Department of Biochemistry and Molecular Biology, Alberta Children's Hospital Research Institute, University of Calgary, Calgary, AB T2N 4N1, Canada.
G3 (Bethesda). 2021 Jul 14;11(7). doi: 10.1093/g3journal/jkab164.
Actin and myosin mediate the epidermal cell contractions that elongate the Caenorhabditis elegans embryo from an ovoid to a tubular-shaped worm. Contraction occurs mainly in the lateral epidermal cells, while the dorsoventral epidermis plays a more passive role. Two parallel pathways trigger actinomyosin contraction, one mediated by LET-502/Rho kinase and the other by PAK-1/p21 activated kinase. A number of genes mediating morphogenesis have been shown to be sufficient when expressed either laterally or dorsoventrally. Additional genes show either lateral or dorsoventral phenotypes. This led us to a model where contractile genes have discrete functions in one or the other cell type. We tested this by examining several genes for either lateral or dorsoventral sufficiency. LET-502 expression in the lateral cells was sufficient to drive elongation. MEL-11/Myosin phosphatase, which antagonizes contraction, and PAK-1 were expected to function dorsoventrally, but we could not detect tissue-specific sufficiency. Double mutants of lethal alleles predicted to decrease lateral contraction with those thought to increase dorsoventral force were previously shown to be viable. We hypothesized that these mutant combinations shifted the contractile force from the lateral to the dorsoventral cells and so the embryos would elongate with less lateral cell contraction. This was tested by examining 10 single and double mutant strains. In most cases, elongation proceeded without a noticeable alteration in lateral contraction. We suggest that many embryonic elongation genes likely act in both lateral and dorsoventral cells, even though they may have their primary focus in one or the other cell type.
肌动蛋白和肌球蛋白介导了表皮细胞的收缩，使秀丽隐杆线虫胚胎从卵圆形拉长为管状蠕虫。收缩主要发生在侧表皮细胞中，而背腹表皮则起更被动的作用。两种平行的途径触发肌动球蛋白收缩，一种由 LET-502/Rho 激酶介导，另一种由 PAK-1/p21 激活激酶介导。许多参与形态发生的基因被证明在侧向或背腹表达时是足够的。其他基因表现出侧向或背腹表型。这使我们得出了一个模型，即收缩基因在一种或另一种细胞类型中具有离散的功能。我们通过检查几个基因的侧向或背腹是否充足来验证这一点。LET-502 在侧表皮细胞中的表达足以驱动伸长。MEL-11/肌球蛋白磷酸酶，它拮抗收缩，和 PAK-1 预计在背腹侧起作用，但我们无法检测到组织特异性充足。致死等位基因的双突变体预计会减少侧向收缩，而那些被认为会增加背腹力的等位基因之前被证明是可行的。我们假设这些突变体组合将收缩力从侧表皮细胞转移到背腹表皮细胞，因此胚胎会在较少的侧表皮细胞收缩的情况下伸长。这通过检查 10 个单突变体和双突变体菌株进行了测试。在大多数情况下，伸长过程没有明显改变侧向收缩。我们认为，许多胚胎伸长基因可能在侧表皮细胞和背腹表皮细胞中都起作用，尽管它们可能主要集中在一种或另一种细胞类型中。
