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保守的 Pelado/ZSWIM8 蛋白通过促进线性肌动蛋白丝聚合来调节肌动蛋白动力学。

The conserved Pelado/ZSWIM8 protein regulates actin dynamics by promoting linear actin filament polymerization.

机构信息

Department of Cell, Developmental, and Regenerative Biology, Graduate School of Biomedical Sciences, Icahn School of Medicine at Mount Sinai, New York, NY, USA.

Departamento de Biología, Centro FONDAP de Regulación del Genoma, Facultad de Ciencias, Universidad de Chile, Santiago, Chile.

出版信息

Life Sci Alliance. 2022 Aug 8;5(12):e202201484. doi: 10.26508/lsa.202201484.

DOI:10.26508/lsa.202201484
PMID:35940847
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC9375228/
Abstract

Actin filament polymerization can be branched or linear, which depends on the associated regulatory proteins. Competition for actin monomers occurs between proteins that induce branched or linear actin polymerization. Cell specialization requires the regulation of actin filaments to allow the formation of cell type-specific structures, like cuticular hairs in <i>Drosophila</i>, formed by linear actin filaments. Here, we report the functional analysis of CG34401/<i>pelado</i>, a gene encoding a SWIM domain-containing protein, conserved throughout the animal kingdom, called ZSWIM8 in mammals. Mutant <i>pelado</i> epithelial cells display actin hair elongation defects. This phenotype is reversed by increasing actin monomer levels or by either pushing linear actin polymerization or reducing branched actin polymerization. Similarly, in hemocytes, Pelado is essential to induce filopodia, a linear actin-based structure. We further show that this function of Pelado/ZSWIM8 is conserved in human cells, where Pelado inhibits branched actin polymerization in a cell migration context. In summary, our data indicate that the function of Pelado/ZSWIM8 in regulating actin cytoskeletal dynamics is conserved, favoring linear actin polymerization at the expense of branched filaments.

摘要

肌动蛋白丝聚合可以是分支的或线性的，这取决于相关的调节蛋白。肌动蛋白单体的竞争发生在诱导分支或线性肌动蛋白聚合的蛋白质之间。细胞特化需要调节肌动蛋白丝，以允许形成细胞类型特异性的结构，如 <i>果蝇</i> 的表皮毛，由线性肌动蛋白丝形成。在这里，我们报告了 CG34401/<i>pelado</i>的功能分析，CG34401 编码一个含有 SWIM 结构域的蛋白，在整个动物界中保守，在哺乳动物中称为 ZSWIM8。突变 <i>pelado</i>上皮细胞显示肌动蛋白毛发伸长缺陷。这种表型可以通过增加肌动蛋白单体水平或推动线性肌动蛋白聚合或减少分支肌动蛋白聚合来逆转。同样，在血细胞中，Pelado 对于诱导丝状伪足（一种基于线性肌动蛋白的结构）是必不可少的。我们进一步表明，Pelado/ZSWIM8 的这种功能在人类细胞中是保守的，在这种细胞迁移的背景下，Pelado 抑制分支肌动蛋白聚合。总之，我们的数据表明，Pelado/ZSWIM8 调节肌动蛋白细胞骨架动力学的功能是保守的，有利于线性肌动蛋白聚合，而不是分支纤维。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b066/9375228/c68f9d458dfc/LSA-2022-01484_FigS6.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b066/9375228/580c28c6ad5f/LSA-2022-01484_Fig1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b066/9375228/81a5187bb2ae/LSA-2022-01484_FigS1.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b066/9375228/c6dfafc1fa68/LSA-2022-01484_FigS3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b066/9375228/fcfeb322c81b/LSA-2022-01484_Fig3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b066/9375228/3e1c71e5523a/LSA-2022-01484_Fig4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b066/9375228/16d3d585ee5d/LSA-2022-01484_FigS4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b066/9375228/c04b930d9004/LSA-2022-01484_Fig5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b066/9375228/a3012dc40bfd/LSA-2022-01484_FigS5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b066/9375228/255f2b4cd7e0/LSA-2022-01484_Fig6.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b066/9375228/c68f9d458dfc/LSA-2022-01484_FigS6.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b066/9375228/580c28c6ad5f/LSA-2022-01484_Fig1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b066/9375228/81a5187bb2ae/LSA-2022-01484_FigS1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b066/9375228/9d47921bec10/LSA-2022-01484_Fig2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b066/9375228/72870074c602/LSA-2022-01484_FigS2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b066/9375228/c6dfafc1fa68/LSA-2022-01484_FigS3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b066/9375228/fcfeb322c81b/LSA-2022-01484_Fig3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b066/9375228/3e1c71e5523a/LSA-2022-01484_Fig4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b066/9375228/16d3d585ee5d/LSA-2022-01484_FigS4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b066/9375228/c04b930d9004/LSA-2022-01484_Fig5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b066/9375228/a3012dc40bfd/LSA-2022-01484_FigS5.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b066/9375228/c68f9d458dfc/LSA-2022-01484_FigS6.jpg

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