DMRT1 is required for Mullerian duct formation in the chicken embryo
DMRT1 is required for Mullerian duct formation in the chicken embryo
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DOI：
10.1016/j.ydbio.2015.02.001
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发表时间：
2015-04-15
影响因子：
2.7
通讯作者：
Smith, C. A.
中科院分区：
文献类型：
--
作者：
Ayers, K. L.;Cutting, A. D.;Smith, C. A.
DMRT1是一种保守的转录因子，在性腺分化中起核心作用。在所有被研究的脊椎动物中，DMRT1在睾丸的发育和/或维持中起着重要的作用。目前还没有研究报道DMRT1在性腺外的作用。在这里，我们证明了DMRT1在鸡胚胎的米氏导管中表达，在那里它是形成导管所必需的。DMRT1的mRNA和蛋白在早期形成的米菲尔脊和在导管形态发生过程中经历上皮向间充质转化的细胞中表达。RNAi介导的DMRT1在卵细胞中的敲除导致间充质层大大减少，这阻止了管腔上皮的尾部延伸。哺乳动物米氏管形成的关键标志，Pax2在导管上皮细胞中和WNT4在间质中，在鸡中保守，它们在DMRT1基因敲除的导管中表达中断。我们得出结论：DMRT1是米氏管形成的早期步骤所必需的。DMRT1调节米氏管脊和间质的形成，它的丢失阻碍了导管的尾部延伸。虽然DMRT1在许多脊椎动物的睾丸发育和维持过程中发挥着重要作用，但这是第一份表明在米氏管发育中需要DMRT1的报告。(C)2015 Elsevier Inc.保留所有权利。
DMRT1 is a conserved transcription factor with a central role in gonadal sex differentiation. In all vertebrates studied, DMRT1 plays an essential function in testis development and/or maintenance. No studies have reported a role for DMRT1 outside the gonads. Here, we show that DMRT1 is expressed in the paired Mfillerian ducts in the chicken embryo, where it is required for duct formation. DMRT1 mRNA and protein are expressed in the early forming Mfillerian ridge, and in cells undergoing an epithelial to mesenchyme transition during duct morphogenesis. RNAi-mediated knockdown of DMRT1 in ovo causes a greatly reduced mesenchymal layer, which blocks caudal extension of the duct luminal epithelium. Critical markers of Mfillerian duct formation in mammals, Pax2 in the duct epithelium and Wnt4 in the mesenchyme, are conserved in chicken and their expression disrupted in DMRT1 knockdown 'ducts. We conclude that DMRT1 is required for the early steps of Mfillerian duct development. DMRT1 regulates Mfillerian ridge and mesenchyme formation and its loss blocks caudal extension of the duct. While DMRT1 plays an important role during testis development and maintenance in many vertebrate species, this is the first report showing a requirement for DMRT1 in Mullerian duct development. (C) 2015 Elsevier Inc. All rights reserved.