DNA repair is crucial for maintaining hematopoietic stem cell function

Laura J. Niedernhofer

doi:10.1016/j.dnarep.2007.11.012

DNA repair is crucial for maintaining hematopoietic stem cell function

Laura J. Niedernhofer

Research output: Contribution to journal › Article › peer-review

58 Scopus citations

Abstract

Richard Cornall and collaborators recently developed a mouse model of Ligase IV syndrome with growth retardation and immunodeficiency due to a defect in nonhomologous end-joining (NHEJ) of DNA double-strand breaks. They demonstrated age-dependent loss of hematopoietic stem cell function in these mice. Simultaneously, Irving Weissman and colleagues demonstrated a similar phenomenon in Ku80^-/- mice defective in NHEJ and telomere maintenance, Xpd^TTD mice defective in nucleotide excision repair, and late generation mTr^-/- missing telomerase activity. These studies strongly support the hypothesis that genomic stress causes aging by limiting the ability of stem cells to indefinitely maintain tissue homeostasis.

Original language	English (US)
Pages (from-to)	523-529
Number of pages	7
Journal	DNA Repair
Volume	7
Issue number	3
DOIs	https://doi.org/10.1016/j.dnarep.2007.11.012
State	Published - Mar 1 2008
Externally published	Yes

Bibliographical note

Funding Information:
L.J.N. is supported by The Ellison Medical Foundation (AG-NS-0303-05), the NCI (CA111525 and CA10370) and the University of Pittsburgh Cancer Institute.

Keywords

Aging
Endogenous damage
Oxidative stress
Progeria

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title = "DNA repair is crucial for maintaining hematopoietic stem cell function",

abstract = "Richard Cornall and collaborators recently developed a mouse model of Ligase IV syndrome with growth retardation and immunodeficiency due to a defect in nonhomologous end-joining (NHEJ) of DNA double-strand breaks. They demonstrated age-dependent loss of hematopoietic stem cell function in these mice. Simultaneously, Irving Weissman and colleagues demonstrated a similar phenomenon in Ku80-/- mice defective in NHEJ and telomere maintenance, XpdTTD mice defective in nucleotide excision repair, and late generation mTr-/- missing telomerase activity. These studies strongly support the hypothesis that genomic stress causes aging by limiting the ability of stem cells to indefinitely maintain tissue homeostasis.",

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N2 - Richard Cornall and collaborators recently developed a mouse model of Ligase IV syndrome with growth retardation and immunodeficiency due to a defect in nonhomologous end-joining (NHEJ) of DNA double-strand breaks. They demonstrated age-dependent loss of hematopoietic stem cell function in these mice. Simultaneously, Irving Weissman and colleagues demonstrated a similar phenomenon in Ku80-/- mice defective in NHEJ and telomere maintenance, XpdTTD mice defective in nucleotide excision repair, and late generation mTr-/- missing telomerase activity. These studies strongly support the hypothesis that genomic stress causes aging by limiting the ability of stem cells to indefinitely maintain tissue homeostasis.

AB - Richard Cornall and collaborators recently developed a mouse model of Ligase IV syndrome with growth retardation and immunodeficiency due to a defect in nonhomologous end-joining (NHEJ) of DNA double-strand breaks. They demonstrated age-dependent loss of hematopoietic stem cell function in these mice. Simultaneously, Irving Weissman and colleagues demonstrated a similar phenomenon in Ku80-/- mice defective in NHEJ and telomere maintenance, XpdTTD mice defective in nucleotide excision repair, and late generation mTr-/- missing telomerase activity. These studies strongly support the hypothesis that genomic stress causes aging by limiting the ability of stem cells to indefinitely maintain tissue homeostasis.

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KW - Oxidative stress

KW - Progeria

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DNA repair is crucial for maintaining hematopoietic stem cell function

Abstract

Bibliographical note

Keywords

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