Hyo Jung Kim *, Hojin Ryu *, Sung Hyun Hong *, Hye Ryun Woo *, Pyung Ok Lim , In Chul Lee *, Jen Sheen , Hong Gil Nam *¶||, and Ildoo Hwang *||
*Division of Molecular and Life Sciences, ¶National Core Research Center for Systems Bio-Dynamics and the I-BIO Graduate Program, Pohang University of Science and Technology, Pohang 790-784, Korea; Department of Science Education, Cheju National University, Cheju 690-756, Korea; and Department of Molecular Biology, Massachusetts General Hospital and Department of Genetics, Harvard Medical School, Boston, MA 02114
Edited by Hans Janos Kende, Michigan State University, East Lansing, MI, and approved November 14, 2005 (received for review June 21, 2005)
Cytokinins are plant hormones with profound roles in growth and development, including control of leaf longevity. Although the cytokinin signal is known to be perceived by histidine kinase receptors, the underlying molecular mechanism and specificity of the receptors leading to delayed leaf senescence have not yet been elucidated. Here, we found that AHK3, one of the three cytokinin receptors in Arabidopsis, plays a major role in controlling cytokinin-mediated leaf longevity through a specific phosphorylation of a response regulator, ARR2. This result was obtained through identification of a gain-of-function Arabidopsis mutant that shows delayed leaf senescence because of a missense mutation in the extracellular domain of AHK3. A loss-of-function mutation in AHK3, but not of the other cytokinin receptors, conferred a reduced sensitivity to cytokinin in cytokinin-dependent delay of leaf senescence and abolished cytokinin-dependent phosphorylation of ARR2. Consistently, transgenic overexpression of wild-type, but not an unphosphorylatable mutant ARR2, led to delayed senescence of leaves.
Author contributions: H.J.K., H.R., S.H.H., H.G.N., and I.H. designed research; H.J.K., H.R., S.H.H., H.R.W., I.C.L., and I.H. performed research; J.S. contributed new reagents/analytic tools; H.J.K., H.R., S.H.H., P.O.L., J.S., H.G.N., and I.H. analyzed data; and H.J.K., H.G.N., and I.H. wrote the paper.
Conflict of interest statement: No conflicts declared.
Present address: Department of Biology, Washington University, St. Louis, MO 63130.
||To whom correspondence may be addressed.