Drosophila brachyenteron regulates gene activity and morphogenesis in the gut.

Drosophila brachyenteron regulates gene activity and morphogenesis in the gut.
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发表时间:
1996-12
期刊:
影响因子:
4.6
通讯作者:
J. Singer;R. Harbecke;T. Kusch;R. Reuter;J. Lengyel
J. Singer;R. Harbecke;T. Kusch;R. Reuter;J. Lengyel
中科院分区:
生物学2区
文献类型:
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作者:
J. Singer;R. Harbecke;T. Kusch;R. Reuter;J. Lengyel

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染色体区域68 D/E是果蝇肠道发育的各个方面所必需的;在该区域内映射了Brachyury同源T相关基因(Trg),其DNA挽救了缺乏68 D/E的后肠缺陷。从13,000条诱变染色体的筛选中,我们鉴定了6个非互补等位基因,它们在68 D/E缺陷时是致命的,并显示出后肠表型。这些突变构成了等位基因系列,并且都被Trg转基因拯救到活力。我们命名的突变等位基因和遗传位点,他们定义brachyenteron(byn);最强的等位基因的表型特征允许确定byn在胚胎发生中的作用。byn的表达被tailless激活,但byn本身不调节。Byn在后肠和肛垫原基中的表达是调控编码转录因子(偶跳、钩状、尾状、腹部B和直足)和细胞信号分子(无翅和十肢麻痹)的基因所必需的。在byn突变胚胎中,这些原基中基因活性的缺陷程序随后是细胞凋亡(由reaper表达启动并由巨噬细胞吞噬完成),导致后肠和肛门垫严重减少。虽然byn在中肠或马氏管中不表达,但它是中肠收缩形成和马氏管伸长所必需的。
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.