Role of Fanconi DNA repair pathway in neural stem cell homeostasis.
Cell Cycle
; 7(13): 1911-5, 2008 Jul 01.
Article
en En
| MEDLINE
| ID: mdl-18604174
ABSTRACT
Defects in DNA repair pathways have been involved in collapse of early neurogenesis leading to brain development abnormalities and embryonic lethality. However, consequences of DNA repair defects in adult neural stem and progenitor cells and their potential contribution in ageing phenotype are poorly understood. The Fanconi anaemia (FA) pathway, which functions primarily as a DNA damage response system, has been examined in neural stem and progenitor cells during developmental and adult neurogenesis. We have shown that loss of fanca and fancg specifically provokes neural progenitor apoptosis during forebrain development, related to DNA repair defects, which persists in adulthood leading to depletion of the neural stem cell pool with ageing. In addition, neural stem cells from FA mice had a reduced capacity to self-renew in vitro. Here, we expand upon our recent work and give further data examining possible implication of oxidative stress. Therefore, FA phenotype might be interpreted as a premature ageing of stem cells, DNA damages being among the driving forces of ageing.
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Colección:
01-internacional
Base de datos:
MEDLINE
Asunto principal:
Células Madre
/
Encéfalo
/
Reparación del ADN
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Proteína del Grupo de Complementación A de la Anemia de Fanconi
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Proteína del Grupo de Complementación G de la Anemia de Fanconi
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Anemia de Fanconi
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Neuronas
Límite:
Animals
Idioma:
En
Revista:
Cell Cycle
Año:
2008
Tipo del documento:
Article
País de afiliación:
Francia