Voelker R A, Huang S M, Wisely G B, Sterling J F, Bainbridge S P, Hiraizumi K
Laboratory of Molecular Genetics, National Institute of Environmental Health Sciences, Research Triangle Park, North Carolina 27709.
Genetics. 1989 Jul;122(3):625-42. doi: 10.1093/genetics/122.3.625.
Recessive mutations at the suppressor of sable [su(s)] locus in Drosophila melanogaster result in suppression of second site mutations caused by insertions of the mobile element 412. In order to determine whether su(s) mutations might have other phenotypes, a saturation mapping of the su(s) region was carried out. The screen yielded 76 mutations that comprise ten genetic complementation groups ordered distal to proximal as follows: l(1)1Bh, l(1)1Bi, M(1)1B, su(s), l(1)1Bk, l(1)1Ca, mul, tw, l(1)lDa and brc. Twenty-three of the mutations are su(s) alleles, and all are suppressors of the 412-insertion-caused v1 allele. Although the screen could have detected su(s) mutations causing sex-specific dominant lethality or sterility as well as all types of recessive lethality or sterility, the only other phenotype observed was male sterility that is enhanced by cold temperature. This type of sterility is exhibited only by alleles induced by base-substitution-causing mutagens. Genetic functions of the poly(A+) messages transcribed from the su(s) microregion were identified by the reintroduction of cloned sequences into embryos by P element transformation. su(s) function has been attributed to a 5-kb message. The segment of DNA encoding only this 5-kb message rescues both the suppression and cold-sensitive male sterility phenotypes of su(s). Minute (1) 1B has been provisionally identified as encoding a 3.5-kb message; lethal (1)1Bi encodes a 1-kb message; and lethal (1)1Bk encodes a 4-kb message. The possible functions of su(s) and M(1)1B are discussed.
黑腹果蝇中黑貂抑制因子[su(s)]位点的隐性突变会导致由移动元件412插入引起的第二位点突变受到抑制。为了确定su(s)突变是否可能具有其他表型,对su(s)区域进行了饱和图谱分析。该筛选产生了76个突变,这些突变包含十个遗传互补群,从远端到近端依次排列如下:l(1)1Bh、l(1)1Bi、M(1)1B、su(s)、l(1)1Bk、l(1)1Ca、mul、tw、l(1)lDa和brc。其中23个突变是su(s)等位基因,并且都是412插入引起的v1等位基因的抑制子。尽管该筛选本可以检测到导致性别特异性显性致死或不育以及所有类型隐性致死或不育的su(s)突变,但观察到的唯一其他表型是低温增强的雄性不育。这种不育类型仅由碱基取代诱变剂诱导的等位基因表现出来。通过P元件转化将克隆序列重新导入胚胎,确定了从su(s)微区域转录的多聚(A+)信息的遗传功能。su(s)功能归因于一个5 kb的信息。仅编码此5 kb信息的DNA片段拯救了su(s)的抑制和冷敏感雄性不育表型。微小(1)1B已被初步确定为编码一个3.5 kb的信息;致死(1)1Bi编码一个1 kb的信息;致死(1)1Bk编码一个4 kb的信息。讨论了su(s)和M(1)1B的可能功能。