AUTHOR=Lehmann Christina , Pohl Christian 

TITLE=A Maternal-Effect Toxin Affects Epithelial Differentiation and Tissue Mechanics in Caenorhabditis elegans

JOURNAL=Frontiers in Cell and Developmental Biology

VOLUME=9

YEAR=2021

URL=https://www.frontiersin.org/journals/cell-and-developmental-biology/articles/10.3389/fcell.2021.743496

DOI=10.3389/fcell.2021.743496

ISSN=2296-634X

ABSTRACT=<p>Selfish genetic elements that act as post-segregation distorters cause lethality in non-carrier individuals after fertilization. Two post-segregation distorters have been previously identified in <italic>Caenorhabditis elegans</italic>, the <italic>peel-1</italic>/<italic>zeel-1</italic> and the <italic>sup-35</italic>/<italic>pha-1</italic> elements. These elements seem to act as modification-rescue systems, also called toxin/antidote pairs. Here we show that the maternal-effect toxin/zygotic antidote pair <italic>sup-35</italic>/<italic>pha-1</italic> is required for proper expression of apical junction (AJ) components in epithelia and that <italic>sup-35</italic> toxicity increases when pathways that establish and maintain basal epithelial characteristics, <italic>die-1</italic>, <italic>elt-1</italic>, <italic>lin-26</italic>, and <italic>vab-10</italic>, are compromised. We demonstrate that <italic>pha-1(e2123)</italic> embryos, which lack the antidote, are defective in epidermal morphogenesis and frequently fail to elongate. Moreover, seam cells are frequently misshaped and mispositioned and cell bond tension is reduced in <italic>pha-1(e2123)</italic> embryos, suggesting altered tissue material properties in the epidermis. Several aspects of this phenotype can also be induced in wild-type embryos by exerting mechanical stress through uniaxial loading. Seam cell shape, tissue mechanics, and elongation can be restored in <italic>pha-1(e2123)</italic> embryos if expression of the AJ molecule DLG-1/Discs large is reduced. Thus, our experiments suggest that maternal-effect toxicity disrupts proper development of the epidermis which involves distinct transcriptional regulators and AJ components.</p>