The subcortical maternal complex controls symmetric division of mouse zygotes by regulating F-actin dynamics

Maternal effect genes play critical roles in early embryogenesis of model organisms where they have been intensively investigated. However, their molecular function in mammals remains largely unknown. Recently, we identified a subcortical maternal complex (SCMC) that contains four proteins encoded b...

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Veröffentlicht in:Nature communications 2014-09, Vol.5 (1), p.4887-4887, Article 4887
Hauptverfasser: Yu, Xing-Jiang, Yi, Zhaohong, Gao, Zheng, Qin, Dandan, Zhai, Yanhua, Chen, Xue, Ou-Yang, Yingchun, Wang, Zhen-Bo, Zheng, Ping, Zhu, Min-Sheng, Wang, Haibin, Sun, Qing-Yuan, Dean, Jurrien, Li, Lei
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Sprache:eng
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Zusammenfassung:Maternal effect genes play critical roles in early embryogenesis of model organisms where they have been intensively investigated. However, their molecular function in mammals remains largely unknown. Recently, we identified a subcortical maternal complex (SCMC) that contains four proteins encoded by maternal effect genes ( Mater , Filia , Floped and Tle6 ). Here we report that TLE6, similar to FLOPED and MATER, stabilizes the SCMC and is necessary for cleavage beyond the two-cell stage of development. We document that the SCMC is required for formation of the cytoplasmic F-actin meshwork that controls the central position of the spindle and ensures symmetric division of mouse zygotes. We further demonstrate that the SCMC controls formation of the actin cytoskeleton specifically via Cofilin, a key regulator of F-actin assembly. Our results provide molecular insight into the physiological function of TLE6, its interaction with the SCMC and their roles in the symmetric division of the zygote in early mouse development. The mammalian subcortical maternal complex is composed of maternally expressed proteins and required for mouse early embryonic cell division. Here the authors show that the complex functions to control spindle positioning through regulation of the actin cytoskeleton.
ISSN:2041-1723
2041-1723
DOI:10.1038/ncomms5887