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It has been a long time since I started writing this story. I lost my muse half way through it and I didn't have the urge to pick it up again. I hope this is better than the last one. We'll see. Thanks for reading and thanks for the comments, I really appreciate them.
Chapter 7 Sharing is Caring Steven had sufficiently loosened up Sean's ass and felt like he was ready for his big dick. He suggested that the two get up on the bed and Sean didn't complain. I doubt the floor was all that comfortable anyway. Sean got up and lay down next to me in the same position in which Steven had first fucked me.
He turned his head to face me. "This is really gonna hurt isn't it?" Sean asked me. "Just at the beginning. You've been fucked before haven't you?" "Yeah.
But nothing this big. This had better be worth it." "Trust me, it will be." Steven had taken this time to lube up his cock and get into position. He was positioned over Sean with his left arm holding him up next to Sean and his right hand holding his dick.
Slowly Steven brought his cock to bear and pressed it against Sean's hole. Sean inhaled sharply and held his breath. "Relax!" I said, "Just go with the flow." Sean exhaled and started to relax as Steven started to rub his cock up and down Sean's crack. Each time Steven's cock made contact with Sean's hole Sean relaxed a little and wanted Steven's cock in him just that much more.
Finally, after Steven decided Sean had relaxed enough, he started to apply pressure on Sean's hole. "Breathe," Steven commanded. Sean consciously tried to relax as Steven pushed.
It took longer than expected but Steven's head eventually popped into Sean's ass. "Jesus!" he yelped. Steven held still not wanting to hurt Sean and also held in place by Sean's tightened sphincter. He sat there as Sean slowly got used to the size.
"Ok," Sean eventually said, "Push." Steven gently started to apply pressure again. Slowly Steven's cock started to sink into Sean.
Sean's face was a mixture of pain, pleasure, and disbelief. From experience I could understand all of it. His eyes were closed and he was breathing very deeply.
After Steven had gotten about two inches of his dick in he paused to let Sean adjust. Steven started to rock his cock in and out little by little. With each inward thrust Pigtail blonde teens toy fuck hardcore and lesbian would push a little more of his cock into Sean's ass.
In a couple minutes of doing this Steven managed to get a bit more than half of his eva adman mom nirmsaaj sex inside Sean and the expression on Sean's face had turned to one of pleasure but Steven couldn't see that.
"How are you doing?" "Great. Ready for more." "You got it." Steven decided that it was time to move on to just pushing his dick in. Now that Sean was ok with what was going on the rocking in was just taking longer than it needed to. He pushed harder than he had before and his cock started to sink deeper into Sean's hole.
"Mmmmm," Sean moaned. Suddenly Steven switched direction and started pulling out of Sean's ass. He didn't stop until he had pulled the full length of his dick was out.
He laughed. "I think I can see straight through you." Sean smirked. "You gonna stick that back in me or am I gonna have to recruit Tyler?" Steven grinned and lined his dick back up with Sean's hole. He pushed half of his dick into Sean in one motion. Sean gasped. "What do you think?" "That I want the rest." "You got it." Sean started pushing his cock into Sean again.
I watched as two more inches of Steven's dick disappeared into Sean's hole. Sean's breathing wasn't deep like it had been earlier. His breathing was much more ragged, the breathing of a man experiencing great pleasure. There was only about two more inches of cock left outside of Sean's body when Steven next stopped pushing in. Once again he backed off but not all the way. He still had about half of his dick inside Sean.
It looked really hard, the veins on his shaft bulging. He must have wanted to fuck Sean like crazy. Can't say I blamed him. With one final thrust and a grunt Steven planted the full length of his dick inside Sean.
His balls smacked against Sean's and their bodies slapped together. "Uggh!" Sean looked to be in pain. His eyes closed tightly and he grabbed the sheets.
Steven held into that position, once again letting Sean get used to having all that meat inside him. He looked to be in a little pain as Sean's sphincter squeezed his cock as he sought to adjust to being so full. I grabbed Sean's hand which was clenching the sheets in his fists. "You ok?" Sean's eyes opened up. There were tears in the corners from the pain.
I repeated myself, "Are you ok?" "Yeah. It was just really sudden." "Sorry," Steven said sheepishly, "It was just so tempting." It wasn't long before Sean had gotten over the pain enough to continue. Steven slowly started to withdraw his cock. He pulled out until just the head of his dick was inside Sean before pushing back in to the hilt. This time Sean moaned in pleasure. Steven repeated the motion, pulling out and pushing in, faster and faster.
With each thrust his balls slapped against Sean. It was so hot to see my 14 year-old brother fucking the brains out of this sexy boy we'd just met earlier in the day. "Knock knock" "Huh?" I looked back. Josh was standing behind me with his hard dick in his hand.
"Can I come in?" He grinned. "Please do." Josh pulled a Steven and just spit in his hand and rubbed it down the length of his shaft to lube it up. He got into the same position that he'd first fucked me in and easily slid his length into me. I didn't need any time to get used to his dick and he started thrusting into me right away.
Next to me my younger brother was fucking Sean while Josh pounded me. It was straight out of a porno and I loved it. Steven and Josh started to synch their thrusting so that they were in rhythm.
They were thrusting together, pounding the living daylights out of me and Sean. I loved Josh's cock just as much now as I had the first time he'd shoved it in me. He didn't fill me up as well as Steven's but he used that dick like a pro. Soon we switched positions. Sean flipped onto his back and I moved over him into a 69 position while Josh fucked me from behind and Steven fucked Sean.
Sean and I sucked each other off. It was wonderfully intense and I loved the feeling of having my dick sucked while I was fucked. The four of us were fucking and sucking like animals oblivious to the world around us. After we were done we would realize that Tyler had gotten dressed and left sometime during our four-way fuck session. Oh well, his loss. For elas gostam e de pau grande kc minutes we continued in that position before Steven announced that he was close to cumming in Sean's ass.
Steven was going to cum deep inside someone's ass and I was going to be able to watch his cock pulse. "Give it to him!" Josh encouraged. Josh slowed down his thrusting to watch. Sean's cock stiffened even more in my mouth at the prospect of Steven cumming inside of him.
This boy better not cum yet, I had other plans for his cum. I let his cock fall out of my mouth. "Ugghh. I'm cumming!" "Yes!" I could see Steven's cock jumping slightly in Sean's hole as he pumped a large load of sperm into Sean's ass. I knew how good it felt to feel Steven's cock shooting cum into me and I envied Sean for a second before I realized that I could get as much of Steven's cock as I wanted until I went off to college.
Steven held his cock in deep, breeding Sean like only a huge cock could. Steven's hands gripped my shoulders as he deposited his large load inside Sean. With each wave of his orgasm he squeezed my shoulders.
Steven slowly pulled his cock out of Sean's ass. His big dick seemed like it went on forever as it left Sean's gaping hole. He was already going soft but was still quite large. It glistened with his sperm.
"Jesus!" Sean moaned between breaths, "That was fucking amazing!" Sean reached back and ran his finger around his hole before sticking it inside himself. "Holy fuck!" Sean couldn't believe how much Steven's dick had stretched him out.
He lay there basking in the euphoria of a great fuck by a big dick while Josh continued to ram me from behind. Sean lay there, breathing heavily, his dick still rock hard. My dick swung above him, bouncing around at each impact of Josh's body against me. Steven sat down on the edge of the bed to watch us. I stared at Sean's cock. I didn't know how much longer Josh would be able to last but I wanted to try something. "Do you think you could both fit inside me?" I wondered out loud.
In the commotion nobody heard me. "Do you think you could both fit inside me?" I asked again, looking at Josh this time. "You mean like both of us fucking you at the same time?" I nodded. "Well, if you can handle that," Josh motioned towards Steven's cock, "I'm sure you can handle the two of us." He was probably right.
I was still really loose from Steven and Tight young blonde with glasses wants hard cock dicks. "Ok, let's do it." Sean said, crawling out from under me.
Once again, the question was asked. "How do we do this?" "I've seen it done," Sean said, "Josh, lay on the edge of the bed and Charlie get on his cock facing him." We arranged ourselves as Sean suggested and waited for what came next. Sean got behind me and placed his cock at my already stuffed hole.
He poked around a bit, pushing against me, trying to force his dick inside. It just wasn't working; my ass wasn't stretched quite enough to have both of them inside of me despite being fucked by both Steven and Tyler.
"Josh, pull out a little bit." Josh backed his hips back a bit, pulling back until less of his dick was in me. His dick wasn't as thick there and there would be more room for Sean to try and slide his in. Once again he pressed his dick against my already occupied hole and tried to force it in. This time I could feel him making some headway. He was able to slide some of his dick in but not much. Despite the stretched out state of my ass I wasn't able to get both of them in quite yet.
Sean kept pressure on my hole as Josh began to slowly fuck me. He didn't pull out his dick entirely, but instead pulled out just enough so that Sean's cock slid in a bit more with each cycle.
It hurt a bit as Josh and Sean slowly stretched out my ass with their dicks but at the same time I knew it would soon feel amazing to have both of them fucking away inside me. After a couple minutes of this back and forth I had both Sean and Josh ball's deep in my ass and I couldn't believe how stretched out I was going to be when this was through.
Josh and Sean started to work their dicks in and out of me opposite one another. As Josh pushed his cock in Sean pulled out and vice versa. In this way I was never lacking in a cock deep inside me and they could fuck me hard. I'd thought having Steven fucking me was heaven but I was wrong.
When he fucked me I only got him going one way at a time. Though he fucked me fast it was nothing like this.
No matter what was going on one of them was always deep inside me. "You really are a slut." Steven grinned, "God I wish I'd known that sooner." All I could do was mew in response as these two horny teens pounded my hole. My cock was rock hard and sandwiched between me and Josh. I couldn't touch it and it was throbbing. I could feel the wetness of my precum between us.
I kissed Josh, taking his tongue into his mouth and he moaned. Sean bit my neck as he thrust into me a little bit harder than he had been, hitting my prostate dead on. My eyes rolled back in pleasure and my mouth dropped open, panting. Holy fuck this was intense. I can't even begin to explain how I felt. I had two roughly average size cocks pounding my ass as I was sandwiched between two really hot guys and they were both going to cum inside me soon enough.
They were thrusting into me hard and fast never giving me time to recover as one's cock filled the void which had just been vacated by the other. And just when I thought it couldn't get any better Steven shoved his cock into my wide open mouth.
He was straddling Josh and I can't begin to understand how I hadn't noticed him. "I think I have some more in there. Let's see if we can't get it out." He didn't have to tell me twice. I started going to town on his cock. I took the head into my mouth and swirled my tongue around it before bobbing up and down the shaft.
But it was hard to keep a good seal with my lips with the constant gasping and moaning that Josh and Sean caused. I could hear their ragged breathing in my ear and knew that this wouldn't be lasting too much longer. I was already surprised they had lasted this long given that they were both pretty close when we started this amazing experiment.
I, too, was getting close from all the constant pounding of my prostate and the rubbing of my cock and our stomachs. I wasn't going to last much longer. "I'm getting close. Oh fuuccc-" Josh moaned and stopped thrusting his hips.
Sean kept thrusting and I looked into Josh's eyes as he began to cum inside me. This was so fucking hot. He was shooting a pent-up load deep inside me. And through all of it I tried to keep sucking Steven's cock though I wasn't doing a great job. "Oh man! I can feel you cumming!" And that was it. Without even touching it my cock burst between us as my ass squeezed their cocks.
My cum sprayed our stomachs and it was quickly smeared between us as Sean kept humping, trying to cum. I couldn't handle it anymore and gave up on Steven's cock.
I let it drop from my mouth and he backed off realizing that I had too much right now. He started to jack off watching.
"Uggh" I groaned as I rode my orgasm to its finish. "Yes! Yes!" Sean planted himself balls deep in me alongside Josh's cock and it started to pulse. His sperm boiled up from his balls, through his cock, and into my bowels where it coated Josh's slowly deflating cock. "Uggh uggh little girl and grandpa sex he breathed out. "You were right, I can feel your dick throbbing and I can feel your cum on my cock." Sean briefly collapsed on top of me to rest.
After he had recovered a bit he gently pulled his cock out of my ass. I felt so empty and I still had Josh's inside me. Josh reached around and slowly pulled his cock out of my ass though we didn't move from the position. "Can I?" Steven asked, "It won't take long." I nodded. Steven moved into position and slid his cock into my hole. He didn't seem so thick anymore. He thrust into me quickly, trying to get his rocks off. It didn't take long before he slammed his dick into me and I got my 7th load of the night inside me.
He pulled out of me and slowly helped me up. I was physically weak from what I had gone through. He lay me down on the bed and I lay there.
Sean and Josh cleaned up and got dressed. Josh thanked me for the fuck and left, leaving Sean behind. Sean thanked me and Steven for a great time.
He kissed me and handed me his phone number on a piece of paper. "Steven said you're thinking about coming here for college. If you do, look me up." He winked at me, walked to the door, and left. "Holy fuck," Steven said. "M'hmm" was all I could manage. "Let's get you cleaned up." Steven turned on the shower and helped me in when it had warmed up.
He got in with me and slowly blonde suck fuck and cumshot me. When we were done he washed me and carried me into bed. He tucked me into bed and covered me with kisses. Steven crawled into bed beside me and snuggled up next to me. "I love you so much Charlie." "I love you too Steven." "If you were to date Sean when you go to college… I… I'd be ok with that. He's a nice guy." I smiled at Steven and he laid his head on my chest.
"But for now, you're mine." "Sounds perfect to me." "Sweet dreams Charlie." "Sweet dreams." End of Chapter 7.


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Our History
Zibo Kang Hui Glassware, founded in 2008, is one of the leading manufacturer and supplier of glassware products in China. And we have a rich experience in the field years before the foundation. Now we can supply a comprehensive range of products including beverage glass, tableware and decorative glass, etc.
11 years focus on the development and production of glassware. With more than 2,000 square meters of plant. It has more than 56 employees, guaranteeing a daily production capacity of 50,000pcs. The founder has more than 15 years of exper... [Details]

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Vintage Tommy Hilfiger Colour Block (XL)
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Check out our sizing guide for more info here.


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With a Pocket Troops Hack Tool, you can add real cash and coins to your game account for free. Lucky for us to have just such a hack for Pocket Troops on our site!
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About Pocket Troops
Pocket Troops is a kind of mouth-sized war game that works well on a mobile platform. It's so involved that it keeps your attention, and you never feel like wasting your time here. Plus the tiny, angry army guys are adorable!
There's a weird backstory with a bad guy planning to take over the world to make everyone wear black – because everyone looks fine in black, obviously – but you'll probably spend more time against other players or to fight any enemy, than to continue with the story. Mostly because story missions increase rather quickly (and can not be repeated) and because the card is constantly overcrowded by such encounters.
These battles are mostly freehand, which can be both good and bad, depending on what you are looking for. When performing in story missions or in random clashes with enemy soldiers, you have a small amount of control – meaning calling things like air strikes, healing troops between battles, and setting goals before the start of a battle.
What I actually get back to Pocket Troops is the progress of my soldiers. To train them (ie to increase certain statistics such as health and accuracy by spending cash in the game and waiting longer), you can acquire / combine / equip them (including some of them) by regularly battling (unlocking the additional slot) and various abilities can be shared with other soldiers), this creates a fairly satisfying sense of achievement. Granted, it may take some time if you have limited training slots and a tiny armory, but I enjoy it more than the actual fight. Which is funny.
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As simple as it is and how little direct interaction it may be, I find the game quite enjoyable. It's perfect for a few minutes at a time whenever you have a free moment and desire. And I love it when I train and improve soldiers. But it will definitely not fade anyone with its strategic depth. Of course you can also do a lot with the Pocket Troops Hack for Android and iOS. Our Pocket Troops cheats are the best on the internet.


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Here it is again Horizontal wind Straightens the flapping flag Stops the dog's wag Clears branches of their leaves Breaks spider webs in the eaves When His wind rolls It's just one direction it goes Stones and twigs Grass and any object no matter how big Is supernaturally pushed Along a path He once took … Continue reading Horizontal Wind
Category: Power
Hallelujah to the God of all Creation!
(Photo credit from a brother in Christ, Steve Keagle). His plenty corn His painted sky Let us dare not pass Him by Heaven's fire Lights the horizon Ablaze ... amazing Overcomes the weakest souls Shouting emboldened praise Glimpse of Christ In all His glory Let our voices unite and raise: Hallelujah! Receiving His power Streaming … Continue reading Hallelujah to the God of all Creation!
Falling in Love with Jesus, A Poetic Journey
As I look into the blank white sky I feel nothing But I believe with every part of my being Every breath I am given Every skin cell Every thought slave be to Jesus He is King of us He is Lord And Savior Sent to be with us Immanuel lowed to earth Literally to … Continue reading Falling in Love with Jesus, A Poetic Journey
She is a Warrior
a warrior she stands alone anchoring to Jesus no matter what comes a warrior she speaks life and hope offers herself as a vessel, a God-given rope a warrior she fears not for she trusts He goes before wherever she trods a warrior her life not her own risking death, meeting scorn she moves within … Continue reading She is a Warrior
Morning Glory
The hint of pink teases those in wait for His glorious day to undress the night leaves thick with ice branches stiff just as our knees crick Pink, His hope-color delivers His promise of valor New … not sudden or flashy Rather, truth living in you and me Passion, bravery Glory to glory Morning to morning … Continue reading Morning Glory


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Molissa with Christiana Axelsen, Betsy Cooper and Holley Farmer present a full evening of dance at the Toscana Dance HUB in Florence and Agropoli.
Please join us at any and all events!
Love, Molissa
Attic short from Michael Mersereau on Vimeo.
Molissa Fenley, one of the most influential artists of postmodern dance, has had a lasting impact on performance. In dance, she has explored extreme effort and duration in highly crafted patterns and performed with an explosive, joyous energy that infused her work with endurance, balance, and life force. She challenged modern dance orthodoxy and redefined the character of a woman's moving body in the late twentieth century, bringing postmodernized ritual to the stage.
Rhythm Field is a vivid and probing portrait of Fenley's four-decade career, written by her fellow artists. The collection functions as a multifaceted look into one woman's complex performing arts legacy. The result is itself an aesthetic undertaking that investigates the ways in which Fenley straddles dance traditions, art genres, and gender norms and has been a model to the field. The collection offers several scholarly analyses of the choreographer's work, and is, above all, a vibrant record from the field. Rhythm Field sits at a necessary midpoint between criticism and scholarship.
Rothwell Theater
May 2, 2020, 3pm - free event
Click here for details
Various venues in Firenze and Agropoli
July 12-25, 2020
Click here for details
September 15, 2020, doors open 7pm, performances at 8pm
Click here for details
Redwood Park (Part 1)


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What Exactly Is Tetrahydrocannabinol (THC)?
Tetrahydrocannabinol (THC) may be the chemical in marijuana in charge of all of the plant's notorious effects that are psychotropic. It had been very first foundin 1964 and had been separated and synthesized through the cannabis plant by way of a Bulgarian-born Israeli organic chemist called Dr. Raphael Mechoulam.
It really works by connecting it self to your cannabinoid receptors in mental performance. These receptors are concentrated within the certain areas connected with memory, time perception, coordination, thought and pleasure. The THC activates the receptors, therefore affecting these certain regions of the mind in several methods.
THC can be found in the resin for the cannabis plant, secreted by glands that are predominantly discovered round the plant's reproductive organs. It's not The chemical that is only present in this resin; you can find about 85 other cannabinoids with cannabidiol (CBD) possibly the most commonly known.
Just Exactly What Effect Does THC Have in the Human Anatomy? (more…)


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Bacon Candy
Bacon Candy! This stuff is CRAZY GOOD and will be ILLEGAL when the food police hear about it! For a special treat think about this. Bacon Candy is so simple to make, only 3 ingredients. Sweet, smoky and just melts in your mouth. Patti and I came to the conclusion that Bacon Candy is just plain Dangerous in a really delicious way. It is so good and rich it's hard not to eat it all. We only ate 2 pieces each, but thought about it the rest of the day, you will be amazed by how it just melts in your mouth.…
Easy to make, we loaded up our Bull Racks on the Green Mountain Grill at 275 degrees for an hour. The rest is just incredibly yummy history.
Bacon Candy
A Pellet Grill Recipe
Prep Time: 5 minutes to mix, few hours to blend
Cook Time: 1 hour @ 275 degrees (135c)
Grill: Green Mountain Wood Pellet Grill
Pellets: Lumberjack Hickory
Ingredients: Bacon Candy
- 1 Lb. thick sliced pepper bacon
- 1 package brown sugar
- ½ cup black pepper, or to taste
Directions: Bacon Candy
Cut your bacon in half for easier handling. Mix the brown sugar and pepper in a large bowl, and then mix in the bacon. Mix well with your hand and set it aside. The sugar will melt and as it does give the bacon a few turns in the bowl. You'll see the sugar will liquefy (an hour or so) and when it does mix the bacon well and you're ready for the Bull Racks and the grill. We did these for 1 hour @ 275 degrees (135c), but that will vary a little by the thick cut of bacon you use and how well you like your bacon done.
When the bacon is done pull it and let it COOL, the sugar glaze is HOT and will stick to you. When it is cool enough to taste you will be amazed by how it just melts in your mouth.
Bacon Candy
A Pellet Grill Recipe
Our Ingredients
Cut the Bacon in Half
Bacon Candy
A Pellet Grill Recipe
Mix Brown Sugar and Pepper
With Time the Sugar Will Liquefy
Mix well for a Nice Coating
Bacon Candy
A Pellet Grill Recipe
Lay Out on Your Bull Racks
In the Smoke
We are so Ready
Note: I get a lot of questions about the kind of pellets you can use with a recipe. Keep in mind that a recipe is just an outline. Some you need to follow closely like when you are making bread, but most you can do anything you can dream, our favorite way to cook. Feel free to mix and match the pellets until you find a combination you really like. Also you are only smoking at temps less than 250 degrees (122c), anything higher is cooking and there will not be much if any smoke so it does not matter what kind of pellet you are using.
Bacon Candy
A Pellet Grill Recipe
Cooking In the Oven:
We have been getting requests for recipe conversions for the Pacific Living Outdoor Oven. I tell folks all the time that cooking on a Wood Pellet Grill/Smoker is just as easy as cooking in your oven. Just about anyone can do it and do it well. Think about it. You set your control knob to the temp you want, put your meat in and leave it for a set time.
It is the same thing, time and temperature is what it is all about. The Green Mountain grill is just like your oven except it uses wood pellets and has wheels.
Do these for 1 hour @ 275 degrees (135c)
Note: The Pacific Living Outdoor Oven also has a smoke box. Let's Eat!!!
Bacon Candy
A Pellet Grill Recipe
About our Recipes
We do our recipes on our patio where we have a lineup of grills, including Louisiana, Green Mountain, Royall, Memphis, Traeger pellet grills, Char Griller side box smoker, Saber, Charmglow, Char-Broil, The Big Easy, Pacific Living Outdoor Oven, Lodge Sportsman's, Brinkman and Weber. I call it our "Wall of Grill". Our grilling styles are healthy and low fat and will fit pelletheads, gas, natural wood and even charcoal purists. Almost any of our recipes can be done on any kind of good BBQ.
The important thing to keep in mind is TIME & TEMPERATURE. You can even do some of them in the oven or crock pot, but, then you lose all the flavors you get from cooking outdoors. But sometimes it does rain.
Remember that a recipe is simply an outline; it is not written in stone. Don't be afraid to make changes to suit your taste. Take it and run with it….
Live your Passion,
Ken & Patti


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We made fine films, once
Irish cinema looked set to conquer the world, but then lost its way and is now struggling to find a way forward. Where did it all go wrong?
Our moment finally came that night in March 1990 at the Dorothy Chandler Pavilion in Los Angeles. Kevin Kline drew Brenda Fricker's name from the envelope and she clutched her chest in shock. She had just beaten Julia Roberts and Anjelica Huston to the Academy Award for best supporting actress for her role in a small Irish film. My Left Foot, Jim Sheridan's debut, had also been nominated for four other awards, including best picture.
"I will take it very proudly back to Ireland," Fricker said, holding the Oscar aloft. Later that night Daniel Day-Lewis strode on stage to pick up the film's second award, for best actor. With his mane of dark hair gleaming, he announced: "You've just provided me with the makings of


text:
The "Organ-Disease".
The fruit fly, Drosophila melanogaster (Meigen, 1830) has been established as a key model organism thanks in part to their considerable biological similarity to mammals and an abundance of available genetic tools. Drosophila have been used to model many human disease states and have been critical in elucidating the genetic mechanisms contributing to them. Part I of this chapter covered basic Drosophila biology and relevant genetic tools available to Drosophila researchers. Here in part II, we review the use of Drosophila as a model organism to study neurodegenerative disorders, cardiovascular diseases, kidney diseases, cancer, metabolic disorders, and immune disorders, as well as key findings made in those fields thanks to Drosophila research.
- animal model
- cancer
- diseases
- Drosophila
- genetic techniques
- heart
- immunology
- kidney
- metabolic disorders
- neurodegeneration
1. Introduction
Please refer to the Introduction of Part I, The fruit fly, Drosophila melanogaster: The Making of a Model.
In this two-part chapter, some of the many aspects that make Drosophila such a fundamental model organism are covered.
Part I covered the basic fly biology and key genetic tools.
Here, Part II provides an overview of important disease states that Drosophila is used to model and some significant advances made in those fields.
2. Drosophila melanogaster as model to study human diseases
Drosophila melanogaster is a widely used model organism to understand many molecular and developmental processes common to higher eukaryotes. A prerogative for a good model system is to share higher physiology within the molecular pathways with humans, and it is remarkable that approximately 75% of genes associated with human diseases have Drosophila homologs and share similarities in their functions, which is of particular interest for medical purposes [2]. Based on this genetic similarity, the fly is a valid tool for understanding the function of genes involved in human disorders. Clearly, Drosophila has the limitation of being an invertebrate system, as some biological processes evolved only within the vertebrate lineage. Despite this, Drosophila exhibits complex behaviors, and each phenotype observed must be contextualized considering that mammalian physiology is not very different from that of the tiny fly. It is not easy to choose an appropriate organism to model a disease due to the higher complexity of humans, and it is necessary to evaluate the nature of the pathology before choosing. Drosophila provides a good background for genetic and biological studies of different pathological conditions such as neurological, cardiac, and metabolic disorders ( Table 1 ).
|Organ system
|Brain and nervous system
The Drosophila brain is two-lobed and contains approximately 100,000 neurons. It is organized into several main structures including: supraesophageal ganglion (optic lobes and cerebrum) and a subesophageal ganglion. Flies also have a segmented nerve cord similar to a mammalian spinal cord (FLYBRAIN neuron Database)
|Immune system
Circulating immune cells called hemocytes (consisting of plasmatocytes, lamellocytes, and crystal cells) fight pathogens by encapsulating them, generating ROS, and/or producing antimicrobial peptides (AMPs). Many tissues are also capable of generating AMPs including the gut and fat body [72]
|Digestive system
Consists of mouth parts for chewing, salivary glands to produce saliva, a crop (similar to a stomach), the proventriculus for grinding food, and a gut (midgut and hindgut) for digestion and nutrient and water absorption
|Excretory system
Structures called Malpighian tubules and nephrocytes function similar to kidneys and filter nitrogenous waste from hemolymph. The tubules connect to the hindgut and excretory waste is eliminated along with digestive waste in the form of uric acid
|Circulatory system
Drosophila has an open circulatory system. The tube-like heart (consisting of the dorsal vessel and the aortic arches) circulates hemolymph (insect blood) around the body cavity
|Respiratory system
Drosophila, like many other insects, does not carry oxygen in their hemolymph. Instead, a system of trachea connects directly with organs for gas exchange. Trachea open to the environment though tiny holes in the exoskeleton called spiracles
|Energy storage
Flies store glycogen and triglycerides in a specialized structure called the fat body. The fat body has functions similar to the mammalian liver and adipose tissue and is heavily involved in regulating growth, metabolism, and the immune system [16, 73, 74, 75].
|Reproductive system
Flies have ovaries for egg production in females, and testes for sperm production in males. These structures develop from imaginal discs in the larva. A fertile female fly can lay hundreds of eggs
|Musculoskeletal system
Flies have an exoskeleton composed mostly of a chitinous cuticle and an outer waxy coating. The cuticle is produced by epithelial cells and can be hard like bone or softer (as in the case of larvae). Muscles attach to points inside the exoskeleton and allow the fly to move
Drosophila has certain characteristics unique to insects such as an open circulatory system, exoskeleton, and tracheal system for gas exchange; however, they also share many similar organs and biological processes with mammals. The following summarizes the major organ and physiological systems in Drosophila and their comparative function to human diseases.
2.1. Neurodegenerative disorders
The Drosophila central nervous system (CNS) is composed of a bilaterally symmetrical brain with two cell types, neurons and glia, both originating from neural progenitors named neuroglioblasts. The fly CNS is considerably simpler than that of vertebrates and the neurodevelopment pattern is conserved among the organisms. Wnt, the mammalian homolog of the Drosophila wingless plays an important function during neuronal development [7] and Notch signaling, which plays a pivotal role during neurogenesis and neuronal differentiation, is also evolutionary conserved [8]. Neurons attend to neurotransmission while glia sustain the neurons during development and adult life mainly by providing trophic factors [9, 10]. When studying neuropathies, it is relevant to consider the interaction between neurons and glia, and research in Drosophila is contributing to this. In fact, the power of the neurodegenerative fly model is in the ability to explore the disease in a physiological context. While glia support neuronal survival and promote recovery in cases of neuronal damage, impairment of glial function induces non-autonomous neuronal death. Glial anti-neurodegenerative functions suggest using them as targets in human neurodegeneration [11]. The Drosophila brain, in particular the visual system, is widely employed for research related to neurodegenerative diseases [12]. The nervous system of people suffering from these debilitating conditions exhibits the progressive loss of neurons. The origins are disparate, and in many cases, they are unknown so it is necessary to intensify the research, aiming to understand how to treat them. Interestingly, insects lack the human hematoencephalic barrier allowing for pharmacological screening directed at the central nervous system. Depending on the mechanisms inducing the disorder and the symptomatology, we can differentiate several types of human neurodegeneration. Most neurodegenerative disorders are characterized by the presence of protein aggregates in the neurons that are different for the various classes of diseases. Despite identifying many causative factors, it remains to be determined how these proteins become neurotoxic. Thanks to the precious genetic tools available, the fly is an excellent model to explore the function of the genes coding for the proteins involved. In addition, the molecular pathways are remarkably conserved allowing for parallels with humans [13]. The simpler fruit fly CNS allows for a better understanding of the function of a gene involved in a disease and its relationship with the other neuronal patterns.
In order to characterize neuronal dysfunction in Drosophila, several approaches can be used including testing motility, individual and social behaviors, hearing, learning, and memory [14, 15, 16]. A histological method based on measuring the vacuoles in adult fly brains allows for the quantification of neuronal degeneration [17]; moreover, electrophysiological assays enable the analysis of synapse functionality [18]. Fruit flies affected by neurodegeneration share behavioral defects and reduced lifespans.
Drosophila is already used to investigate proteinopathies (protein misfolding diseases) such as Huntington's disease, amyotrophic lateral sclerosis, and spinocerebellar ataxia [19, 20, 21]. The cause of Huntington's disease (HD) is the expansion of CAG repeats in the huntingtin gene, leading to a polyglutamine (poliQ) repeats in the huntingtin (htt) protein. Htt is required for axonal transport and synapsis, and the fly homolog shares the same expression pattern and function [22]. The poliQ expansion is toxic also for Drosophila neurons; in fact, the fly gradually loses photoreceptors when human htt is expressed in the eye compartment. When human mutated genes encoding for polyQ are expressed in Drosophila, there is a phenotype comparable to the human disease, for instance late onset, progressive loss of neurons and motility, and premature death, and the formation of large protein aggregates of mutant Htt visible also in neurons of Drosophila ( Figure 1 ). The Drosophila HD model has contributed to some findings, for instance it uncovered that the histone deacetylase (HDAC) controls the level of neurodegeneration, making it an important achievement for human poliQ diseases [23]. In the fly, as in humans, the neurodegeneration rate is related to polyQ repeat length [24]. Spinocerebellar ataxia (SCA) is another disorder originating from abnormal CAG repeats. Humans can be affected by several types of SCA and ataxin is the mutated gene. Autophagy is a fundamental process to limit the poliQ aggregation, and in a fly model of SCA3, autophagy proteins are overexpressed allowing for a rescue of the toxicity [25]. Amyotrophic lateral sclerosis (ALS) is a disease characterized by loss of cortical and spinal motor neurons [26]. Several genes are involved in ALS and most of them can be expressed in Drosophila to assess their contribution to neurodegeneration. A causative factor of ASL is a mutation in superoxide dismutase SOD1 [27], and interestingly, loss of Drosophila SOD1 causes neuronal death while human SOD1 expression increases the fly lifespan [28, 29].
Tauopathies, including Alzheimer's, Parkinson's, and others, refer to disorders caused by aberrant accumulation of the microtubule-associated protein tau [30]. Drosophila has a tau homolog and the pathways involved in tau neurotoxicity such as wnt, JNK, and TOR are shared with humans [31, 32, 33]. More than 30 transgenic fly models have been established that express various forms of human wild-type and mutant tau and have uncovered many potential mechanisms for tau toxicity in a variety of neurodegenerative diseases [34]. Alzheimer's disease (AD) is one of the most common neurodegenerative disorders and yet its pathogenesis is still unclear. The tiny fly is once again a good organism to model this affliction because the AD-associated genes, such as APP and presenilins, are evolutionarily conserved. The brains of Alzheimer's patients are marked by aggregation of beta-amyloid protein and neurofibrillary tangles (NFTs) originating from hyperphosphorylation of Tau [35]. Tau expression induces learning and memory deficits in Drosophila, mimicking AD in humans [36]. Some recent advances uncovered by Drosophila Alzheimer's models include: explaining the mechanisms behind the phosphorylation of tau and its toxicity [37, 38, 39, 40] along with ways to reverse it [41, 42], as well as linking DNA damage and oxidative stress triggered by tau phosphorylation in causing neurotoxicity [33, 43]. Moreover, Drosophila models are helping researchers to uncover the interaction between beta-amyloid proteins and tau and how they cause neuronal death [34]. Parkinson's disease (PD) is characterized by the progressive loss of dopamine neurons in the substantia nigra, a part of the brain responsible for motor control, as well as the formation of protein accumulations known as Lewy bodies, which are composed primarily of alpha synuclein [44]. Many mechanisms have been proposed for the cause of this neuronal death including disruptions in protein degradation, oxidative stress, mitochondrial dysfunction, autophagy and lysosomal dysfunction, and problems with calcium homeostasis [45] Furthermore, phosphorylated tau has been found to be associated with alpha synuclein in Lewy bodies [46, 47] and the two may function together to destabilize microtubules and damage axonal transport, also contributing to cell death [48]. Many fly models exist to study Parkinson's disease [49]. The fly dopamine neurotransmitter is similar to the human version and its function in movement is conserved [50]. Homologs of several PD-related genes are present in Drosophila, allowing researchers to model this neurodegenerative disease [51]. Drosophila models are currently being used to test a variety of potential therapeutic approaches, including boosting antioxidant mechanisms, reducing the oxidative stress caused by dopamine metabolites, and using inhibitors for members of the TOR pathway to improve Parkinson's symptoms [49].
2.2. Cardiovascular diseases
Drosophila melanogaster and humans share some aspects of heart development and function making the fly a good model for studying cardiovascular diseases, which are the leading causes of death worldwide. The heart precursors of Drosophila originate in the lateral mesoderm and converge on the dorsal midline to form a linear tubular structure comparable to the early vertebrate embryo heart. In Drosophila, a simple contractile tube pumps the hemolymph through the larval body cavity in an open cardiovascular system and regulates cardiac rhythm ( Figure 2 ). The cardiovascular system has an anteroposterior polarity and it consists of the posterior portion named the dorsal vessel, corresponding to the heart, and the narrow anterior portion named the aorta, which facilitates the transport of hemolymph to the head [52]. The dorsal vessel is made up of two cell types: the cardiomyocytes, which are the inner contractile muscle cells, and the pericardial non-contractile cells, which flank the cardiomyocytes. The human heart has four distinct chambers, likewise the fly heart is divided into four chambers, each one consisting of six myocardial cells [53] that have a sarcomere structure similar to mammalian cardiac cells. The hemolymph flow moves nutrients, immune cells, and molecules required for homeostasis; however, oxygen is transported through diffusion from spiracles that invaginate from the cuticle into the interior of the animal. Despite the fly dorsal vessel being much simpler than the mammalian looped heart, the signaling pathways involved are remarkably conserved [54]. Cardiogenic genes required for the proper development of the Drosophila embryonic heart were identified through genome wide screens [55] showing that many molecules important for heart development and morphogenesis are conserved in humans [56]. Tinman is a homeobox transcription factor discovered in Drosophila and it is a master gene of cardiac development conserved in higher organisms [57, 58]. In addition, pannier and hand, which play crucial roles for heart specification as well as neuromancer, have counterparts in humans [59, 60, 61]. Moreover, these signaling pathways are required for some adult function both in Drosophila and in mammals suggesting that they have a conserved physiology [62].
Even if most studies are based on the embryonic development of the fly heart, nowadays the focus is shifting to the function and structure of the Drosophila adult heart as a model of human heart defects. Indeed, the great availability of genetic tools in Drosophila allows for the identification of elements important for heart functions and facilitates the analysis of mutant isoforms associated with congenital heart defects [63]. The physiological mechanisms are conserved among Drosophila and vertebrates supporting the utility of the fly to investigate cardiomyopathies and arrhythmias [52]. The improvement of techniques for the measurement of cardiac performance in Drosophila also permits the analysis of the effect of aging and the stress response on the heart [64]. Cardiac dysfunction can occur naturally in Drosophila, and this phenotype depends on age, just like in humans [64]. Some strategies allow heart rate monitoring in response to externally applied electric pacing in order to understand the effects of aging in adult flies. Insulin-IGF receptor (InR) and TOR signaling play an important role in regulation of age-dependent cardiac performance [65]. Drosophila is also one of the most efficient model organism used to discern the mechanism underlying channelopathies and cardiomyopathies as many impaired pathways are evolutionarily conserved [66]. Cardiomyopathies affecting Drosophila resemble those of humans both in terms of the genes responsible and the resulting effect. Such a similarity among the fly and humans is also found in the case of channelopathies and arrhythmias.
Several assay systems are helpful in characterizing Drosophila heart function, such as optical coherence tomography (OCT), an imaging of the Drosophila heart tube to observe contraction in vivo similar to clinical echocardiography [62]. In addition, semi-automated measurements allow researchers to record heart function to quantify cardiac impairment in Drosophila.
2.3. Kidney diseases
Despite millions of people suffering from kidney disorders, there is a disconcerting lack of therapies available to patients because the primary causes of kidney disorders are not completely characterized. Drosophila is advantageous to model renal disorders since many genes, proteins, and even some functions of the vertebrate kidney have parallels with the fruit fly. Despite many differences due the greater complexity of the human kidney, several orthologous genes have an important role in renal development and function, both in humans and in Drosophila [67]. For example, many genes encoding for electrolyte transporting proteins affected in congenital renal disorders have fly counterparts [68, 69].
The insect Malpighian tubules and the nephrocytes are functionally analogous to the vertebrate kidney; in fact, these two organs in Drosophila guide the metabolite homeostasis and the excretory process ( Figure 3 ). Nephrocytes, which surround the heart and esophagus, are responsible for filtering the hemolymph, similar to the podocytes in the human glomerulus. In addition, nephrocytes have filtration diaphragms similar to the podocyte slit diaphragms that work as a filtration barrier in higher organisms [70, 71]. The Malpighian tubules, corresponding to the tubular part of nephrons, are two pairs of elongated and thin tubes connected to the hindgut that secrete urine after absorption of water, ions, solutes, and organic metabolites from the hemolymph. The principal cells and the stellate cells are the two main cell types in Malpighian tubules involved in excretion [72].
Nephrotic syndrome refers to ultrafiltration dysfunction leading mostly to extra protein in the urine and deficiency of protein in blood [73]. Given the evolutionary conservation of the diaphragms and their regulative mechanisms, Drosophila is a good option to look into this kind of disease. Some events during the renal development are shared between the fly and humans and the molecular pathways are conserved. All the genes playing a pivotal role in renal development, such as Kruppel and Cut involved in cell specification, Dwnt in tubulogenesis, and Sns, a nephrin-like protein, in cell differentiation, have a counterpart in mammals. One of the fundamental phases of Malpighian tubules formation is a mesenchymal-to-epithelial transition that resembles the steps of kidney development [74]. This makes the fruit fly organ able to provide insights on disorders affecting the tubular nephrons such as polycystic kidney disease and renal agenesis [75, 76]. Drosophila is also useful to study nephrolithiasis, also known as kidney stones, since insects also produce stone formations like calcium phosphate and calcium oxalate [77]. A simple method exists to score the filtration and the uptake of a secreted fluorescently tagged protein (ANFRFP) that accumulates in nephrocytes to assess the renal function in Drosophila [75].
The similarities among the species definitely allow the use of the Drosophila renal structure as a model to better understand the basis of human kidney impairments and consequently to develop personalized therapeutic agents. Furthermore, immune and inflammatory responses are trigger factors of kidney diseases so they should be taken into account when analyzing these pathologies [78].
2.4. Cancer and growth
The fly is a simple model to improve the understanding of tumor biology and progression [79, 80, 81, 82, 83] as the available genetic tools support the analysis of the mechanisms underlying growth regulation in an intact epithelium rather than in cell cultures. The advantage is remarkable since cell-cell and cell-environment interactions contribute to tissue size regulation. The Drosophila cell cycle can escape the normal control system leading to the typical cancer hyperproliferation. Reproducing human tumors in Drosophila allowed for the identification of many oncosuppressor genes that regulate cell division and differentiation [84]. In the fly, the tumor hallmarks mimic the human ones: autonomous proliferation signals and overgrowth, irregular cell morphology, bypassed apoptosis, and metastasis [85]. In spite of these similarities, there are several limitations including lack in flies of processes such as telomere maintenance and angiogenesis that participate in cancer development.
A great conservation across species is detected in regards to the signaling pathways affecting growth. Initial studies using activated proto-oncogenes such as the receptor tyrosine kinase (ret), a gene responsible for medullary thyroid carcinoma (MTC), allowed researchers to perform genetic screens for suppressors or enhancers of the rough eye phenotype, which indicates an overproliferation of cells in the eye [86]. These studies evolved to include tumors that were induced by the activation of growth signaling pathways, such as PI3K and EGFR in glia, which resemble human glioma [87], or studies involving tuberous sclerosis, an autosomal dominant disorder characterized by benign tumors in multiple organs induced by the loss of function activity of the TSC1 and 2 tumor suppressor genes [88]. A large number of studies also demonstrated how the Hippo pathway, which regulates growth through the activation of Yki, is highly conserved and required for cellular proliferation as well as for apoptosis, has a human counterpart that retains sequence and function, and is mutated within the context of cancer [89, 90]. The same goes for Salvador, a gene promoting apoptosis, and Archipelago [91, 92, 93, 94]. The two organisms also share PTEN, a tumor suppressor that plays a crucial role in carcinogenesis both in humans and in flies [95].
New studies defined how the loss of cell polarity could be considered a hallmark of malignancy [96]. Members of discs large (dlg) and lethal giant larvae (lgl) were identified as tumor suppressors in the fly by promoting cell invasion if mutated, with a similar role also seen in human neoplasm [97]. The role of proteins involved in cellular adhesion, such as Rho1 and E-cadherin, was also shown to be conserved and relevant for migration and invasion helping the study of the metastatic process [98, 99]. Other well-studied oncogenes in Drosophila that promote overgrowth and cell survival are Ras and Notch and were also shown to play a role in cellular polarity [100]. Dpp, the homolog of human bone morphogenetic protein/transforming growth factor-beta (BMP/TGF beta), is also responsible for epithelial integrity [101] and implicated in a model for cancer in Drosophila. All these parallelisms provide the potential to dissect in vivo the interacting patterns causing the tumor growth.
As anticipated, the communication between neighboring cells must be taken into consideration when analyzing a tumor tissue. Competitive interactions occur among cells with different growth rates in a process known as cell competition, which was first described in Drosophila using ribosomal proteins [102, 103] and then characterized using dMyc, the fly homolog of human cMyc [104]. Cells expressing higher levels of Myc behave as supercompetitors: they survive and acquire a proliferative advantage inducing apoptosis in the weaker nearby cells, termed losers [105, 106, 107]. The mechanisms controlling overproliferation and metastasis are comparable to those involved in cell competition since in human cancer, cells overexpressing Myc acquire the capacity to grow more than normal and to invade the neighboring normal cells. Since then, a few additional oncogenes and tumor suppressor genes have been associated with a competitive behavior, and cell competition is now thought to have an important role in human cancer [108, 109, 110, 111, 112]. This similitude underscores the utility of using flies for studying how cells compete for survival.
More studies are arising on the connection between the insurgence of tumors and diet or obesity. Recent studies linked the growth of prostate tumors and the status of obesity [113]. Caloric restriction reduces the growth of tumor cells in rodent models through reduced systemic insulin and IGF-1 signaling [114], while the activation of PI3K induces tumors to be resistant to diet restriction [115] suggesting an important relationship between PI3K signaling in tumors and the nutrients in the tumor environment. The exact link between obesity and cancer has not yet been established and the fly may facilitate this research thanks to the ability to combine obesity and tumor models in Drosophila. Insulin signaling is the main regulator of metabolic homeostasis, and it is also involved in cancer development and progression [116] but we have yet to understand how hyperinsulinemia promotes tumor formation. Interestingly, the oncogenes Src and Ras were overexpressed in a Drosophila model of obesity and increasing the level of insulin exacerbates the malignant phenotype due to wingless activity [117]. The interplay between obesity and cancer is an important area of study to understand the relevance of fat to tumor growth, since fatty acids are unable to penetrate the biological membranes and need to be cleaved by lipases (lipolysis). Recent studies indicate that in the peritumoural area, an increase in adipose triglyceride lipase (ATGL) that mediates lipolysis results in tumor survival [118, 119]. The ability to manipulate flies genetically and the possibility to change the composition of lipids or nutrients in their food will likely put Drosophila as a key model to investigate the relationship between obesity and cancer and the mechanisms that control cellular overgrowth. Cancer research can only benefit from the ability to create specific disease models in Drosophila. This approach lets researchers detect oncogenes and tumor suppressors, allowing a detailed in vivo analysis of the mechanisms triggering cancer. From these findings, drug therapy compounds can then be developed and tested.
2.5. Metabolic disorders
Hepatic diseases affect a large proportion of the population worldwide making it crucial to investigate the underlying pathogenic mechanisms that still remain unclear. Identification of the molecular defects underlying liver disease requires studies in model organisms, and recently Drosophila has been proposed for this purpose [120].
The use of the fruit fly in the study of hepatic disorders is partially restricted due to the absence of a homologous organ for the liver. The fat body in Drosophila acts as storage for sugar and fat and also performs metabolic functions similar to those of the mammalian hepatocytes, regulated by insulin through an evolutionarily conserved mechanism [121, 122]. During starvation, triglycerides are transported from the fat body into the hemolymph where they are captured by the oenocytes, clusters of hepatocyte-like cells that are important for lipid metabolism [123]. Therefore, some functions of hepatocytes are performed by oenocytes, which are located near the body wall surface and play a prominent role in the fly lipid processing. Drosophila homologs of genes specifically expressed in human hepatocytes are expressed in larval oenocytes and the fat metabolism pathway is similar among the organisms [123]. An interesting aspect regarding lipid metabolism is the interaction between oenocytes and fat cells, as oenocytes control lipolysis in fat cells through a feedback similar to that in mammals [123]. Underfed Drosophila stores many fat droplets resulting in the accumulation of triacylglycerols in the liver, a condition called steatosis, and forms an excellent model for understanding human non-alcoholic fatty liver disease (NAFLD) [124]. Moreover, the relationship between oenocytes and fat cells needs to be elucidated because it contributes to the pathogenesis of metabolic syndrome [125], and fly modeling can be useful for this purpose.
It is necessary to improve assays examining the function of the fat body and oenocytes to solidify Drosophila as a liver disease model. To date, the analyses are based on evaluating lipid accumulation depending on different nutritional conditions. Fly lipid homeostasis can be monitored by Raman scattering microscopy that allows for the visualization of the lipid content in larval oenocytes and in the fat body by in vivo imaging [126]. Oil Red-O and BODIPY are dyes permitting the assessment of lipid content [123, 127].
Several proteins that contribute to lipid metabolism in Drosophila, including proteins responsible for lipid storage, transport, and utilization, have counterparts in higher organisms [128, 129]. This similitude makes the fruit fly helpful in describing the main pathways controlling homeostasis and provides an opportunity to examine metabolic disorders affecting humans such as diabetes and obesity [122]. For example, the main regulator of sugar and fat metabolism is the nutrient-sensing target of rapamycin (TOR) both in Drosophila and in mammals [130]. Flies are able to regulate carbohydrate metabolism by cellular storage of excess nutrients. The hormone insulin controls hemolymph sugar levels and maintains carbohydrate homeostasis through a phylogenetically conserved signaling pathway [122, 131]. Drosophila insulin induces an increase in fat cell mass, just as in mammals, because insulin acts on triglyceride storage and on fat body cell number. Shaggy is a serine/threonine protein kinase orthologous to glycogen synthase kinase 3 (GSK3), and it is responsible for the lipid accumulation in Drosophila fat cells while the transcription factor Drosophila FOXO (dFOXO) influences the adipocyte cell number [121]. Both of these key factors are regulated by the conserved insulin pathway [121]. Dilp2, 3 and 5, members of the Drosophila insulin-like peptides (Dilps) are expressed in the insulin-producing cells (IPCs), a cluster of cells in the brain that function similarly to human pancreatic β cells [132]. Additionally, the adipokinetic hormone participates in fly glucose regulation with a glucagon-like function [55]. Functional changes to these metabolic regulators in Drosophila cause a phenotype similar to metabolic impairment as well as affecting body size [132, 133]. The resemblance between Drosophila and mammals helps to elucidate the main mechanisms of metabolic homeostasis involved in common pathologies such as type 2 diabetes mellitus (T2DM), which is characterized by insulin resistance, hyperglycemia, and defects in lipid metabolism [134]. High-glycemic diets promote obesity, a disorder characterized by excessive fat storage. Drosophila fed a high fat diet store fat in the fat body and in the midgut [135]. This condition changes the animal physiology and lifespan mainly due to insulin resistance [136, 137]. Moreover, obesity is considered among the risk factors for diabetes, cardiac diseases, and several types of cancer [138, 139]. Insulin resistance is also related to NFALD, the most frequent chronic hepatic disorder [140]. NAFLD originates from metabolic impairment highlighting the strong relationship between the liver and metabolism and the subsequent need to examine the pathways linking them [124].
Drosophila has facilitated the study of metabolic pathways thanks to the availability of several assays of metabolic function, including some that are available for use only in Drosophila, which allow for the quantification of lipids, sugars, ATP, and mitochondria. In spite of the anatomical differences between flies and humans, the identification of novel genes and pathways in the fruit fly could arrange for new therapies to treat metabolic disease in humans.
2.6. Immunological diseases
The mechanism of the innate immune system is fairly conserved across species, and Drosophila is a leading organism for elucidating the process of defense from pathogens and its evolution [141]. Since the adaptive immune response of vertebrates could hide some aspects of the innate immunity, it is beneficial to use Drosophila to detail the regulation of innate immunity because this organism does not have an adaptive one [141]. Pathogenic microorganisms, such as bacteria, fungi, nematodes, and viruses, can infect Drosophila, priming an immune reaction. Despite the greater refinement of mammalian immunity, Drosophila and humans share general defense strategies like epithelial barriers, phagocytosis, and antimicrobial peptides. The fly's first line of defense against to pathogens is a physical barrier represented by the epithelia of the epidermis, trachea, and gut. Clotting factors in the hemolymph provide a second barrier because they can entrap invaders by means of their protein filaments [142]. Epithelia then release antimicrobial peptides (AMPs) and reactive oxygen species (ROS), triggering a local immune response [143, 144]. Beside their toxic activity, ROS are involved in wound healing and tissue repair both in Drosophila and mammals [145]. In addition to epithelia, blood cells and the fat body are also required for Drosophila immunity. The external agents are phagocytized by hemocytes; the circulating blood cells and different types of hemocytes are involved in this reaction. Plasmatocytes are monocyte-like cells, which able to phagocytose pathogens, apoptotic bodies, and other foreign particles. Crystal cells, another type of hemocyte, are involved in the production of melanin, a protein involved in both encapsulating and killing microorganisms as well as being implicated in wound healing. Hemocytes differentiate into lamellocytes if a more specialized response is required, and lamellocytes can trap larger parasites, producing a cellular capsule around it in a process named encapsulation [146, 147]. In Drosophila, the majority of blood cells have phagocytic activity.
Some fly macrophages originate via self-renewing and others from progenitor cells that are located in the lymph gland, a specialized hematopoietic organ. The great importance of the lymph gland in controlling the blood cell homeostasis makes this Drosophila organ comparable with the hematopoietic stem cell niche in the bone marrow [148, 149]. ROS levels have a crucial role in the regulation of Drosophila hematopoiesis [150]. Moreover, the signaling pathways regulating blood cell differentiation are conserved from Drosophila to humans [151, 152]. These similarities with vertebrate hematopoiesis underscore the utility of the fly to elucidate the basis of hematopoietic injury, necessary because an impairment in hematopoietic differentiation and homeostasis causes several diseases such as leukemia. Drosophila has already been used to study acute myeloid leukemia, a widespread form of leukemia, in particular to identify the genes promoting the disease. AML1 is one of the transcription factors activating myeloid differentiation and it has a counterpart in the fly [153]. When AML1 is fused with the repressor ETO, the differentiation is inhibited while the proliferation of multilineage progenitors is activated, leading to acute myeloid leukemia. AML1-ETO expression in Drosophila causes the same effect, confirming the fly as a good genetic model for leukemia [153, 154].
The great availability of genetic tools in the fly contributed to defining the innate immune system and to establishing that it is a specific mechanism. In fact, Drosophila can respond specifically to pathogens, discriminating between classes of surface molecules on different intruders. AMPs have different targets, for instance drosomycin acts on fungi, defensin on Gram-positive bacteria, and drosocin on Gram-negative bacteria [155]. Moreover, the sequences of AMPs are conserved between humans and insects [156]. Not only is the defense mechanism evolutionarily conserved, but also is the molecular pattern promoting innate immune reactions. Toll and Imd are the two master genes of Drosophila immunity, but FoxO, JAK/STAT, and JNK transduction also play a part [157]. After pathogen detection, Toll and Imd induce a cascade of events that finally release the antimicrobial peptides in fat body cells through the activation of the NF-κB transcription factors Dif, homolog of Dorsal, and Relish, respectively [155]. Toll encodes an interleukin 1 receptor-like protein that in Drosophila acts in parallel during two different processes: the dorsoventral specification and the immune response regulation [158]. Toll is activated by fungi and most Gram-positive bacteria and has a pivotal function both in the humoral response and in phagocytosis. Dissecting Toll signaling in Drosophila helped to understand toll-like receptors that play an important role in inflammatory responses [159, 160, 161]. The Immune deficiency (Imd) signaling is mainly involved in the Drosophila reaction to Gram-negative bacterial infection [162]. The flies are also helpful in examining the defense against viral infection as they share with humans some proteins, named restriction factors, involved in the reaction to viral infection. Restriction factors, for instance Pastrel in Drosophila, are induced in host cells by virus infection and they can recognize specific viral elements, but the mechanism by which they act in insects is not very clear yet [163].
In order to examine immunity in the fly, an efficient and simple procedure has been developed to elucidate the physiological effect after infection and to quantify the pathogen load. It consists in scoring bacterial load, fly mortality, and also evaluating the effect on immune transcription factors after the direct introduction of bacteria in the fly body cavity, eluding the epithelial barrier [164].
The innate immunity contributes to Drosophila homeostasis and it is regulated by endocrine and metabolic systems. Since immune dysfunction leads to several human diseases, including autoimmune disorders, allergy, and intestinal infections, it is fruitful to use this model organism to better understand how all these systems are regulated. The fruit fly is also used to investigate the association between the microbiome and host, trying to characterize the resistance and tolerance mechanisms that are conserved in humans [165, 166, 167]. Circadian rhythms also participate in immune regulation both in Drosophila and in humans providing another similarity between organisms [168].
3. Conclusions
As illustrated throughout these two chapters, Drosophila melanogaster has been an invaluable tool for unlocking mechanisms contributing to the pathogenesis of many diseases such as cancer, diabetes, obesity, neurodegenerative disorders, kidney disease, immunological impairments, and many others. Given the advances in the field of genetics, new tools and techniques are continually being developed that will keep flies at the forefront of biomedical research.
We thanks the Confocal facility at IFOM-Milan, Matteo Cascinelli, Matteo Frattaroli, Valeria Lupi, and John Benedict Pollard from Liceo Scientifico "A. Einstein Milano" and Zhasmine Mirzoyan University of Milan for helping with the images. Funding from Cariplo Foundation and EHDN to PB and from CiBio to MTC.
Conflict of interest
The authors declare no conflict of interest.


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Every Billboard Hot 100 Single 1970- #29 "The Ghetto"- Donny Hathaway. The final entry onto the charts for January 17, 1970.
- Single: "The Ghetto"- Donny Hathaway
- Record Company- Atco
- Genre: Soul
- Written by Donny Hathaway and Leroy Hutson
- Time: 2:42
- B-side: 'Part 2″
- Album: Everything Is Everything
- Grade: A+
- Peaked at #87 8 weeks in the Billboard Hot 100
While "The Ghetto" wasn't a hit [it did go to #23 on the Soul Singles Chart} is is a great song. The debut single on Donny Hathaway's debut album. Listening to "The Ghetto" gives me the feeling of watching a movie. You get the sounds of men talking on the corner, a baby crying [the baby was Donny's daughter Lalah}
Donny Hathaway's story is a sad and tragic one. Hathaway suffered from severe bouts of depression during his life and was diagnosed as being a paranoid schizophrenic and was taking strong medication to control that illness. According to his wife he wasn't always taking his medication and he would require several hospitalizations throughout the 1970's. At a recording session in January 1979 he began behaving irrationally . The recording session was called off. Hours later he was found dead on the sidewalk below his 15th floor room at the Essex House hotel in NYC. He was only 33 years old. Hathaway's big pop hits were duets with his college friend Roberta Flack- "Where Is The Love" #5 1972 and "The Closer I Get To You" #2 1978.
Justin Timberflake has called Hathaway "the greatest singer of all time", Stevie Wonder said "When Donny sings any song he owns it" and Amy Winehouse said he was her favorite artist of all time.


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SCOTTSDALE, Ariz. — Tiger Woods and Phil Mickelson are gone but the party goes on. Nothing personal, fellas, but you were hardly missed at the Waste Management Phoenix Open.
It's Saturday, so there's a billion people out here. Or maybe only 150,000, I don't know.
It's the Phoenix Open and there is the 16th hole. Therefore, we've got more excitement than we can handle.
Saturday is the day when we don't really care who is winning the WM Phoenix Open. We only care who got cheered, who got booed, who handed out party gifts, who played to the crowd and hey, where are those hot chicks headed?
For the record, Scotsman Martin Laird finished the third round with a three-shot lead over Brooks Koepka, Memorial Tournament champ Hideki Matsuyama and Mr. Iowa, Zach Johnson.
The roars Tiger and Phil would've likely provided today had they not missed the cut? Don't worry, Francesco Molinari singlehandedly had them covered.
The likable Italian sparked a thunderous roar that was heard throughout the course in the middle of the day when he made a hole-in-one at the 16th, golf's only stadium-enclosed golf hole and the place where crowds come to twist and shout and beers go to die.
Bowling has the Beer Frame. Golf has TPC Scottsdale's 16th. Somebody's trying give it a nickname — The Colosseum. Not bad. It might stick. It does feel a little like the Christians hitting golf shots for the pleasure of the lions at times. Gladiators, emperors, wild animals. Only Russell Crowe is missing.
Anyway, Molinari's Shot Heard 'Round the Foam carried with it unintended consequence. Maybe because Golf Channel has been replaying Tiger's famous ace there from 1997 a hundred times and the chaotic scene that followed as beer cups and cans flew everywhere, fans subconsciously wanted to recreate that video moment. Molinari's shot hit, spun back and dropped in the back of the cup, the roar went up. It was soon followed by plastic cups and plastic beer bottles thrown through the air. Those high-priced luxury box patrons? They're just as excitable as the rowdies, apparently.
Brian Davis, who was paired with Molinari, still had to hit his shot. He had to wait for the craziness to die down.
"I was smiling but Brian had to wait a while to let the guys clear the green and the bunkers. I don't know how to describe it. You have to see it. It was amazing for me to be there."
There are a few places where a hole-in-one means even more than it would anywhere else. Most golfers would kill for one. But if you could pick one place for an ace, it would probably be at a famous spot such as the seventh at Pebble Beach, the 12th at Augusta National, the Postage Stamp at Royal Troon, the 16th at Cypress Point or, perhaps, the 16th at TPC Scottsdale during the Waste Management Phoenix Open.
"It's just my third hole-in-one in my life and to get one there, it is special," Molinari said. "The reaction was something else."
It has become the place to be in golf like no other. The hole itself is fairly nondescript. Just a medium-length par-3 with a crowned green and a couple of bunkers lurking. I played it again a few weeks ago when the grandstands were already up. It was kind of spooky, really, and when I pulled a lousy 9-iron into the left bunker, I almost imagined I heard boos. I'm pretty sure it wasn't my caddie, although I can't prove it.
When Molinari was heading out to the range at 7 a.m. to finish up his second round, it was still pretty dark and there were already fans in view. "There were a few guys running towards the 16th green," he said. "They had been waiting awhile."
Saturday at the Phoenix Open, the 16th is the center of the golfing universe. Even Golf Channel acknowledged this by setting up its golf studio right there.
The legend of the 16th just keeps getting bigger. The stands are bigger. It's starting to look like the old Tiger Stadium a little bit. It's got the scoreboard running around the mezzanine front, like at a baseball game. There used to be an open section behind the green but it's completely enclosed now.
It's the place to be. Those guys Molinari spotted hurrying out to 16? They pale in comparison to the guys who climbed a fence Thursday night, sneaked onto the grounds and spent the night in the grandstands — in the rain! — in order to have front-row seats for Friday. They really did it because they emailed a photo of them in the rainy darkness to their buddy, who showed it around Friday to fellow spectators, including my wife, like a badge of honor.
Nuts, yes. Kind of cool, I suppose. And memo to security: Make a note.
Famous rich guy Mark Cuban camped out in the stands Saturday. He's got a reputation for knowing what he's doing.
Russell Knox had the first tee time for the third round and was first to hit when his threesome got to 16. "They sang the national anthem, which was cool," Knox said. "Then I think I almost made it. I hit it to three feet and it looked like it shaved the edge of the hole. I love that. I hit it to three feet the first day, eight feet yesterday and three feet today. Something about that hole brings out the best of me."
Something about it brings out some kind of reaction from everyone. Molinari, the Ace Hole of the Day Saturday, was inspired enough to toss his hole-in-one ball into the stands. Strangely enough, he wound up getting it back.
"The fans threw it back onto the green and nearly hit Brian Davis again," Molinari said. "A volunteer raked it out of the bunker and gave it to me at the end of the round. It was nice to get it back. I don't know if I will keep it or give it to someone. I wasn't expecting to see it come back from the stands."
It was different from the first ace he made as a pro. That one happened in Malaysia after a rain delay the previous day so he was playing at 7:15 in the morning.
"No one was there," he said. "It was the opposite of today."
The party went on as scheduled without Phil or Tiger. Bubba Watson put on a Russell Wilson Seahawks jersey and tossed signed visors into the stands, disregarding the Tour's new policy against tossing gear to fans on that hole. Justin Thomas, a Tour rookie, made a birdie putt and immediately cupped a hand to one ear, and then the other hand to the other ear, to make sure he got the appropriate reaction from the crowd.
No need to beg, Rook. They're going to roar. It's guaranteed. But if you miss the green next time, prepare to get booed.
The tournament proper will resume Sunday. Then the scores and the standings and the race to the wire will matter. The fun will be more in the finish — the contenders who have the guts to go for the 15th green in two or the 17th green in one or are nervy enough to find the fairway at the 18th.
Zach Johnson, former Masters champ and frequent Ryder Cupper, will be one of the prime contenders Sunday. He was really pleased when he hit a superb bunker shot to two feet to save par at the 18th and stay tied for second, three shots behind Laird. That might prove to be a big shot on Sunday, even though few will remember it. Saturday, it was all about the 16th. Johnson was at the fourth tee when heard an extended roar from the distance. He didn't know it was Molinari but he knew what it meant.
"We all looked at each other and said, That's a one," Johnson said.
It was. Too bad Tiger and Phil missed it.
For more news that golfers everywhere are talking about, follow @si_golf on Twitter, like us on Facebook, and subscribe to our YouTube video channel.


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Sahher Bamba Wiki, Biography, Age, Birthday, Movies, Boyfriend & More
Today we are going to know about the upcoming Bollywood Actress Sahher Bamba Wiki, Biography, Age, Weight, Height, Birthday, Father, Mother, Brother, Sister, Family, School, College, Hometown, Upcoming Movies & More…
Sahher Bamba Biography
Sahher Bamba is upcoming Indian Bollywood Actress born in Shimla, Himachal Pradesh in 1999. Currently staying at Mumbai & pursuing his graduation from Jai Hind College, Mumbai.
Sahher Bamba Family
Belongs to hindu family consists of father Sunil Bamba, mother Shilpa Bamba & elder sister Saachi Bamba.
Sahher Bamba Upcoming Movies
Sahher Bamba is going to debut in Bollywood Film Industry with the movie "Pal Pal Dil Ke Pass" as a lead actress opposite Sunny Deol son name Karan Deol.
Pal pal dil ke pass movie releasing on 20 September 2019.
Sahher Bamba Wiki
|Sahher Bamba Age
|20 Years Old (in 2019)
|Sahher Bamba Mother
|Shilpa Bamba
|Sahher Bamba Father
|Sunil Bamba
|Saher Bamba Hometown
|Shimla, Himachal Pradesh
|Saher Bamba Birthday
|10 May 1999
|Sahher Bamba Caste / Religion
|Sahher Bamba Height
|Sahher Bamba Weight
|50 Kg
|Sahher Bamba Figure
|Sahher Bamba Sister
|Saachi Bamba
|Sahher Bamba Instagram
|Sahher Bamba College
|Jai Hind College, Mumbai
|Sahher Bamba Boyfriend
|Not Known
|Sahher Bamba Husband
|Sahher Bamba Movie
|Pal Pal Dil Ke Pass
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The last 24 hours have been nothing short of amazing. Thank you for welcoming us with open arms ❤
Also Check:- SAHIL SANGHA WIKI
Sahher Bamba Facts:-
- Sahher is trained Kathak Dancer
- She is also fitness freak & loves to do yoga regularly
- In 2016 Won "Oppo Bombay Times Fresh Face"
- Sahher loves a dog a lot & loves to spend her free time with them.