Genetics. Published Articles Ahead of Print: September 2, 2005, Copyright © 2005
doi:10.1534/genetics.105.047340


A more recent version of this article appeared on January 1, 2006.


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spe-10 Encodes a DHHC-CRD Zinc Finger Membrane Protein Required for ER/Golgi Membrane Morphogenesis During Caenorhabditis elegans Spermatogenesis

1 Emory University
2 Rutgers University

* To whom correspondence should be addressed. E-mail: bioslh{at}biology.emory.edu.

Submitted on June 27, 2005
Revised on August 2, 2005
Accepted on 17 August 2005


Abstract

C. elegans spermatogenesis employs lysosome-related fibrous body-membranous organelles (FB-MOs) for transport of many cellular components. Previous work showed that spe-10 mutants contain FB-MOs that prematurely disassemble, resulting in defective transport of FB components into developing spermatids. Consequently, spe-10 spermatids are smaller than wild type and contain defective FB-MO derivatives. In this paper, we show that spe-10 encodes a four-pass integral membrane protein that has a DHHC-CRD zinc-finger motif. The DHHC-CRD motif is found in a large, diverse family of proteins that have been implicated in palmitoyl transfer during protein lipidation. Seven spe-10 mutants were analyzed, including missense, nonsense and deletion mutants. An antiserum to SPE-10 showed significant co-localization with a known marker for the FB-MOs during wild-type spermatogenesis. In contrast, the spe-10(ok1149) deletion mutant lacked detectable SPE-10 staining; this mutant lacks a spe-10 promoter and most coding sequence. The spe-10(eb64) missense mutation, which changes a conserved residue within the DHHC-CRD domain in all homologs, behaves as a null mutant. These results suggest that wild-type SPE-10 is required for the MO to properly deliver the FB to the C. elegans spermatid and the DHHC-CRD domain is essential for this function.

Key Words: C. elegans spermatogenesis, DHHC-CRD zinc fingers, ER/Golgi, palmitoylation, vesicular trafficking