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Plant Cell Advance Online Publication
Published on January 12, 2007; 10.1105/tpc.106.045658

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Received July 7, 2006
Returned for revision November 9, 2006
Accepted November 27, 2006

PIP5K9, an Arabidopsis Phosphatidylinositol Monophosphate Kinase, Interacts with a Cytosolic Invertase to Negatively Regulate Sugar-Mediated Root Growth

Ying Lou 1, Jin-Ying Gou 2, and Hong-Wei Xue 1*

1 National Key Laboratory of Plant Molecular Genetics, Institute of Plant Physiology and Ecology, Shanghai Institutes for Biological Science, Chinese Academy of Sciences, 200032 Shanghai, People's Republic of China; Partner Group of Max-Planck-Institute of Molecular Plant Physiology on Plant Molecular Physiology and Signal Transduction, 200032 Shanghai, People's Republic of China
2 National Key Laboratory of Plant Molecular Genetics, Institute of Plant Physiology and Ecology, Shanghai Institutes for Biological Science, Chinese Academy of Sciences, 200032 Shanghai, People's Republic of China

* To whom correspondence should be addressed. E-mail: hwxue{at}sibs.ac.cn.

Phosphatidylinositol monophosphate 5-kinase (PIP5K) plays an essential role in coordinating plant growth, especially in response to environmental factors. To explore the physiological function of PIP5K, we characterized Arabidopsis thaliana PIP5K9, which is constitutively expressed. We found that a T-DNA insertion mutant, pip5k9-d, which showed enhanced PIP5K9 transcript levels, had shortened primary roots owing to reduced cell elongation. Transgenic plants overexpressing PIP5K9 displayed a similar root phenotype. Yeast two-hybrid assays identified a cytosolic invertase, CINV1, that interacted with PIP5K9, and the physiological relevance of this interaction was confirmed by coimmunoprecipitation studies using plant extracts. CINV1-deficient plants, cinv1, had reduced activities of both neutral and acid invertases as well as shortened roots. Invertase activities in pip5k9-d seedlings were also reduced, suggesting a negative regulation of CINV1 by PIP5K9. In vitro studies showed that PIP5K9 interaction indeed repressed CINV1 activities. Genome-wide expression studies revealed that genes involved in sugar metabolism and multiple developmental processes were altered in pip5k9-d and cinv1, and the altered sugar metabolism in these mutants was confirmed by metabolite profiling. Together, our results indicate that PIP5K9 interacts with CINV1 to negatively regulate sugar-mediated root cell elongation.




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