Activation and repression activities of ash2 in Drosophila wing imaginal discs
Activation and repression activities of ash2 in Drosophila wing imaginal discs
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DOI：
10.1242/dev.01380
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发表时间：
2004-10-01
期刊：
影响因子：
4.6
通讯作者：
Serras, F
中科院分区：
文献类型：
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作者：
Angulo, M;Corominas, M;Serras, F
多梳（PcG）和三胸（trxG）组基因是参与维持发育决策的染色质调节因子。虽然它们作为同源异型基因的转录调节因子的功能已经有了很好的记录，但很少有人知道它们对其他靶基因的影响或它们在其他发育过程中的作用。在这项研究中，我们使用的图案的静脉和interveins在翅膀作为一个模型，以了解功能的trxG基因ash 2（缺席，小或同源异型光盘2）。我们表明，ash 2是维持激活的静脉间促进基因净和benefred（BS）和抑制菱形（rho），EGF受体（Egfr）途径的一个组成部分。此外，Egfr途径的功能丧失表型被ash 2突变体抑制，而功能获得表型被增强。我们的研究结果还表明，阿什2作为静脉L2组织基因knirps（kni），其表达上调整个翼成虫盘在阿什2突变体和有丝分裂克隆的阻遏物。此外，ash 2介导的kni抑制作用不依赖于spalt-major和spalt-related。总之，这些实验表明，ash 2在翅膀发育过程中的两个过程中发挥作用：（1）通过激活脉间基因或抑制脉分化基因来维持脉间细胞的命运;（2）在L2脉以外的组织中保持kni处于关闭状态。我们建议，阿什2复合物提供了一个分子框架所需的机制，以保持细胞的身份在翅膀的发展。
Polycomb (PcG) and trithorax (trxG) group genes are chromatin regulators involved in the maintenance of developmental decisions. Although their function as transcriptional regulators of homeotic genes has been well documented, little is known about their effect on other target genes or their role in other developmental processes. In this study, we have used the patterning of veins and interveins in the wing as a model with which to understand the function of the trxG gene ash2 (absent, small or homeotic discs 2). We show that ash2 is required to sustain the activation of the intervein-promoting genes net and blistered (bs) and to repress rhomboid (rho), a component of the EGF receptor (Egfr) pathway. Moreover, loss-of-function phenotypes of the Egfr pathway are suppressed by ash2 mutants, while gain-of-function phenotypes are enhanced. Our results also show that ash2 acts as a repressor of the vein L2-organising gene knirps (kni), whose expression is upregulated throughout the whole wing imaginal disc in ash2 mutants and mitotic clones. Furthermore, ash2-mediated inhibition of kni is independent of spalt-major and spalt-related. Together, these experiments indicate that ash2 plays a role in two processes during wing development: (1) maintaining intervein cell fate, either by activation of intervein genes or inhibition of vein differentiation genes; and (2) keeping kni in an off state in tissues beyond the L2 vein. We propose that the Ash2 complex provides a molecular framework for a mechanism required to maintain cellular identities in the wing development.