INITIATION OF SPERMIOGENESIS IN C-ELEGANS - A PHARMACOLOGICAL AND GENETIC-ANALYSIS
INITIATION OF SPERMIOGENESIS IN C-ELEGANS - A PHARMACOLOGICAL AND GENETIC-ANALYSIS
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DOI:
10.1016/0012-1606(89)90088-2
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发表时间:
1989-07-01
影响因子:
2.7
通讯作者:
WARD, S
中科院分区:
文献类型:
--
作者:
SHAKES, DC;WARD, S
Spermiogensis in Caenorhabditis elegans involves the conversion of spherical, sessile spermatids into bipolar, crawling spermatozoa. In males, spermiogenesis is induced by mating, while in hermaphrodites, spermiogenesis occurs before the first oocytes ar fertilized. Alternatively, spermiogenesis can be induced in vitro by treatemtn with monensin, triethanolamine, or pronase. Treatment with the calmodulin inhibitors, trifluoperazine, chlorpromazine, or W7, also induces spermiogenesis in vitro with a half maximal effect at 20 .mu.M. Upon initial activation, spermatids extend long, thin spikes and undergo extensive cellular movements. Eventually, a single motile pseudopod forms through the restructuring of one or more of these spikes. These transient spikes can be prolonged in vitro by removing triethanolamine as soon as the spermatids first form spikes. Spermatids from spe-8 and spe-12 spermatogenesis-defective (spe) mutants activate in vivo with male but not hermaphrodite sperm activator. In vitro, the mutant spermatids arrest spermiogenesis at the spike stage with pronase, but form normal spermatozoa if subsequently or initially treated with monesin or triethanolamine. We present a model of spermiogenesis in which the mutant defects and the action of the pharmacological agents are ordered relative to one another.