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对果蝇中编码液泡ATP酶B亚基的基因vha55进行分析和失活,揭示了一种幼虫致死表型。

Analysis and inactivation of vha55, the gene encoding the vacuolar ATPase B-subunit in Drosophila melanogaster reveals a larval lethal phenotype.

作者信息

Davies S A, Goodwin S F, Kelly D C, Wang Z, Sözen M A, Kaiser K, Dow J A

机构信息

Division of Molecular Genetics, Institute for Biomedical and Life Sciences, University of Glasgow, Glasgow G12 8QQ, United Kingdom.

出版信息

J Biol Chem. 1996 Nov 29;271(48):30677-84. doi: 10.1074/jbc.271.48.30677.

Abstract

Vacuolar ATPases play major roles in endomembrane and plasma membrane proton transport in eukaryotes. A Drosophila melanogaster cDNA encoding vha55, the 55-kDa vacuolar ATPase (V-ATPase) regulatory B-subunit, was characterized and mapped to 87C2-4 on chromosome 3R. A fly line was identified that carried a single lethal P-element insertion within the coding portion of gene, and its LacZ reporter gene revealed elevated expression in Malpighian tubules, rectum, antennal palps, and oviduct, regions where V-ATPases are believed to play a plasma membrane, rather than an endomembrane, role. The P-element vha55 insertion was shown to be allelic to a known lethal complementation group l(3)SzA (= l(3)87Ca) at 87C, for which many alleles have been described previously. Deletions of the locus have been shown to be larval lethal, whereas point mutations show a range of phenotypes from subvital to embryonic lethal, implying that severe alleles confer a partial dominant negative phenotype. The P-element null allele of vha55 was shown also to suppress ectopic sex combs in Polycomb males, suggesting that transcriptional silencing may be modulated by genes other than those with known homeotic or DNA binding functions.

摘要

液泡型ATP酶在真核生物的内膜和质膜质子转运中起主要作用。对果蝇中编码vha55(55 kDa液泡型ATP酶(V-ATP酶)调节性B亚基)的cDNA进行了表征,并将其定位到3R染色体上的87C2-4。鉴定出一条果蝇品系,其在该基因的编码部分携带单个致死性P因子插入,其LacZ报告基因显示在马氏管、直肠、触角须和输卵管中表达升高,这些区域被认为V-ATP酶发挥质膜而非内膜的作用。P因子vha55插入显示与87C处已知的致死互补群l(3)SzA(= l(3)87Ca)等位,此前已描述了许多该互补群的等位基因。该基因座的缺失已被证明是幼虫致死的,而点突变表现出从亚活力到胚胎致死的一系列表型,这意味着严重的等位基因具有部分显性负表型。vha55的P因子无效等位基因也被证明可抑制多梳蛋白雄性果蝇中的异位性梳,这表明转录沉默可能受除具有已知同源异型或DNA结合功能的基因以外的其他基因调节。

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