{'fraction_non_alphanumeric': 0.018948655256723717, 'fraction_numerical': 0.0024449877750611247, 'mean_word_length': 5.44488188976378, '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}}
Temporal control over the initiation of cell motility by a regulator of G-protein signaling

Significance Cell motility is critical for a wide range of processes in development, homeostasis, and immune response. Conversely, abnormal regulation of cell migration leads to pathological consequences like cancer metastasis. In this study, we investigate the mechanisms controlling the timing of motility acquisition, using zebrafish primordial germ cells as an in vivo model. We defined a previously unknown role for the signaling scaffold molecule and regulator of Gα protein signaling Rgs14a in coordinating the onset of migration with the presence of migration guidance cues. Furthermore, we show that this control level involves the regulation of the cell–cell adhesion molecule E-cadherin, a molecule implicated in motility acquisition in a range of normal physiological events and in disease conditions. The control over the acquisition of cell motility is central for a variety of biological processes in development, homeostasis, and disease. An attractive in vivo model for investigating the regulation of migration initiation is that of primordial germ cells (PGCs) in zebrafish embryos. In this study, we show that, following PGC specification, the cells can polarize but do not migrate before the time chemokine-encoded directional cues are established. We found that the regulator of G-protein signaling 14a protein, whose RNA is a newly identified germ plasm component, regulates the temporal relations between the appearance of the guidance molecules and the acquisition of cellular motility by regulating E-cadherin levels.