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Title: Mouse Bone Marrow and Peripheral Blood Erythroid Cell Counts are Regulated by Different Autosomal Genetic Loci
Authors: Jawad, M.
Giotopoulos, G.
Fitch, S.
Cole, C.
Plumb, M.
Talbot, Christopher J.
First Published: 2007
Publisher: Elsevier
Citation: Blood Cells Molecules and Diseases, 2007, 38 (2), pp. 69-77.
Abstract: Erythropoiesis is under fine control and genetic loci that effect it are likely to be important in a range of conditions. To assess the relative contributions of different genetic loci to parameters of erythropoiesis we have measured RBC counts in the peripheral circulation and committed erythroid cells (RBC and small normoblasts) in the bone marrow in a cohort of (CBA/H x C57BL/6) F2 mice to map quantitative trait loci (QTL). Candidate genes were assessed using bioinformatics and DNA sequencing. Different autosomal loci affect bone marrow (chromosomes 5, 11, and 19) and peripheral blood (chromosome 4) erythroid cell counts but there may be a common chromosome X locus. Spleen weight QTL were found on chromosomes 3, 15 and 17. Surprisingly, erythropoietin (EPO) is the best candidate quantitative trait gene (QTG) in the chromosome 5 locus that affects bone marrow but not peripheral blood erythroid cell counts. Epo gene expression is known to be genetically regulated in mice, but our data suggests a tissue-specific role for epo in mouse erythropoiesis that is also genetically determined. The identity of the other QTG will be important both to further knowledge of the control of erythropoiesis and as potential modifier genes for haematological disorders.
DOI Link: 10.1016/j.bcmd.2006.10.009
ISSN: 1079-9796
Type: Article
Description: NOTICE: this is the author’s version of a work that was accepted for publication in Blood Cells Molecules and Diseases. Changes resulting from the publishing process, such as peer review, editing, corrections, structural formatting, and other quality control mechanisms may not be reflected in this document. Changes may have been made to this work since it was submitted for publication. A definitive version was subsequently published in Blood Cells Molecules and Diseases, [38 (2), pp. 69-77 (2007)] 10.1016/j.bcmd.2006.10.009
Appears in Collections:Published Articles, Dept. of Genetics

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