Functional p85α gene is required for normal murine fetal erythropoiesis

Hannah Huddleston, Bailin Tan, Feng-Chun Yang, Hilary White, Mary Jo Wenning, Attilio Orazi, Mervin C. Yoder, Reuben Kapur, David A. Ingram

Research output: Contribution to journalArticle

27 Scopus citations


In vitro studies suggest that activation of class IA phosphatidyiinositol 3 (PI-3) kinase is necessary for normal erythroid cell development. However, when class IA PI-3 kinase-deficient mice were generated by a targeted deletion of the p85α regulatory subunit, fetal erythropoiesis was reportedly unaffected. Given the discrepancies between these studies, we performed a more detailed in vivo analysis of class IA PI-3 kinase-deficient embryos. Day-14.5 p85α-/- embryos are pale with a marked reduction of mature erythrocytes in their peripheral blood. Further, the absolute number and frequency of both early (erythroid burst-forming unit [BFU-E]) and late erythroid progenitors (erythroid colony-forming unit [CFU-E]) are reduced in p85α-/- fetal livers compared with wild-type controls, which is associated with reduced proliferation. Taken together, these data establish an important role for p85α and class IA PI-3 kinase in regulating the development of both early and late erythroid progenitors in fetal liver.

Original languageEnglish (US)
Pages (from-to)142-145
Number of pages4
Issue number1
StatePublished - Jul 1 2003
Externally publishedYes


ASJC Scopus subject areas

  • Hematology

Cite this

Huddleston, H., Tan, B., Yang, F-C., White, H., Wenning, M. J., Orazi, A., Yoder, M. C., Kapur, R., & Ingram, D. A. (2003). Functional p85α gene is required for normal murine fetal erythropoiesis. Blood, 102(1), 142-145.