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WDR62调节人类多能干细胞的早期神经和神经胶质祖细胞特化。

WDR62 Regulates Early Neural and Glial Progenitor Specification of Human Pluripotent Stem Cells.

作者信息

Alshawaf Abdullah J, Antonic Ana, Skafidas Efstratios, Ng Dominic Chi-Hung, Dottori Mirella

机构信息

Centre for Neural Engineering, The University of Melbourne, Carlton, VIC 3010, Australia.

Department of Psychiatry, The University of Melbourne, Carlton, VIC 3010, Australia.

出版信息

Stem Cells Int. 2017;2017:7848932. doi: 10.1155/2017/7848932. Epub 2017 Jun 13.

DOI:10.1155/2017/7848932
PMID:28690640
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC5485354/
Abstract

Mutations in WD40-repeat protein 62 () are commonly associated with primary microcephaly and other developmental cortical malformations. We used human pluripotent stem cells (hPSC) to examine WDR62 function during human neural differentiation and model early stages of human corticogenesis. Neurospheres lacking WDR62 expression showed decreased expression of intermediate progenitor marker, TBR2, and also glial marker, S100. In contrast, inhibition of c-Jun N-terminal kinase (JNK) signalling during hPSC neural differentiation induced upregulation of WDR62 with a corresponding increase in neural and glial progenitor markers, PAX6 and EAAT1, respectively. These findings may signify a role of WDR62 in specifying intermediate neural and glial progenitors during human pluripotent stem cell differentiation.

摘要

WD40重复蛋白62（WDR62）的突变通常与原发性小头畸形和其他发育性皮质畸形有关。我们使用人类多能干细胞（hPSC）来研究WDR62在人类神经分化过程中的功能，并模拟人类皮质发生的早期阶段。缺乏WDR62表达的神经球显示中间祖细胞标志物TBR2以及神经胶质标志物S100的表达降低。相反，在hPSC神经分化过程中抑制c-Jun氨基末端激酶（JNK）信号传导可诱导WDR62上调，同时神经和神经胶质祖细胞标志物PAX6和EAAT1分别相应增加。这些发现可能表明WDR62在人类多能干细胞分化过程中确定中间神经和神经胶质祖细胞方面发挥作用。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3ba0/5485354/94613b2a6c56/SCI2017-7848932.005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3ba0/5485354/b2d7f92301f6/SCI2017-7848932.001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3ba0/5485354/913e2c4a2577/SCI2017-7848932.002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3ba0/5485354/4d0461fd6aee/SCI2017-7848932.003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3ba0/5485354/67a82019569f/SCI2017-7848932.004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3ba0/5485354/94613b2a6c56/SCI2017-7848932.005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3ba0/5485354/b2d7f92301f6/SCI2017-7848932.001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3ba0/5485354/913e2c4a2577/SCI2017-7848932.002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3ba0/5485354/4d0461fd6aee/SCI2017-7848932.003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3ba0/5485354/67a82019569f/SCI2017-7848932.004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3ba0/5485354/94613b2a6c56/SCI2017-7848932.005.jpg

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Opposing roles for JNK and Aurora A in regulating the association of WDR62 with spindle microtubules.
一种综合的功能和临床基因组学方法揭示了驱动侵袭性转移性前列腺癌的基因。
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YTHDF2 destabilizes mA-modified neural-specific RNAs to restrain differentiation in induced pluripotent stem cells.YTHDF2 使 mA 修饰的神经特异性 RNA 不稳定，从而抑制诱导多能干细胞的分化。
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