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Severe NDE1-mediated microcephaly results from neural progenitor cell cycle arrests at multiple specific stages.

Abstract：

:Microcephaly is a cortical malformation disorder characterized by an abnormally small brain. Recent studies have revealed severe cases of microcephaly resulting from human mutations in the NDE1 gene, which is involved in the regulation of cytoplasmic dynein. Here using in utero electroporation of NDE1 short hairpin RNA (shRNA) in embryonic rat brains, we observe cell cycle arrest of proliferating neural progenitors at three distinct stages: during apical interkinetic nuclear migration, at the G2-to-M transition and in regulation of primary cilia at the G1-to-S transition. RNAi against the NDE1 paralogue NDEL1 has no such effects. However, NDEL1 overexpression can functionally compensate for NDE1, except at the G2-to-M transition, revealing a unique NDE1 role. In contrast, NDE1 and NDEL1 RNAi have comparable effects on postmitotic neuronal migration. These results reveal that the severity of NDE1-associated microcephaly results not from defects in mitosis, but rather the inability of neural progenitors to ever reach this stage.

journal_name

Nat Commun

journal_title

Nature communications

authors

Doobin DJ,Kemal S,Dantas TJ,Vallee RB

doi

10.1038/ncomms12551

subject

Has Abstract

pub_date

2016-08-24 00:00:00

pages

12551

issn

2041-1723

pii

ncomms12551

journal_volume

7

pub_type

杂志文章

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