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 <i>Caenorhabditis elegans</i>, the <i>
peel-1</i>/<i>
zeel-1</i> and the <i>
sup-35</i>/<i>
pha-1</i> 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 <i>
sup-35</i>/<i>
pha-1</i> is required for proper expression of apical junction (AJ) components in epithelia and that <i>
sup-35</i> toxicity increases when pathways that establish and maintain basal epithelial characteristics, <i>
die-1</i>, <i>
elt-1</i>, <i>
lin-26</i>, and <i>
vab-10</i>, are compromised. We demonstrate that <i>
pha-1(
e2123)</i> 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 <i>
pha-1(
e2123)</i> 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 <i>
pha-1(
e2123)</i> 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.