School of Biomedical Sciences, Faculty of Medicine, University of Queensland, St Lucia, QLD, Australia.
Department of Biochemistry and Molecular Biology, University of Melbourne, Parkville, VIC, Australia.
Mol Neurobiol. 2018 Jul;55(7):5409-5424. doi: 10.1007/s12035-017-0778-x. Epub 2017 Sep 22.
Genetic disruptions of spindle/centrosome-associated WD40-repeat protein 62 (WDR62) are causative for autosomal recessive primary microcephaly (MCPH) and a broader range of cortical malformations. Since the identification of WDR62 as encoded by the MCPH2 locus in 2010, recent studies that have deleted/depleted WDR62 in various animal models of cortical development have highlighted conserved functions in brain growth. Here, we provide a timely review of our current understanding of WDR62 contributions in the self-renewal, expansion and fate specification of neural stem and progenitor cells that are critical for neocortical development. Recent studies have revealed multiple functions for WDR62 in the regulation of spindle organization, mitotic progression and the duplication and biased inheritance of centrosomes during asymmetric divisions. We also discuss recently elaborated WDR62 interaction partners that include Aurora and c-Jun N-terminal kinases as part of complex signalling mechanisms that may define its neural functions. These studies provide new insights into the molecular and cellular processes that are required for brain formation and implicated in the genesis of primary microcephaly.
WDR62 是纺锤体/中心体相关 WD40 重复蛋白,其遗传紊乱可导致常染色体隐性原发性小头畸形(MCPH)和更广泛的皮质畸形。自 2010 年将 WDR62 鉴定为 MCPH2 基因座编码的蛋白以来,最近在各种皮质发育的动物模型中删除/耗尽 WDR62 的研究强调了其在大脑生长中的保守功能。在这里,我们及时回顾了我们目前对 WDR62 在神经干细胞和祖细胞的自我更新、扩增和命运特化中的作用的理解,这些细胞对新皮质的发育至关重要。最近的研究揭示了 WDR62 在调节纺锤体组织、有丝分裂进展以及中心体在不对称分裂中的复制和偏向性遗传中的多种功能。我们还讨论了最近详细阐述的 WDR62 相互作用伙伴,包括 Aurora 和 c-Jun N 端激酶,作为可能定义其神经功能的复杂信号机制的一部分。这些研究为大脑形成所需的分子和细胞过程提供了新的见解,并暗示了原发性小头畸形的发生。