- THIS ARTICLE
- Full Text (Rapid PDF)
-
All Versions of this Article:
genetics.105.047340v1
172/1/145 most recent - Alert me when this article is cited
- Alert me if a correction is posted
- SERVICES
- Similar articles in this journal
- Similar articles in PubMed
- Alert me to new issues of the journal
- Download to citation manager
- Reprints & Permissions
- CITING ARTICLES
- Citing Articles via Google Scholar
- GOOGLE SCHOLAR
- Articles by Gleason, E. J.
- Articles by L'Hernault, S. W.
- Search for Related Content
- PUBMED
- PubMed Citation
- Articles by Gleason, E. J.
- Articles by L'Hernault, S. W.
doi:10.1534/genetics.105.047340
A more recent version of this article appeared on January 1, 2006.
REGULAR RESEARCH PAPERS |
spe-10 Encodes a DHHC-CRD Zinc Finger Membrane Protein Required for ER/Golgi Membrane Morphogenesis During Caenorhabditis elegans Spermatogenesis
Elizabeth J. Gleason 1, Wesley C. Lindsey 1, Tim L. Kroft 1, Andrew W. Singson 2 and Steven W. L'Hernault 1*
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
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