The Rac1 homolog CED-10 is a component of the MES-1/SRC-1 pathway for asymmetric division of the C. elegans EMS blastomere.

IF 3.3 3区生物学 Q2 GENETICS & HEREDITY

Genetics Pub Date : 2025-02-01 DOI:10.1093/genetics/iyaf020

Helen Lamb, McKenzi Fernholz, Małgorzata J Liro, Krista M Myles, Holly Anderson, Lesilee S Rose

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引用次数: 0

Abstract

Asymmetric cell division is essential for the creation of cell types with different identities and functions. The EMS blastomere of the four-cell Caenorhabditis elegans embryo undergoes an asymmetric division in response to partially redundant signaling pathways. One pathway involves a Wnt signal from the neighboring P2 cell, while the other pathway is defined by the receptor-like MES-1 transmembrane protein localized at the EMS-P2 cell contact, and the cytoplasmic kinase SRC-1. In response to these signals, the EMS nuclear-centrosome complex rotates so that the spindle forms on the anterior-posterior axis; after division, the daughter cell contacting P2 becomes the endodermal precursor cell. Here we identify the Rac1 homolog CED-10 as a new component of the MES-1/SRC-1 pathway. Loss of CED-10 affects both spindle positioning and endoderm specification in the EMS cell. SRC-1 dependent phosphorylation at the EMS-P2 contact is reduced. However, the asymmetric division of the P2 cell, which is also MES-1 and SRC-1 dependent, appears normal in ced-10 mutants. These and other results suggest that CED-10 acts upstream of, or at the level of, SRC-1 activity in the EMS cell. In addition, we find that the branched actin regulator ARX-2 is enriched at the EMS-P2 cell contact site, in a CED-10 dependent manner. Loss of ARX-2 results in EMS spindle orientation defects, suggesting that CED-10 acts through branched actin to promote spindle orientation in the EMS cell.

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Rac1 同源物 CED-10 是 elegans EMS 胚泡不对称分裂的 MES-1/SRC-1 通路的一个组成部分。

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来源期刊

Genetics GENETICS & HEREDITY-

CiteScore

6.90

自引率

6.10%

发文量

177

审稿时长

1.5 months

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