Src64 is required for actomyosin contraction during cellularization of the Drosophila embryonic blastoderm. The mechanism of actomyosin ring constriction is poorly understood even though a number of cytoskeletal regulators have been implicated in the assembly, organization, and contraction of these microfilament rings. How these cytoskeletal processes are regulated during development is even less well understood. To investigate the role of Src64 as an upstream regulator of actomyosin contraction, we conducted a proteomics screen to identify proteins whose expression levels are controlled by src64. Global levels of actin are reduced in src64 mutant embryos. Furthermore, we show that reduction of the actin isoform Actin 5C causes defects in actomyosin contraction during cellularization similar to those caused by src64 mutation, indicating that a relatively high level of Actin 5C is required for normal actomyosin contraction and furrow canal structure. However, reduction of Actin 5C levels only slows down actomyosin ring constriction rather than preventing it, suggesting that src64 acts not only to modulate actin levels, but also to regulate the actomyosin cytoskeleton by other means.

中文翻译：

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细胞化过程中的肌动球蛋白收缩部分受肌动蛋白5C蛋白水平的Src64控制。

果蝇胚胎胚盘细胞化过程中肌动球蛋白收缩需要Src64。尽管已经有许多细胞骨架调节剂参与了这些微丝环的组装，组织和收缩，但对肌动球蛋白环收缩的机制知之甚少。在发育过程中如何调节这些细胞骨架过程的了解甚至更少。为了研究Src64作为肌动球蛋白收缩的上游调节剂的作用，我们进行了蛋白质组学筛选，以鉴定其表达水平受src64控制的蛋白质。src64中肌动蛋白的整体水平降低突变体胚胎。此外，我们表明肌动蛋白同工型肌动蛋白5C的减少导致细胞化过程中的肌动球蛋白收缩缺陷，类似于由src64突变引起的缺陷，表明正常肌动球蛋白收缩和沟管结构需要相对较高水平的肌动蛋白5C。但是，肌动蛋白5C水平的降低只会减慢肌动蛋白环收缩而不是阻止它，这表明src64不仅可以调节肌动蛋白水平，还可以通过其他方式调节肌动蛋白细胞骨架。