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Author Notes:

Corresponding author: Department of Biology, Emory University, 1510 Clifton Rd. NE, Atlanta, GA 30322. E-mail: bioslh@emory.edu

Supporting information is available online at http://www.genetics.org/content/suppl/2012/03/23/genetics.112.139618.DC1.

The first four authors contributed equally to this work and are listed alphabetically.

PDH Present address: Department of Cellular and Molecular Pharmacology, University of California, 1700 4th St., MC 2530, San Francisco, CA 94158.

KLHH Present address: Powell Gene Therapy Center, Department of Pediatrics, University of Florida, Gainesville, FL 32610.

RMW Present address: Genentech Inc., 1 DNA Way, South San Francisco, CA 94080.

TLK Present address: Department of Biology, 1035 Kirby Dr., University of Minnesota, Duluth, MN 55812.

GZ Present address: Pathway Genomics Corporation, 4045 Sorrento Valley Blvd., San Diego, CA, 92121.

SC Present address: National Center for Environmental Health, Centers for Disease Control and Prevention, Atlanta, GA 30341.


Research Funding:

This work was supported by NIH grants GM040697 and GM082932 to S.W.L. and R43 GM071317 to Abeome Inc.


  • V-ATPase
  • lysosomes
  • SPE-5
  • spermatogenesis
  • Caenorhabditis elegans

Developmental Genetics of Secretory Vesicle Acidification During Caenorhabditis elegans Spermatogenesis


Journal Title:



Volume 191, Number 2


, Pages 477-491

Type of Work:

Article | Post-print: After Peer Review


Secretory vesicles are used during spermatogenesis to deliver proteins to the cell surface. In Caenorhabditis elegans, secretory membranous organelles (MO) fuse with the plasma membrane to transform spermatids into fertilization-competent spermatozoa. We show that, like the acrosomal vesicle of mammalian sperm, MOs undergo acidification during development. Treatment of spermatids with the V-ATPase inhibitor bafilomycin blocks both MO acidification and formation of functional spermatozoa. There are several spermatogenesis-defective mutants that cause defects in MO morphogenesis, including spe-5. We determined that spe-5, which is on chromosome I, encodes one of two V-ATPase B paralogous subunits. The spe-5 null mutant is viable but sterile because it forms arrested, multi-nucleate spermatocytes. Immunofluorescence with a SPE-5-specific monoclonal antibody shows that SPE-5 expression begins in spermatocytes and is found in all subsequent stages of spermatogenesis. Most SPE-5 is discarded into the residual body during spermatid budding, but a small amount remains in budded spermatids where it localizes to MOs as a discrete dot. The other V-ATPase B subunit is encoded by vha-12, which is located on the X chromosome. Usually, spe-5 mutants are self-sterile in a wild-type vha-12 background. However, an extrachromosomal transgene containing wild-type vha-12 driven by its own promoter allows spe-5 mutant hermaphrodites to produce progeny, indicating that VHA-12 can at least partially substitute for SPE-5. Others have shown that the X chromosome is transcriptionally silent in the male germline, so expression of the autosomally located spe-5 gene ensures that a V-ATPase B subunit is present during spermatogenesis.

Copyright information:

© 2012 by the Genetics Society of America

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