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Decapentaplegic and growth control in the developing Drosophila wing

机译:发育中的果蝇翅膀的十足功能和生长控制

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摘要

As a central model for morphogen action during animal development, the bone morphogenetic protein 2/4 (BMP2/4)-like ligand Decapentaplegic (Dpp) is proposed to form a long-range signalling gradient that directs both growth and pattern formation during Drosophila wing disc development(1-6). While the patterning role of Dpp secreted from a stripe of cells along the anterior-posterior compartmental boundary is well established(1,2,6), the mechanism by which a Dpp gradient directs uniform cell proliferation remains controversial and poorly understood(7-13). Here, to determine the precise spatiotemporal requirements for Dpp during wing disc development, we use CRISPR-Cas9-mediated genome editing to generate a flippase recognition target (FRT)-dependent conditional null allele. By genetically removing Dpp from its endogenous stripe domain, we confirm the requirement of Dpp for the activation of a downstream phospho-Mothers against dpp (p-Mad) gradient and the regulation of the patterning targets spalt (sal), optomotor blind (omb; also known as bifid) and brinker (brk). Surprisingly, however, third-instar wing blade primordia devoid of compartmental dpp expression maintain relatively normal rates of cell proliferation and exhibit only mild defects in growth. These results indicate that during the latter half of larval development, the Dpp morphogen gradient emanating from the anterior-posterior compartment boundary is not directly required for wing disc growth.
机译:作为动物发育过程中形态发生素作用的中心模型,提出了骨形态发生蛋白2/4(BMP2 / 4)样配体去Capcappleplegic(Dpp)形成长距离的信号梯度,指导果蝇翅的生长和模式形成光盘开发(1-6)。虽然沿前后隔室边界的细胞条带分泌的Dpp的模式作用已经确立(1,2,6),但Dpp梯度指导均匀细胞增殖的机制仍然存在争议并且了解甚少(7-13) )。在这里,为了确定翼片发育过程中Dpp的精确时空要求,我们使用CRISPR-Cas9介导的基因组编辑来生成依赖于flippase识别靶标(FRT)的条件性无效等位基因。通过从其内源条带结构域中遗传去除Dpp,我们证实了Dpp对于激活下游磷酸化母亲对抗dpp(p-Mad)梯度和调节构图靶标口角(sal),光致盲(omb;也称为bifid)和brinker(brk)。然而,令人惊讶的是,缺乏隔室dpp表达的三龄翼状原基维持相对正常的细胞增殖速率,并且仅表现出轻微的生长缺陷。这些结果表明,在幼体发育的后半段,从前-后室边界发出的Dpp形态发生子梯度并不是翼盘生长直接需要的。

著录项

  • 来源
    《Nature》 |2015年第7578期|375-378|共4页
  • 作者单位

    Stowers Inst Med Res, Kansas City, MO 64110 USA;

    Stowers Inst Med Res, Kansas City, MO 64110 USA|Univ Kansas, Sch Med, Dept Anat & Cell Biol, Kansas City, KS 66160 USA;

  • 收录信息 美国《科学引文索引》(SCI);美国《工程索引》(EI);美国《生物学医学文摘》(MEDLINE);美国《化学文摘》(CA);
  • 原文格式 PDF
  • 正文语种 eng
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