biostudies-literatureUnknownLamb HNCRR NIH HHSNIGMS NIH HHSNIH HHSAsymmetric cell division is essential for the creation of cell types with different identities and functions. The EMS blastomere of the four-cell <i>Caenorhabditis elegans</i> embryo undergoes an asymmetric division in response to partially redundant signaling pathways. One pathway involves a Wnt signal emanating from the neighboring P2 cell, while the other pathway is defined by the receptor-like MES-1 protein localized at the EMS/P2 cell contact, and the cytoplasmic kinase SRC-1. In response to these pathways, 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. Although MES-1 is still present at the EMS/P2 contact in <i>ced-10</i> embryos, SRC-1 dependent phosphorylation is reduced. These and other results suggest that CED-10 acts downstream of MES-1 and upstream of, or at the level of, SRC-1 activity. 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 spindle positioning defects, suggesting that CED-10 acts through branched actin to promote the asymmetric division of the EMS cell.bioRxiv : the preprint server for biology2024.04.04.588162https://www.ebi.ac.uk/biostudies/studies/S-EPMC11030239biostudies-literatureThe Rac1 homolog CED-10 is a component of the MES-1/SRC-1 pathway for asymmetric division of the &lt;i&gt;C. elegans&lt;/i&gt; EMS blastomere.PMC11030239S10 RR024543T32 GM007377P40 OD010440R01 GM068744Myles KFernholz MRose LSLamb HLiro MAnderson HfalseThe Rac1 homolog CED-10 is a component of the MES-1/SRC-1 pathway for asymmetric division of the &lt;i&gt;C. elegans&lt;/i&gt; EMS blastomere.Asymmetric cell division is essential for the creation of cell types with different identities and functions. The EMS blastomere of the four-cell <i>Caenorhabditis elegans</i> embryo undergoes an asymmetric division in response to partially redundant signaling pathways. One pathway involves a Wnt signal emanating from the neighboring P2 cell, while the other pathway is defined by the receptor-like MES-1 protein localized at the EMS/P2 cell contact, and the cytoplasmic kinase SRC-1. In response to these pathways, 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. Although MES-1 is still present at the EMS/P2 contact in <i>ced-10</i> embryos, SRC-1 dependent phosphorylation is reduced. These and other results suggest that CED-10 acts downstream of MES-1 and upstream of, or at the level of, SRC-1 activity. 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 spindle positioning defects, suggesting that CED-10 acts through branched actin to promote the asymmetric division of the EMS cell.2024-01-01T00:00:00Z2024 May2026-04-07T22:52:32.668Z2026-04-07T18:47:42.907ZS-EPMC110302393864519510.1101/2024.04.04.588162