schnurri is required for dpp-dependent patterning of the Drosophila wing.
schnurri is required for dpp-dependent patterning of the Drosophila wing.
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DOI：
10.1006/dbio.2000.9900
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发表时间：
2000-11
影响因子：
2.7
通讯作者：
Jesús Torres-Vázquez;R. Warrior;K. Arora
中科院分区：
文献类型：
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作者：
Jesús Torres-Vázquez;R. Warrior;K. Arora
BMP相关配体Decapentaplegic（Dpp）在果蝇胚胎发生和幼虫发育过程中的模式形成中具有良好的作用。先前的工作已经表明，Dpp应答基因的转录需要BMP特异性Smad（Mothers against dpp，Mad）的活性。在这项研究中，我们研究了锌指转录因子Schnurri（Shn）在介导的核反应DPP在成人图案的作用。使用克隆分析，我们表明，翅成虫盘细胞突变SHN未能转录基因spalt，optomotor盲，残留，爸爸，这是已知的诱导DPP信号。shn克隆还异位表达brinker，一种响应于dpp而下调的基因，从而暗示Shn参与Dpp靶基因的激活和抑制。我们证明，损失的SHN活性影响前后图案和细胞增殖的机翼叶片，在某种程度上，反映了在这些过程中的DPP的分级要求。此外，我们发现shn在蛹翅中表达，并在此阶段介导依赖dpp的静脉分化中起着独特的作用。SHN活性的缺乏导致缺陷，这些缺陷在性质和严重程度上与消除Mad所引起的缺陷相似，这表明SHN在发育中的翅膀中的DPP信号转导中具有重要作用。我们的数据是一致的模型中，Shn作为一个辅因子的疯狂。
The BMP-related ligand Decapentaplegic (Dpp) has a well-characterized role in pattern formation during Drosophila embryogenesis and in larval development. Previous work has shown that transcription of Dpp-responsive genes requires the activity of the BMP-specific Smad, Mothers against dpp (Mad). In this study we investigated the role of the zinc finger transcription factor Schnurri (Shn) in mediating the nuclear response to Dpp during adult patterning. Using clonal analysis, we show that wing imaginal disc cells mutant for shn fail to transcribe the genes spalt, optomotor blind, vestigial, and Dad, that are known to be induced by dpp signaling. shn clones also ectopically express brinker, a gene that is downregulated in response to dpp, thus implicating Shn in both activation and repression of Dpp target genes. We demonstrate that loss of shn activity affects anterior-posterior patterning and cell proliferation in the wing blade, in a manner that reflects the graded requirement for Dpp in these processes. Furthermore, we find that shn is expressed in the pupal wing and plays a distinct role in mediating dpp-dependent vein differentiation at this stage. The absence of shn activity results in defects that are similar in nature and severity to those caused by elimination of Mad, suggesting that Shn has an essential role in dpp signal transduction in the developing wing. Our data are consistent with a model in which Shn acts as a cofactor for Mad.