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Reduced hematopoietic reserves in DNA interstrand crosslink repair-deficient Ercc1−/− mice
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Reduced hematopoietic reserves in DNA interstrand crosslink repair-deficient Ercc1−/− mice
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Reduced hematopoietic reserves in DNA interstrand crosslink repair-deficient Ercc1−/− mice
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Journal Article
Reduced hematopoietic reserves in DNA interstrand crosslink repair-deficient Ercc1−/− mice
2005
Overview
The ERCC1‐XPF heterodimer is a structure‐specific endonuclease involved in both nucleotide excision repair and interstrand crosslink repair. Mice carrying a genetic defect in
Ercc1
display symptoms suggestive of a progressive, segmental progeria, indicating that disruption of one or both of these DNA damage repair pathways accelerates aging. In the hematopoietic system, there are defined age‐associated changes for which the cause is unknown. To determine if DNA repair is critical to prolonged hematopoietic function, hematopoiesis in
Ercc1
−/−
mice was compared to that in young and old wild‐type mice.
Ercc1
−/−
mice (3‐week‐old) exhibited multilineage cytopenia and fatty replacement of bone marrow, similar to old wild‐type mice. In addition, the proliferative reserves of hematopoietic progenitors and stress erythropoiesis were significantly reduced in
Ercc1
−/−
mice compared to age‐matched controls. These features were not seen in nucleotide excision repair‐deficient
Xpa
−/−
mice, but are characteristic of Fanconi anemia, a human cancer syndrome caused by defects in interstrand crosslink repair. These data support the hypothesis that spontaneous interstrand crosslink damage contributes to the functional decline of the hematopoietic system associated with aging.
Publisher
John Wiley & Sons, Ltd,Nature Publishing Group UK,Springer Nature B.V
