Department of Biology and Genetics Institute, University of Florida, Gainesville, FL 32611, USA.
G3 (Bethesda). 2022 Nov 4;12(11). doi: 10.1093/g3journal/jkac221.
Mutation or loss of 6 extracellular matrix collagen genes disrupts annular furrows in adult C. elegans cuticles, causes a wide "Dumpy" body morphology, and activates osmotic, detoxification, and antimicrobial defense genes. High environmental osmolarity reduces internal turgor pressure, physically distorts the epidermis, and activates the same stress responses. Collagen gene mutations that cause Dumpy without furrow disruption do not activate stress responses. These results are consistent with an extracellular damage sensor associated with furrows in the adult cuticle that regulates environmental stress responses in adjacent cells. Several cuticle characteristics change between molts, but all stages have annular furrows and express furrow collagen genes. We compared body shape, furrow organization imaged with differential interference contrast microscopy, and stress response gene expression in furrow collagen gene mutants at all postembryonic stages. We find that most body shape and furrow disorganization phenotypes start at the L3 stage and increase in severity with each molt afterwards. Stress response genes were induced the strongest in adults, correlating with the greatest Dumpy and furrow phenotypes. Although weaker than in adults, osmolyte transporter gene hmit-1.1 and antimicrobial gene nlp-29 were also induced in some early larvae that had weak or undetectable cuticle phenotypes. Our data are consistent with progressive cuticle phenotypes in which each new cuticle is at least partially directed by organization of the former cuticle. Gene expression and cuticle data support the role of furrow disruption as a signal in L4 larvae and adults, but also suggest a role for other cuticle organization or epidermal cell effects in early larvae.
6 个细胞外基质胶原蛋白基因突变或缺失会破坏成年秀丽隐杆线虫表皮的环形凹痕，导致“矮胖”的体型，并激活渗透、解毒和抗菌防御基因。高环境渗透压会降低内部膨压，使表皮物理变形，并激活相同的应激反应。不会破坏凹痕但导致矮胖的胶原蛋白基因突变不会激活应激反应。这些结果与与成年表皮凹痕相关的细胞外损伤传感器一致，该传感器调节相邻细胞的环境应激反应。蜕皮过程中会发生几种表皮特征的变化，但所有阶段都有环形凹痕并表达凹痕胶原蛋白基因。我们比较了所有后生阶段的凹痕胶原基因突变体的体型、用微分干涉对比显微镜成像的凹痕组织以及应激反应基因表达。我们发现，大多数体型和凹痕组织紊乱表型始于 L3 阶段，并随着每次蜕皮后变得更加严重。应激反应基因在成虫中诱导最强，与最大的矮胖和凹痕表型相关。尽管不如成虫中强烈，但在一些早期幼虫中，渗透调节剂转运基因 hmit-1.1 和抗菌基因 nlp-29 也被诱导，这些幼虫的表皮表型较弱或无法检测到。我们的数据与渐进性表皮表型一致，其中每个新表皮至少部分由前一个表皮的组织决定。基因表达和表皮数据支持凹痕破坏作为 L4 幼虫和成虫中信号的作用，但也表明在早期幼虫中，其他表皮组织或表皮细胞效应也发挥了作用。
