Minniti A N, Sadler C, Ward S
Department of Molecular and Cellular Biology, University of Arizona, Tucson 85721, USA.
Genetics. 1996 May;143(1):213-23. doi: 10.1093/genetics/143.1.213.
Hermaphrodites with mutations in the spe-27 gene are self-sterile, laying only unfertilized eggs; mutant males are fertile. Hermaphrodites make spermatids that fail to activate to crawling spermatozoa so passing oocytes sweep them out of the spermatheca. These spermatids do activate and produce self-progeny if young mutant hermaphrodites are mated by fertile (or sterile) males. Spermatids isolated from either mutant males or hermaphrodites initiate activation in vitro when treated with proteases, but then arrest with spiky membrane projections that resemble those of a normal intermediate in pseudopod formation. These phenotypes are identical to spe-8 and spe-12 mutants. They can be explained if males and hermaphrodites have distinct pathways for spermatid activation, and these three genes are necessary only for the hermaphrodite pathway. Consistent with this model, when spe-27 mutant male spermatids without seminal fluid are artificially inseminated into hermaphrodites, they fail to activate. The spe-27 gene has been isolated, sequenced and its regulatory regions identified. The sequence predicts a 131 amino acid polypeptide that has no striking structural motifs and no resemblance to known proteins. Two of the mutations in spe-27 alter mRNA splicing; a third mutation is a temperature-sensitive missense mutation.
spe-27基因发生突变的雌雄同体是自我不育的,只产未受精的卵;突变的雄性是可育的。雌雄同体产生的精细胞无法激活成为游动的精子,因此经过的卵母细胞会将它们从受精囊中排出。如果年轻的突变雌雄同体与可育(或不育)雄性交配,这些精细胞会被激活并产生自产后代。从突变雄性或雌雄同体中分离出的精细胞在体外经蛋白酶处理后会启动激活,但随后会停滞,带有类似于伪足形成过程中正常中间体的尖刺状膜突起。这些表型与spe-8和spe-12突变体相同。如果雄性和雌雄同体有不同的精细胞激活途径,且这三个基因仅对雌雄同体途径是必需的,那么这些现象就可以得到解释。与此模型一致的是,当没有精液的spe-27突变雄性精细胞被人工授精到雌雄同体中时,它们无法被激活。spe-27基因已被分离、测序并确定了其调控区域。该序列预测有一个131个氨基酸的多肽,没有明显的结构基序,与已知蛋白质也没有相似之处。spe-27中的两个突变改变了mRNA剪接;第三个突变是一个温度敏感的错义突变。