Abstract
The Caenorhabditis elegans gene lin-29 encodes a zinc-finger transcription factor that is required for hypodermal cell terminal differentiation and proper vulva morphogenesis. Here we demonstrate that lin- 29 is also required in males for productive mating. We show that lin-29 males can perform the early mating behaviors including response to hermaphrodite contact and vulva location, but they do not perform the subsequent steps of vulva attachment via spicule insertion and sperm transfer. Consistent with this observation, we found that lin-29 mutant spicules are on average 43% shorter than wild-type spicules while other male mating structures appear unaltered. In lin-29 mutants, spicule development goes awry after the generation of spicule cells, when spicule morphogenesis occurs in wild-type males. We show that LIN-29 accumulates in many cells of the wild-type male tail, including those that form the spicules. We demonstrate, through analysis of genetic mosaics, that the formation of wild-type-length spicules requires lin-29(+) in the AB.p lineage, the lineage that gives rise to the spicules and other male copulatory structures. Our mosaic analysis also reveals a role for lin-29(+) in the P1 lineage, which mainly produces sex muscles, cells of the somatic gonad, and body wall muscles.
| Original language | English (US) |
|---|---|
| Pages (from-to) | 142-156 |
| Number of pages | 15 |
| Journal | Developmental Biology |
| Volume | 206 |
| Issue number | 2 |
| DOIs | |
| State | Published - Feb 15 1999 |
Bibliographical note
Funding Information:We thank Helen Chamberlin for invaluable advice on B cell lineage analysis and spicule defects; Jocelyn Shaw and Jeff Simon for critical reading of the manuscript; Andrew Robinson for help with statistical analyses; Mike Herman for advice about males; members of our laboratory and the Twin Cities Worm Labs for useful discussions; and Craig Mello, Geraldine Seydoux, and Gary Ruvkun for generously allowing S.E. to complete portions of this work in their labs. S.E. was partially supported by a grant from the Department of Genetics and Cell Biology at the University of Minnesota. Some of the strains used in this study were provided by the Caenorhabditis elegans Genetics Center which is funded by the NIH. This work was funded by National Institutes of Health Grant GM 50227 to A.E.R.