Morphogenetic furrow initiation and progression during eye development in Drosophila: the roles of decapentaplegic, hedgehog and eyes absent.
Morphogenetic furrow initiation and progression during eye development in Drosophila: the roles of decapentaplegic, hedgehog and eyes absent.
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发表时间：
2000-03
期刊：
影响因子：
4.6
通讯作者：
J. Curtiss;M. Mlodzik
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文献类型：
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作者：
J. Curtiss;M. Mlodzik
果蝇信号因子Decapentaplegic(DPP)通过调节组织特异性基因的表达来介导刺猬(HH)在组织构型中的作用。在眼盘中，转录因子无眼(EY)、无眼(EYA)、正弦Oculis(SO)和腊肠(DAC)与这些信号分子一起参与一个复杂的调控网络，导致眼睛发育的启动。我们对早期眼盘功能关系的分析表明，HH和DPP在调节EY方面没有作用，但对eya、So和Dac的表达是必需的。我们表明，在功能缺失的DPP突变背景中恢复eya的表达足以诱导SO和DAC的表达，并挽救眼睛的发育。因此，一旦表达出来，eya就可以在没有民进党的情况下发挥其功能。这些实验表明，DPP在EY下游或与EY并行，但在EYA、SO和DAC的上游起作用。另外的控制由维持eya和so的表达并包括DPP的反馈环提供。外源性EY、EYA、SO和DAC的过度表达干扰了野生型眼睛的发育，这一事实表明了在眼睛发育的早期维持这些因子的适当水平的复杂机制的重要性。虽然在HH或DPP信号突变体中眼睛发育的启动都失败了，但随后的形态发生皱纹的进展只是放缓了。然而，我们发现同时突变了HH和DPP信号成分的克隆完全阻止了皱纹的进展和眼睛的分化，这表明HH和DPP在这一过程中起着部分冗余的功能。有趣的是，eya、so和dac与皱纹相关的表达不受双突变组织的影响，这表明在皱纹进展过程中，某些其他因子(S)调节它们的表达。
The Drosophila signaling factor decapentaplegic (dpp) mediates the effects of hedgehog (hh) in tissue patterning by regulating the expression of tissue-specific genes. In the eye disc, the transcription factors eyeless (ey), eyes absent (eya), sine oculis (so) and dachshund (dac) participate with these signaling molecules in a complex regulatory network that results in the initiation of eye development. Our analysis of functional relationships in the early eye disc indicates that hh and dpp play no role in regulating ey, but are required for eya, so and dac expression. We show that restoring expression of eya in loss-of-function dpp mutant backgrounds is sufficient to induce so and dac expression and to rescue eye development. Thus, once expressed, eya can carry out its functions in the absence of dpp. These experiments indicate that dpp functions downstream of or in parallel with ey, but upstream of eya, so and dac. Additional control is provided by a feedback loop that maintains expression of eya and so and includes dpp. The fact that exogenous overexpression of ey, eya, so and dac interferes with wild-type eye development demonstrates the importance of such a complicated mechanism for maintaining proper levels of these factors during early eye development. Whereas initiation of eye development fails in either Hh or Dpp signaling mutants, the subsequent progression of the morphogenetic furrow is only slowed down. However, we find that clones that are simultaneously mutant for Hh and Dpp signaling components completely block furrow progression and eye differentiation, suggesting that Hh and Dpp serve partially redundant functions in this process. Interestingly, furrow-associated expression of eya, so and dac is not affected by double mutant tissue, suggesting that some other factor(s) regulates their expression during furrow progression.