{'fraction_non_alphanumeric': 0.02162579648580807, 'fraction_numerical': 0.009847460899787604, 'mean_word_length': 5.598726114649682, 'pattern_counts': {'":': 0, '<': 0, '<?xml version=': 0, '>': 0, 'https://': 0, 'lorem ipsum': 0, 'www.': 0, 'xml': 0}, 'pii_count': 0, 'substrings_counts': 0, 'word_list_counts': {'cursed_substrings.json': 0, 'profanity_word_list.json': 0, 'sexual_word_list.json': 0, 'zh_pornsignals.json': 0}}
The Hormonal Regulation of Cell Elongation Through Changes in Microtubule Orientation

Plant morphogenesis is defined by the expansion characteristics of the individual cells making up the plant body. Understanding the mechanisms that control plant morphogenesis has occupied the efforts of botanists for decades. Manipulation of cell expansion characteristics through the application of plant hormones has proved to be fertile ground for unraveling the mechanisms of plant development (for review, see Scott [1972]; Jones [1973]; Eisinger [1983]; Graebe [1987]). Certain hormones, such as gibberellic acid (GA) and auxin, augment cell elongation, while others, such as abscisic acid (ABA) and ethylene, inhibit elongation (see Ishida and Katsumi, in this issue, for references). What is not known is how these hormones elicit this response in cell elongation. What are the mechanisms that control cell expansion characteristics and define final cell size and shape? Are all cells equally involved in controlling organ elongation or are there specific tissues that are ultimately responsible for controlling final organ development? There are many factors that must be coordinated to achieve the end result of an elongated plant cell. Cells must undergo turgor-pressuredriven cell expansion, and that expansion must be controlled to produce an elongated cell rather than a swollen, isodiametric cell. Controlled cell expansion is achieved through the organization of the load-bearing, innermost layer of wall microfibrils (Green 1969). If wall microfibrils are organized in parallel arrays, strong hydrogen bonding between adjacent microfibrils provides a substantial force to resist turgor pressure and cell expansion. If wall microfibrils maintain a random organization, then hydrogen bonding between adjacent microfibrils is reduced, and the wall is less able to resist turgor pressure. In elongating tissues such as roots and stems, radial and tangential cell walls contain arrays of highly organized wall microfibrils oriented transversely to the long axis of the organ. These walls restrict lateral expansion, thereby promoting elongation of the cells and the entire plant organ. The role of the cytoplasm in controlling microfibril organization and orientation has been intensely investigated. An extensive literature provides a body of largely circumstantial evidence that the orientation of the innermost layer of wall microfibrils is controlled by arrays of microtubules located in the cortical cytoplasm close to, and possibly connected with, the plasmalemma (for reviews, see Hepler and Palevitz [1974]; Robinson and Quader [1982]; Seagull [1989]; Giddings and Staehelin [1991]). With few exceptions, when organized arrays of microfibrils are deposited, the innermost layer of microfibrils mimics the cortical arrays of microtubules in both orientation and organization. The study of microtubule involvement in wall deposition has intensified with the introduction of immunofluorescence techniques to plant cell biology (Lloyd 1987). It is now clear that microtubules are very dynamic, responding to environmental or developmental signals to elicit a developmental response. Microtubule patterns not only change throughout the cell cycle but also during cell differentiation, when changes in cell shape often precede the establishment of specific cell function. In this issue, Ishida and Katsumi report on the relationship between cell elongation, hormone application, and the orientation of microtubule arrays in elongating cucumber seedlings. Microtubule orientation in tangential and radial walls of epidermal cells and tangential walls of cortical cells at two locations in the hypocotyl were examined after exposure to GA and ABA. The application of GA induced an increase in: (1) hypocotyl elongation and (2) the percentage of epidermal cells with transversely oriented microtubules. As all the cells of the cortex have transversely oriented microtubules in the control experiment, GA did not exhibit an effect in these cells. On the other hand, ABA treatment resulted in a decrease in the percentage of cells with transversely oriented microtubules in all areas examined. ABA also antagonized the GA response by diminishing the extent of hypocotyl elongation and microtubule reorientation. The authors noted a direct correlation between the extent of hormone-mediated hypocotyl elongation and the transverse orientation of microtubules along the tangential walls of epidermal cells. This relationship was not evident in data from other walls examined. Hormone-induced modification of microtubule orientation may occur as a normal physiological response. Katsumi et al. (1989) showed that a stress-induced decrease in hypocotyl elongation was correlated with increases in both ABA concentration and the numbers of cells containing longitudinal microtubules. Previous studies by these authors (Ishida and Katsumi 1991) have indicated that the orientation of microtubules along the tangential walls of epidermal cells may be responsible for dwarfing in the d5 mutant of Zea mays L. and that dwarfing is overcome through a GA-induced reorientation of microtubules.