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 journalArticlepeer-review

27 Scopus citations

Abstract

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
JournalBlood
Volume102
Issue number1
DOIs
StatePublished - Jul 1 2003

ASJC Scopus subject areas

  • Biochemistry
  • Immunology
  • Hematology
  • Cell Biology

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