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Zbed3 participates in the subcortical maternal complex and regulates the distribution of organelles Free
Zheng Gao 1,2,† , Xiaoxin Zhang 1,† , Xingjiang Yu 1 , Dandan Qin 1 , Yi Xiao 1 , Yang Yu 1 , Yunlong Xiang 1 ,Xiaoqing Nie 1 , Xukun Lu 1 , Wenbo Liu 1 , Zhaohong Yi 3 , and Lei Li 1,2, *
1 State Key Laboratory of Stem Cell and Reproductive Biology, Institute of Zoology, Chinese Academy of Sciences, Beijing 100101, China
2 University of Chinese Academy of Sciences, Beijing 100049, China
3 Key Laboratory of Urban Agriculture (North) of Ministry of Agriculture, College of Biological Science and Engineering, Beijing University of Agriculture, Beijing 102206, China
These authors contributed equally to this work *Correspondence to:Lei Li, E-mail: lil@ioz.ac.cn
J Mol Cell Biol, Volume 10, Issue 1, February 2018, Pages 74-88  https://doi.org/10.1093/jmcb/mjx035
Keyword: Zbed3, SCMC, organelle distribution, maternal effect gene, cytoskeleton, early embryogenesis, cytoplasmic lattices

We previously identified a subcortical maternal complex (SCMC) that is essential for early embryogenesis and female fertility in mice. However, the molecular mechanism by which the SCMC affects female fertility remains largely uncharacterized. Here, we report that a novel maternal protein, zinc finger BED-type containing 3 (Zbed3), participates in the SCMC. Depletion of maternal Zbed3 results in reduced fecundity of females, because of the impaired and delayed development in a proportion of mutant embryos. The loss of maternal Zbed3 results in asymmetric zygotic division and abnormal distributions of organelles in the affected oocytes and zygotes, similar to the phenotypes observed in females with disrupted core SCMC genes. Further investigation revealed that these phenotypes are associated with disrupted dynamics of microtubules and/or formation of cytoplasmic lattices (CPLs). The stability and localization of Zbed3 depend on, but are not required for, the formation of the SCMC. Thus, our data suggest Zbed3 as one of downstream proteins mediating SCMC functions and provide further insights into the roles of the SCMC and CPLs in female fertility.