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T-box基因optomotor-blind在果蝇翅膀图案形成中的作用。

The role of the T-box gene optomotor-blind in patterning the Drosophila wing.

作者信息

del Alamo Rodríguez David, Terriente Felix Javier, Díaz-Benjumea Fernando J

机构信息

Centro de Biología Molecular-C.S.I.C, Universidad Autónoma de Madrid-Cantoblanco, Madrid E-28049, Spain.

出版信息

Dev Biol. 2004 Apr 15;268(2):481-92. doi: 10.1016/j.ydbio.2004.01.005.

Abstract

The development of the Drosophila wing is governed by the action of two morphogens encoded by the genes decapentaplegic (dpp; a member of the BMP gene family) and wingless (wg; a member of the WNT gene family), which promote cell proliferation and pattern the wing. Along the anterior/posterior (A/P) axis, the precise expression of decapentaplegic and its receptors is required for the transcriptional regulation of specific target genes. In the present work, we analyze the function of the T-box gene optomotor-blind (omb), a decapentaplegic target gene. The wings of optomotor-blind mutants have two apparently opposite phenotypes: the central wing is severely reduced and shows massive cell death, mainly in the distal-most wing, and the lateral wing shows extra cell proliferation. Here, we present genetic evidence that optomotor-blind is required to establish the graded expression of the decapentaplegic type I receptor encoded by the gene thick veins (tkv) to repress the expression of the gene master of thick veins and also to activate the expression of spalt (sal) and vestigial (vg), two decapentaplegic target genes. optomotor-blind plays a role in wing development downstream of decapentaplegic by controlling the expression of its receptor thick veins and by mediating the activation of target genes required for the correct development of the wing. The lack of optomotor-blind produces massive cell death in its expression domain, which leads to the mis-activation of the Notch pathway and the overproliferation of lateral wing cells.

摘要

果蝇翅膀的发育受由基因“截瘫”(dpp;BMP基因家族成员)和“无翅”(wg;WNT基因家族成员)编码的两种形态发生素的作用控制,它们促进细胞增殖并为翅膀定型。沿前后(A/P)轴,“截瘫”及其受体的精确表达对于特定靶基因的转录调控是必需的。在本研究中,我们分析了T-box基因“视动性失明”(omb)的功能,它是“截瘫”的一个靶基因。“视动性失明”突变体的翅膀有两种明显相反的表型:翅膀中部严重缩小并显示大量细胞死亡,主要在翅膀最远端,而侧翼显示额外的细胞增殖。在此,我们提供遗传学证据表明,需要“视动性失明”来建立由基因“粗脉”(tkv)编码的“截瘫”I型受体的梯度表达,以抑制“粗脉主控”基因的表达,并激活“spalt”(sal)和“残翅”(vg)这两个“截瘫”靶基因的表达。“视动性失明”通过控制其受体“粗脉”的表达以及介导翅膀正常发育所需靶基因的激活,在“截瘫”下游的翅膀发育中发挥作用。“视动性失明”的缺失在其表达域产生大量细胞死亡,这导致Notch信号通路的错误激活和侧翼细胞的过度增殖。

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