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果蝇JNK信号通路控制卵背侧附属物和卵孔的形态发生。

The Drosophila JNK pathway controls the morphogenesis of the egg dorsal appendages and micropyle.

作者信息

Suzanne M, Perrimon N, Noselli S

机构信息

Centro de Biología Molecular Severo Ochoa, Universidad Autónoma de Madrid, 28049 Madrid, Spain.

出版信息

Dev Biol. 2001 Sep 15;237(2):282-94. doi: 10.1006/dbio.2001.0384.

Abstract

During Drosophila oogenesis, the formation of the egg respiratory appendages and the micropyle require the shaping of anterior and dorsal follicle cells. Prior to their morphogenesis, cells of the presumptive appendages are determined by integrating dorsal-ventral and anterior-posterior positional information provided by the epidermal growth factor receptor (EGFR) and Decapentaplegic (Dpp) pathways, respectively. We show here that another signaling pathway, the Drosophila Jun-N-terminal kinase (JNK) cascade, is essential for the correct morphogenesis of the dorsal appendages and the micropyle during oogenesis. Mutant follicle cell clones of members of the JNK pathway, including DJNKK/hemipterous (hep), DJNK/basket (bsk), and Djun, block dorsal appendage formation and affect the micropyle shape and size, suggesting a late requirement for the JNK pathway in anterior chorion morphogenesis. In support of this view, hep does not affect early follicle cell patterning as indicated by the normal expression of kekkon (kek) and Broad-Complex (BR-C), two of the targets of the EGFR pathway in dorsal follicle cells. Furthermore, the expression of the TGF-beta homolog dpp, which is under the control of hep in embryos, is not coupled to JNK activity during oogenesis. We show that hep controls the expression of puckered (puc) in the follicular epithelium in a cell-autonomous manner. Since puc overexpression in the egg follicular epithelium mimics JNK appendages and micropyle phenotypes, it indicates a negative role of puc in their morphogenesis. The role of the JNK pathway in the morphogenesis of follicle cells and other epithelia during development is discussed.

摘要

在果蝇卵子发生过程中,卵呼吸附属器和卵孔的形成需要前卵泡细胞和背卵泡细胞的塑形。在其形态发生之前,假定附属器的细胞通过整合分别由表皮生长因子受体(EGFR)和骨形态发生蛋白(Dpp)信号通路提供的背腹和前后位置信息来确定。我们在此表明,另一个信号通路,即果蝇Jun氨基末端激酶(JNK)级联反应,对于卵子发生过程中背附属器和卵孔的正确形态发生至关重要。JNK信号通路成员的突变卵泡细胞克隆,包括DJNKK/半翅目(hep)、DJNK/篮状蛋白(bsk)和Djun,会阻断背附属器的形成,并影响卵孔的形状和大小,这表明JNK信号通路在绒毛膜前体形态发生中存在后期需求。支持这一观点的是,如背卵泡细胞中EGFR信号通路的两个靶标kekkon(kek)和广谱复合体(BR-C)的正常表达所示,hep不影响早期卵泡细胞的模式形成。此外,在胚胎中受hep调控的TGF-β同源物dpp的表达在卵子发生过程中与JNK活性无关。我们表明,hep以细胞自主方式控制卵泡上皮中褶皱蛋白(puc)的表达。由于puc在卵泡上皮中的过表达模拟了JNK附属器和卵孔的表型,这表明puc在其形态发生中起负作用。本文还讨论了JNK信号通路在卵泡细胞和发育过程中其他上皮细胞形态发生中的作用。

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