Roberts Brett, Clucas Caroline, Johnstone Iain L
The Wellcome Centre for Molecular Parasitology, The University of Glasgow, Glasgow G11 6NU, United Kingdom.
Mol Biol Cell. 2003 Nov;14(11):4414-26. doi: 10.1091/mbc.e03-03-0162. Epub 2003 Aug 7.
SEC-23 is a component of coat protein complex II (COPII)-coated vesicles involved in the endoplasmic reticulum-to-Golgi transport pathway of eukaryotes. During postembryonic life, Caenorhabditis elegans is surrounded by a collagenous exoskeleton termed the cuticle. From a screen for mutants defective in cuticle secretion, we identified and characterized a sec-23 mutant of C. elegans. By sequence homology, C. elegans has only the single sec-23 gene described herein. In addition to the cuticle secretion defect, mutants fail to complete embryonic morphogenesis. However, they progress through the earlier stages of embryogenesis, including gastrulation, and achieve substantial morphogenesis before death. We demonstrated a maternal component of SEC-23 function sufficient for progression through the earlier stages of embryogenesis and explaining the limited phenotype of the zygotic mutant. By RNA-mediated interference, we investigated the effects of perturbing COPII function during various postembryonic stages. During larval stages, major defects in cuticle synthesis and molting were observed. In the adult hermaphrodite, reduction of SEC-23 function by RNA-mediated interference caused a rapid onset of sterility, with defects in oogenesis including early maturation of the germline nuclei, probably a result of the observed loss of the GLP-1 receptor from the membrane surfaces adjacent to the developing germline nuclei.
SEC-23是包被蛋白复合物II（COPII）包被囊泡的一个组成部分，参与真核生物内质网到高尔基体的运输途径。在胚胎后期生活中，秀丽隐杆线虫被一种称为角质层的胶原质外骨骼所包围。通过筛选角质层分泌缺陷的突变体，我们鉴定并表征了秀丽隐杆线虫的一个sec-23突变体。通过序列同源性分析，秀丽隐杆线虫只有本文所述的单个sec-23基因。除了角质层分泌缺陷外，突变体无法完成胚胎形态发生。然而，它们能经历胚胎发育的早期阶段，包括原肠胚形成，并在死亡前实现显著的形态发生。我们证明了SEC-23功能的母体成分足以支持胚胎发育的早期阶段，并解释了合子突变体有限的表型。通过RNA介导的干扰，我们研究了在胚胎后期各个阶段干扰COPII功能的影响。在幼虫阶段，观察到角质层合成和蜕皮的主要缺陷。在成年雌雄同体中，通过RNA介导的干扰降低SEC-23功能会导致迅速不育，卵子发生出现缺陷，包括生殖系细胞核过早成熟，这可能是由于观察到GLP-1受体从与发育中的生殖系细胞核相邻的膜表面丢失所致。
