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Published on April 13, 2007; 10.1104/pp.106.092163

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Received November 2, 2006
Accepted March 28, 2007

Arabidopsis Inositol Polyphosphate 6-/3-kinase (AtIpk2[beta]) Is Involved in Axillary Shoot Branching via Auxin Signaling

Zai-Bao Zhang , Guang Yang , Fernando Arana , Zhen Chen , Yan Li , and Hui-Jun Xia *

Key Laboratory of MOE for Plant Developmental Biology, College of Life Sciences, Wuhan University, Wuhan, Hubei 430072, P.R.China; Institute of Biochemistry and Biology, University of Potsdam, Potsdam14469, Germany

* Corresponding author; email: hjxia{at}whu.edu.cn.

The Arabidopsis inositol polyphosphate 6-/3-kinase gene (AtIpk2{beta}) is known to participate in inositol phosphate metabolism. However, little is known about its physiological functions in higher plants. Here, we report that AtIpk2{beta} regulates Arabidopsis axillary shoot branching. By overexpressing AtIpk2{beta} in wild-type and mutants, we found that overexpression of AtIpk2{beta} leads to more axillary shoot branches. Further analysis of AtIpk2{beta} overexpression lines showed that axillary meristem forms earlier and the bud outgrowth rate is also accelerated, resulting in more axillary shoot branches. AtIpk2{beta} promoter/{beta}-glucuronidase (GUS) fusions (AtIpk2{beta}::GUS) expression pattern is similar to that of the auxin reporter DR5::GUS. Moreover, AtIpk2{beta} can be induced in response to exogenous IAA treatments. In addition, AtIpk2{beta} overexpression plants exhibite auxin-related phenotypes and are more resistance to exogenous auxin treatment. Further analysis employing RT-PCR shows that some genes involved in auxin biosynthesis (CYP83B1), auxin transport (PIN4) and auxin-mediated branching regulation (MAX4 and SPS) are regulated by AtIpk2{beta}. Taken together, our data provide insights into a role for AtIpk2{beta} in axillary shoot branching through auxin signaling pathway.






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