Worm Breeder's Gazette 16(4): 25 (October 1, 2000)
These abstracts should not be cited in bibliographies. Material contained herein should be treated as personal communication and should be cited as such only with the consent of the author.
|1||Department of Molecular and Cellular Biology, University of Arizona, Tucson 85704 firstname.lastname@example.org|
|2||Department of Molecular and Cellular Biology, University of Arizona, Tucson 85704 email@example.com|
Spermiogenesis is the rapid and dramatic differentiation of a spherical immotile spermatid to a mature crawling spermatozoon. Spermiogenesis normally occurs in response to an extracellular signal received just before the sperm gains its first opportunity to fertilize oocytes. For hermaphrodites, spermiogenesis takes place after sperm have entered the fertilization chambers--the spermathecae; male sperm undergo spermiogenesis when they enter the hermaphrodite uterus. A collection of mutants in four genes (spe-8, -12, -27, and -29) fail to undergo spermiogenesis in response to the hermaphrodite-derived signal. In a screen for suppressors of spe-27, we isolated numerous mutants, which all turned out to be alleles of the same gene, spe-6. These mutants, which suppress all four of the spermiogenesis defective genes named above, have spermatids that undergo spermiogenesis precociously. spe-6 was previously identified in our lab by its null mutants, in whose spermatocytes the major sperm protein (MSP) fails to assemble into the paracrystalline fibrous bodies. Spermatocytes from null spe-6 mutants also have defects in chromosome segregation, and almost never produce spermatids. To understand the causes and relationships between these two disparate sets of phenotypes caused by different alleles of the same gene, we identified spe-6 by microinjection rescue of a null spe-6 mutant with a PCR fragment encoding the putative spe-6 gene (see the accompanying article on how we located spe-6). spe-6 encodes a member of the large (88 member) casein kinase I family of serine/threonine protein kinases. Sterile alleles have either a premature translational stop or a mutation of a universally conserved T/S in the catalytic domain. All of the suppressor alleles we sequenced (18 to date) have mutations that appear unlikely to eliminate the enzyme's activity, consistent with their non-null phenotype. Amazingly, fully half of the casein kinase I members appear to be spermatogenesis-specific or -enriched, according to our microarray data, pointing to a prominent role for this gene family in sperm development and signaling.