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Functional maintenance of hematopoietic stem cells (HSCs) is constantly challenged by stresses like DNA damage and oxidative stress. Foxo factors, particularly Foxo3a, function to regulate the self-renewal of HSCs and contribute to the maintenance of the HSC pool during aging by providing resistance to oxidative stress. Fancd2 -deficient mice had multiple hematopoietic defects, including HSC loss in early development and in response to cellular stresses including oxidative stress. The cellular mechanisms underlying HSC loss in Fancd2 -deficient mice include abnormal cell cycle status, loss of quiescence, and compromised hematopoietic repopulating capacity of HSCs. To address on a genome wide level the genes and pathways that are impacted by deletion of the Fancd2 and Foxo3a , we performed microarray analysis on phenotypic HSCs (Lin - cki + Sca-1 + CD150 + CD48 - ) from Fancd2 single knockout, Foxo3a single knockout and Fancd2-/-Foxo3a-/- double-knockout (dKO) mice. Here we provide detailed methods and analysis on these microarray data which has been deposited in Gene Expression Omnibus (GEO): GSE64215.

Transcriptional profiling of Foxo3a and Fancd2 regulated genes in mouse hematopoietic stem cells