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首页> 外文期刊>Molecular biology of the cell >Cytoplasmic carboxypeptidase 5 regulates tubulin glutamylation and zebrafish cilia formation and function
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Cytoplasmic carboxypeptidase 5 regulates tubulin glutamylation and zebrafish cilia formation and function

机译：细胞质羧肽酶5调节小管蛋白谷氨酸和斑马鱼纤毛形成和功能

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Glutamylation is a functionally important tubulin posttranslational modification enriched on stable microtubules of neuronal axons, mitotic spindles, centrioles, and cilia. In vertebrates, balanced activities of tubulin glutamyl ligase and cytoplasmic carboxypeptidase deglutamylase enzymes maintain organelle- and cell type–specific tubulin glutamylation patterns. Tubulin glutamylation in cilia is regulated via restricted subcellular localization or expression of tubulin glutamyl ligases ( ttll s) and nonenzymatic proteins, including the zebrafish TPR repeat protein Fleer/Ift70. Here we analyze the expression patterns of ccp deglutamylase genes during zebrafish development and the effects of ccp gene knockdown on cilia formation, morphology, and tubulin glutamylation. The deglutamylases ccp2 , ccp5 , and ccp6 are expressed in ciliated cells, whereas ccp1 expression is restricted to the nervous system. Only ccp5 knockdown increases cilia tubulin glutamylation, induces ciliopathy phenotypes, including axis curvature, hydrocephalus, and pronephric cysts, and disrupts multicilia motility, suggesting that Ccp5 is the principal tubulin deglutamylase that maintains functional levels of cilia tubulin glutamylation. The ability of ccp5 knockdown to restore cilia tubulin glutamylation in fleer/ift70 mutants and rescue pronephric multicilia formation in both fleer - and ift88 -deficient zebrafish indicates that tubulin glutamylation is a key driver of ciliogenesis.
机译：戊二化是一种功能重要的微管蛋白的富含神经元轴突，有丝分子纺锤，纤维素和纤毛的微管状的微管状改性。在脊椎动物中，管蛋白谷氨酸胶酶和细胞质羧肽酶脱谷酰基酶的平衡活性维持细胞石和细胞类型特异性小管蛋白戊二酰胺化图案。 Cilia中的管蛋白戊二酰化通过限制的亚细胞定位或小管蛋白谷氨酸胶酶（TTLL）和非酶蛋白的表达来调节，包括斑马鱼TPR重复蛋白润滑/ IFT70。在这里，我们在斑马鱼发育过程中分析CCP脱氮酶基因的表达模式及CCP基因敲低对纤毛形成，形态和小管蛋白谷氨酸的影响。将甲酰基酶CCP2，CCP5和CCP6表示在纤毛细胞中，而CCP1表达仅限于神经系统。只有CCP5敲低增加纤毛细胞蛋白谷氨酸，诱导患有轴曲率，脑积水和静脉囊肿，并破坏多利时动力，表明CCP5是维持纤毛细胞蛋白谷氨酸功能水平的主要管蛋白含淀粉酶。 CCP5敲低止血管/ IFT70突变体恢复纤毛细胞蛋白谷氨酸的能力和悬浮在苗圃和IFT88 - 斑马鱼中抢救幽门多体子形成表明小管蛋白谷氨酸是纤氯酶的关键驱动器。

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