首页> 外文期刊>Genetics: A Periodical Record of Investigations Bearing on Heredity and Variation >Mutations in the bli-4 (I) locus of Caenorhabditis elegans disrupt both adult cuticle and early larval development.
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Mutations in the bli-4 (I) locus of Caenorhabditis elegans disrupt both adult cuticle and early larval development.

机译:秀丽隐杆线虫的bli-4(I)基因座中的突变破坏了成年表皮和早期幼虫的发育。

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The bli-4 (I) gene of Caenorhabditis elegans had been previously defined by a single recessive mutation, e937, which disrupts the structure of adult-stage cuticle causing the formation of fluid-filled separations of the cuticle layers, or blisters. We report the identification of 11 new alleles of bli-4, all early larval lethals, including an allele induced by transposon mutagenesis. Nine of the lethal alleles failed to complement the blistered phenotype of e937; two alleles, s90 and h754, complement e937. The complementing alleles arrested development somewhat later than the noncomplementing alleles, which blocked just prior to hatching. We conclude that bli-4 is a complex locus with an essential function late in embryogenesis. We investigated the blistered phenotype of e937 through interactions with other mutations that alter worm morphology or cuticle structure. Recessive and dominant epistasis of several dumpy mutations over the blistered phenotype was observed. Using two heterochronic mutations that alter the developmental stage at which adult cuticle is expressed, we observed that adult worms that lack an adult-stage cuticle could not express blisters. However, late larval worms that expressed the adult cuticle did not express blisters either. It seems likely that the presence of the adult cuticle is necessary, but not sufficient, for blister expression. Blistering resulting from e937 is more severe in trans to null alleles, indicating that e937 is hypomorphic. We postulate that the adult-specific blistering is due to an altered or reduced function of bli-4 gene product in the adult cuticle.(ABSTRACT TRUNCATED AT 250 WORDS)
机译:秀丽隐杆线虫的bli-4(I)基因先前已由单个隐性突变e937定义,该突变会破坏成年阶段角质层的结构,从而导致角质层或水泡形成液体填充的分离。我们报告了11个新的bli-4等位基因的鉴定,所有这些幼虫致死率包括由转座子诱变诱导的等位基因。致命的等位基因中有9个未能补充e937的水泡表型。 s90和h754这两个等位基因与e937互补。互补等位基因比非互补等位基因在孵化之前受阻的发育迟缓要晚一些。我们得出结论,bli-4是一个复杂的基因座,在胚胎发生后期具有重要功能。我们通过与改变蠕虫形态或表皮结构的其他突变相互作用研究了e937的水泡表型。观察到在水泡表型上有几个突变的隐性和显性上位性。使用两个异时突变来改变成年角质层表达的发育阶段,我们观察到缺少成年角质层的成虫不表达水泡。但是,表达成年角质层的晚期幼虫蠕虫也不表达水泡。成人角质层的存在似乎对于水泡表达是必要的,但并不足够。反式至无效等位基因由e937引起的起泡更为严重,表明e937是亚型的。我们推测成人特异性水疱是由于成人角质层中bli-4基因产物的功能改变或减少所致(摘要截短为250字)

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