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Mtx2通过调节微丝形成来指导斑马鱼在卵黄栓形成期间的形态发生运动。

Mtx2 directs zebrafish morphogenetic movements during epiboly by regulating microfilament formation.

作者信息

Wilkins Simon J, Yoong Simon, Verkade Heather, Mizoguchi Takamasa, Plowman Sarah J, Hancock John F, Kikuchi Yutaka, Heath Joan K, Perkins Andrew C

机构信息

Institute for Molecular Bioscience, University of Queensland, Brisbane, 4072, Australia.

出版信息

Dev Biol. 2008 Feb 1;314(1):12-22. doi: 10.1016/j.ydbio.2007.10.050. Epub 2007 Nov 12.

DOI:10.1016/j.ydbio.2007.10.050
PMID:18154948
Abstract

The homeobox transcription factor Mtx2 is essential for epiboly, the first morphogenetic movement of gastrulation in zebrafish. Morpholino knockdown of Mtx2 results in stalling of epiboly and lysis due to yolk rupture. However, the mechanism of Mtx2 action is unknown. The role of mtx2 is surprising as most mix/bix family genes are thought to have roles in mesendoderm specification. Using a transgenic sox17-promoter driven EGFP line, we show that Mtx2 is not required for endoderm specification but is required for correct morphogenetic movements of endoderm and axial mesoderm. During normal zebrafish development, mtx2 is expressed at both the blastoderm margin and in the zebrafish equivalent of visceral endoderm, the extra-embryonic yolk syncytial layer (YSL). We show that formation of the YSL is not Mtx2 dependent, but that Mtx2 directs spatial arrangement of YSL nuclei. Furthermore, we demonstrate that Mtx2 knockdown results in loss of the YSL F-actin ring, a microfilament structure previously shown to be necessary for epiboly progression. In summary, we propose that Mtx2 acts within the YSL to regulate morphogenetic movements of both embryonic and extra-embryonic tissues, independently of cell fate specification.

摘要

同源框转录因子Mtx2对于斑马鱼原肠胚形成过程中的外包运动(原肠胚形成的首个形态发生运动)至关重要。用吗啉代寡核苷酸敲低Mtx2会导致外包运动停滞,并因卵黄破裂而溶解。然而,Mtx2的作用机制尚不清楚。mtx2的作用令人惊讶,因为大多数mix/bix家族基因被认为在中内胚层特化中发挥作用。利用转基因的sox17启动子驱动的EGFP品系,我们发现内胚层特化不需要Mtx2,但内胚层和轴向中胚层的正确形态发生运动需要Mtx2。在正常斑马鱼发育过程中,mtx2在胚盘边缘以及斑马鱼相当于脏内胚层的部位(即胚外卵黄合胞体层,YSL)均有表达。我们发现YSL的形成不依赖于Mtx2,但Mtx2指导YSL细胞核的空间排列。此外,我们证明敲低Mtx2会导致YSL F-肌动蛋白环缺失,这是一种微丝结构,先前已证明其对于外包运动的进行是必需的。总之,我们提出Mtx2在YSL内发挥作用,以调节胚胎组织和胚外组织的形态发生运动,而与细胞命运特化无关。

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