ArrayExpress Uploader0mouse24 monthswild type24 monthswild type24 monthswild type9-12 weekswild type9-12 weeks 9-12 weeks 32 weeksPolgtm1Lrsn-/-32 weeksPolgtm1Lrsn-/-32 weeksPolgtm1Lrsn-/-32 weeksPolgtm1Lrsn+/+32 weeksPolgtm1Lrsn+/+32 weeksPolgtm1Lrsn+/+8-12 weekswild type8-12 weekswild type8-12 weekswild type8-12 weekswild type6386arrayexpress_sid6Somatic stem cells mediate tissue maintenance for the lifetime of an organism. Despite the well-established longevity that is a...21549326E-GEOD-27686/profile/8773/arrayexpressuploader216anemiacelllymphopeniastem cellDec.12, 2014FalseE-GEOD-27686_A-AFFY-45accumulating-mitochondrial-dna-mutations-drive-preAccumulating mitochondrial DNA mutations drive premature hematopoietic aging phenotypes molecularly distinct from physiologic stem cell agingNov.11, 2014Somatic stem cells mediate tissue maintenance for the lifetime of an organism. Despite the well-established longevity that is a prerequisite for such function, accumulating data argue for compromised stem cell function with age. Identifying the mechanisms underlying age-dependent stem cell dysfunction is therefore key to understand the aging process. Using a model that carries a proofreading defective mitochondrial DNA polymerase, we demonstrate hematopoietic defects reminiscent of premature HSC aging including anemia, lymphopenia and myeloid lineage skewing. However, in contrast to physiologic stem cell aging, rapidly accumulating mitochondrial DNA mutations displayed little involvement of the hematopoietic stem cell pool but rather with distinct differentiation blocks and/or disappearance of downstream progenitors. Hematopoietic stem cells (HSC) has been sorted out from midaged wildtype and mutator mice and compared with stem cells sorted from young and and old wt micehttp://www.ebi.ac.uk/arrayexpress/experiments/E-GEOD-27686http://www.ebi.ac.uk/arrayexpress/experiments/E-GEOD-27686/samples/