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Originally published as MBC in Press, 10.1091/mbc.E03-03-0162 on August 7, 2003

Vol. 14, Issue 11, 4414-4426, November 2003

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Loss of SEC-23 in Caenorhabditis elegans Causes Defects in Oogenesis, Morphogenesis, and Extracellular Matrix Secretion

Brett Roberts, Caroline Clucas, and Iain L. Johnstone *

The Wellcome Centre for Molecular Parasitology, The University of Glasgow, Glasgow G11 6NU, United Kingdom

Submitted March 20, 2003; Revised June 25, 2003; Accepted June 26, 2003
Monitoring Editor: John Pringle

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.


* Corresponding author. E-mail address: i.johnstone{at}vet.gla.ac.uk.




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