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Published 18 December 2006. doi:10.1083/jcb.200604073
The Rockefeller University Press, 0021-9525 $8.00
JCB, Volume 175, Number 6, 937-946
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Article

 Rac1 and a GTPase-activating protein, MgcRacGAP, are required for nuclear translocation of STAT transcription factors

Toshiyuki Kawashima1, Ying Chun Bao1, Yasushi Nomura1, Yuseok Moon1,4, Yukio Tonozuka1, Yukinori Minoshima1, Tomonori Hatori1, Akiho Tsuchiya1, Mari Kiyono2, Tetsuya Nosaka2, Hideaki Nakajima3, David A. Williams5, and Toshio Kitamura1

1 Division of Cellular Therapy, 2 Division of Hematopoietic Factors, and 3 Center of Excellence, The Institute of Medical Science, University of Tokyo, Minato-ku, Tokyo 108-8639, Japan
4 Department of Microbiology and Immunology, Medical Research Institute, Pusan National University Medical School, Busan 602-739, Korea
5 Division of Experimental Hematology, Cincinnati Children's Hospital Medical Center, Cincinnati, OH 45229

Correspondence to Toshio Kitamura: kitamura{at}ims.u-tokyo.ac.jp

STAT transcription factors are tyrosine phosphorylated upon cytokine stimulation and enter the nucleus to activate target genes. We show that Rac1 and a GTPase-activating protein, MgcRacGAP, bind directly to p-STAT5A and are required to promote its nuclear translocation. Using permeabilized cells, we find that nuclear translocation of purified p-STAT5A is dependent on the addition of GTP-bound Rac1, MgcRacGAP, importin {alpha}, and importin ß. p-STAT3 also enters the nucleus via this transport machinery, and mutant STATs lacking the MgcRacGAP binding site do not enter the nucleus even after phosphorylation. We conclude that GTP-bound Rac1 and MgcRacGAP function as a nuclear transport chaperone for activated STATs.

Abbreviations used in this paper: DBD, DNA binding domain; EMSA, electrophoretic mobility shift analysis; GAP, GTPase-activating protein; ITD, internal tandem duplication; MBP, maltose binding protein; MgcRacGAP, male germ cell Rac-GAP; STAT, signal transducer and activator of transcription; TB, transport buffer.


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