Induction and autoregulation of the anti-proneural gene Bar during retinal neurogenesis in Drosophila
Induction and autoregulation of the anti-proneural gene Bar during retinal neurogenesis in Drosophila
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DOI：
10.1242/dev.01426
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发表时间：
2004-11-01
期刊：
影响因子：
4.6
通讯作者：
Choi, KW
中科院分区：
文献类型：
--
作者：
Lim, JH;Choi, KW
果蝇眼成虫盘神经发生受正负调控基因的相互作用控制。碱性螺旋-环-螺旋（bHLH）转录因子Atonal（Ato）在形态发生沟中起着诱导R8创始神经元形成的重要原神经功能。Bar同源结构域蛋白是基底未分化视网膜前体细胞中ato转录抑制所必需的，以防止眼盘沟后的异位神经发生。因此，在基底未分化细胞中Bar表达的精确调节对于眼睛中的神经模式至关重要。我们的证据表明，酒吧在基础未分化细胞的表达是由至少三种不同的途径，这取决于发育时间和在眼盘的位置。首先，在沟起始时，Bar表达通过来自椎间盘后缘的Hedgehog（Hh）信号传导独立于Ato诱导。第二，在沟进展期间，Bar表达也由来自迁移沟的Ato依赖性EGFR（表皮生长因子受体）信号传导诱导。最后，一旦启动，Bar表达可以通过正性自动调节来维持。因此，我们提出，Bar表达的Ato抑制域的建立和维护的非自主Hh/EGFR信号通路和Bar的自动调节的组合。
Neurogenesis in Drosophila eye imaginal disc is controlled by interactions of positive and negative regulatory genes. The basic helix-loop-helix (bHLH) transcription factor Atonal (Ato) plays an essential proneural function in the morphogenetic furrow to induce the formation of R8 founder neurons. Bar homeodomain proteins are required for transcriptional repression of ato in the basal undifferentiated retinal precursor cells to prevent ectopic neurogenesis posterior to the furrow of the eye disc. Thus, precise regulation of Bar expression in the basal undifferentiated cells is crucial for neural patterning in the eye. We show evidence that Bar expression in the basal undifferentiated cells is regulated by at least three different pathways, depending on the developmental time and the position in the eye disc. First, at the time of furrow initiation, Bar expression is induced independent of Ato by Hedgehog (Hh) signaling from the posterior margin of the disc. Second, during furrow progression, Bar expression is also induced by Ato-dependent EGFR (epidermal growth factor receptor) signaling from the migrating furrow. Finally, once initiated, Bar expression can be maintained by positive autoregulation. Therefore, we propose that the domain of Bar expression for Ato repression is established and maintained by a combination of non autonomous Hh/EGFR signaling pathways and autoregulation of Bar.