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Pot1a prevents telomere dysfunction and ATM-dependent neuronal loss.

Authors
Lee, Y  | Brown, EJ | Chang, S | McKinnon, PJ
Citation
The Journal of neuroscience, 34(23). : 7836-7844, 2014
Journal Title
The Journal of neuroscience
ISSN
0270-64741529-2401
Abstract
Genome stability is essential for neural development and the prevention of neurological disease. Here we determined how DNA damage signaling from dysfunctional telomeres affects neurogenesis. We found that telomere uncapping by Pot1a inactivation resulted in an Atm-dependent loss of cerebellar interneurons and granule neuron precursors in the mouse nervous system. The activation of Atm by Pot1a loss occurred in an Atr-dependent manner, revealing an Atr to Atm signaling axis in the nervous system after telomere dysfunction. In contrast to telomere lesions, Brca2 inactivation in neural progenitors also led to ablation of cerebellar interneurons, but this did not require Atm. These data reveal that neural cell loss after DNA damage selectively engages Atm signaling, highlighting how specific DNA lesions can dictate neuropathology arising in human neurodegenerative syndromes.
MeSH

DOI
10.1523/JNEUROSCI.4245-13.2014
PMID
24899707
Appears in Collections:
Journal Papers > Research Organization > Institute for Medical Sciences
Ajou Authors
이, 영수
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