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黑腹果蝇异常卵母细胞基因的发育遗传学分析与分子克隆

Developmental genetical analysis and molecular cloning of the abnormal oocyte gene of Drosophila melanogaster.

作者信息

Tomkiel J, Fanti L, Berloco M, Spinelli L, Tamkun J W, Wakimoto B T, Pimpinelli S

机构信息

Department of Genetics, University of Washington, Seattle 98195, USA.

出版信息

Genetics. 1995 Jun;140(2):615-27. doi: 10.1093/genetics/140.2.615.

Abstract

Studies of the abnormal oocyte (abo) gene of Drosophila melanogaster have previously been limited to the analysis of a single mutant allele, abnormal oocyte1 (abo1). The abo1 mutation causes a maternal-effect lethality that can be partially rescued zygotically by the abo+ allele and by increasing the dosage of specific regions of heterochromatin denoted ABO. This report describes the properties of abo2, a new P-element-induced allele that allowed us to reexamine the nature of maternal-effect defect. Comparisons of the phenotype of progeny of abo1/abo1 and abo1/abo2 females show that the preblastoderm lethality previously described as a component of the abo mutant maternal effect results from a recessive fertilization defect associated with the abo1 chromosome. We demonstrate here that the abo-induced maternal effect lethality occurs predominately late in embryogenesis after cuticle deposition but before hatching. The phenocritical period for zygotic rescue by heterochromatin coincides with this period of late embryogenesis. We have used the abo2 mutation to map and molecularly clone the gene. We show that the abo gene is located in the 32C cytogenetic interval and identify the putative abo transcript from mRNA isolated from adult females. Using germline transformation, we show that a 9-kb genomic fragment to which the transcript maps, partially fulfills requirement for maternal and zygotic abo+ function.

摘要

此前,对黑腹果蝇异常卵母细胞(abo)基因的研究仅限于对单个突变等位基因——异常卵母细胞1(abo1)的分析。abo1突变会导致母性效应致死,这种致死效应可通过abo +等位基因以及增加异染色质特定区域(称为ABO)的剂量在合子阶段得到部分挽救。本报告描述了abo2的特性,abo2是一个新的P因子诱导等位基因,它使我们能够重新审视母性效应缺陷的本质。对abo1/abo1和abo1/abo2雌性后代的表型比较表明,先前被描述为abo突变母性效应一部分的胚盘形成前致死是由与abo1染色体相关的隐性受精缺陷导致的。我们在此证明,abo诱导的母性效应致死主要发生在胚胎发育后期,即角质层沉积之后但孵化之前。异染色质合子挽救的表型关键期与胚胎发育后期这一时期一致。我们利用abo2突变对该基因进行了定位并进行了分子克隆。我们表明,abo基因位于32C细胞遗传学区间,并从成年雌性分离的mRNA中鉴定出了推定的abo转录本。通过种系转化,我们表明转录本所对应的一个9 kb基因组片段部分满足了母性和合子abo +功能的要求。

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