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果蝇短肠基因调节肠道中的基因活性和形态发生。

Drosophila brachyenteron regulates gene activity and morphogenesis in the gut.

作者信息

Singer J B, Harbecke R, Kusch T, Reuter R, Lengyel J A

机构信息

Department of Molecular, Cell and Developmental Biology, UCLA, Los Angeles, CA 90095-1606, USA.

出版信息

Development. 1996 Dec;122(12):3707-18. doi: 10.1242/dev.122.12.3707.

Abstract

Chromosomal region 68D/E is required for various aspects of Drosophila gut development; within this region maps the Brachyury homolog T-related gene (Trg), DNA of which rescues the hindgut defects of deficiency 68D/E. From a screen of 13,000 mutagenized chromosomes we identified six non-complementing alleles that are lethal over deficiencies of 68D/E and show a hindgut phenotype. These mutations constitute an allelic series and are all rescued to viability by a Trg transgene. We have named the mutant alleles and the genetic locus they define brachyenteron (byn); phenotypic characterization of the strongest alleles allows determination of the role of byn in embryogenesis. byn expression is activated by tailless, but byn does not regulate itself. byn expression in the hindgut and anal pad primordia is required for the regulation of genes encoding transcription factors (even-skipped, engrailed, caudal, AbdominalB and orthopedia) and cell signaling molecules (wingless and decapentaplegic). In byn mutant embryos, the defective program of gene activity in these primordia is followed by apoptosis (initiated by reaper expression and completed by macrophage engulfment), resulting in severely reduced hindgut and anal pads. Although byn is not expressed in the midgut or the Malpighian tubules, it is required for the formation of midgut constrictions and for the elongation of the Malpighian tubules.

摘要

果蝇肠道发育的多个方面都需要68D/E染色体区域;在该区域定位了短尾同源物T相关基因(Trg),其DNA可挽救68D/E缺失的后肠缺陷。通过对13000条诱变染色体的筛选,我们鉴定出6个非互补等位基因,它们在68D/E缺失时致死,并表现出后肠表型。这些突变构成一个等位基因系列,并且都能被Trg转基因挽救至存活状态。我们将这些突变等位基因及其所定义的基因座命名为短肠(byn);对最强等位基因的表型特征分析有助于确定byn在胚胎发生中的作用。byn的表达由无尾激活,但byn并不自我调节。后肠和肛垫原基中byn的表达对于调控编码转录因子(偶数跳、 engrailed、尾、腹B和正位)和细胞信号分子(无翅和脱壳蛋白)的基因是必需的。在byn突变胚胎中,这些原基中基因活性的缺陷程序随后会发生凋亡(由收割者表达启动并由巨噬细胞吞噬完成),导致后肠和肛垫严重减少。虽然byn在中肠或马氏管中不表达,但它对于中肠收缩的形成和马氏管的伸长是必需的。

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