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Blood, 1 August 2004, Vol. 104, No. 3, pp. 784-787.
Prepublished online as a Blood First Edition Paper on April 6, 2004; DOI 10.1182/blood-2003-09-3071.
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IMMUNOBIOLOGY
Brief report
Optimal B-cell proliferation requires phosphoinositide 3-kinase–dependent inactivation of FOXO transcription factors
Isharat Yusuf,
Xiaocui Zhu,
Michael G. Kharas,
Jing Chen, and
David A. Fruman
From the Department of Molecular Biology and Biochemistry, University of California, Irvine.
Transcription factors of the Forkhead Box, class O (FOXO) family promote cell-cycle arrest and/or apoptosis in a variety of cell types. Mitogenic stimuli inactivate FOXO function by way of an evolutionarily conserved pathway involving the activation of phosphoinositide 3-kinase (PI3K) and its downstream effector, Akt. Although PI3K activation is required for B-lymphocyte proliferation, it is not known whether PI3K-dependent inactivation of FOXO proteins is important for cell-cycle progression and survival of these cells. Here, we show that B-cell receptor (BCR) engagement triggers PI3K-dependent phosphorylation and nuclear export of FOXO1. Furthermore, forced expression of PI3K-independent variants of FOXO1 or FOXO3a in activated B cells induces partial arrest in G1 phase of the cell cycle and increases apoptosis. These findings establish that FOXO inactivation is a functionally important consequence of PI3K signaling in primary B cells.
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