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MBC in Press, published online ahead of print August 7, 2003
Mol. Biol. Cell 10.1091/mbc.E03-03-0162

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Submitted on March 20, 2003
Revised on June 25, 2003
Accepted on June 26, 2003

Loss of SEC-23 in Caenorhabditis elegans causes defects in oogenesis, morphogenesis, and ECM secretion

Brett Roberts1, Caroline Clucas1, and Iain L. Johnstone1*

1 The Wellcome Centre for Molecular Parasitology, The University of Glasgow, Anderson College, 56 Dumbarton Rd., Glasgow, G11 6NU, UK

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

SEC-23 is a component of COPII coated vesicles involved in the ER 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 here. 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 {clubsuit}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 (RNAi), 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 RNAi 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.




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