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First published online January 22, 2004; 10.1104/pp.103.030650

Plant Physiology 134:790-800 (2004)
© 2004 American Society of Plant Biologists

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DEVELOPMENT AND HORMONE ACTION

High Pigment1 Mutation Negatively Regulates Phototropic Signal Transduction in Tomato Seedlings1

Ankanagari Srinivas, Rajendra K. Behera, Takatoshi Kagawa, Masamitsu Wada and Rameshwar Sharma*

School of Life Sciences, University of Hyderabad, Hyderabad-500046, India (A.S., R.K.B., R.S.); Division of Biological Regulation and Photobiology, National Institute for Basic Biology, Okazaki 444–8585, Japan (T.K., M.W., R.S.); and Department of Biological Sciences, Graduate School of Science, Tokyo Metropolitan University, Tokyo 192–0397, Japan (M.W.)

Phototropins and phytochromes are the major photosensory receptors in plants and they regulate distinct photomorphogenic responses. The molecular mechanisms underlying functional interactions of phototropins and phytochromes remain largely unclear. We show that the tomato (Lycopersicon esculentum) phytochrome A deficient mutant fri lacks phototropic curvature to low fluence blue light, indicating requirement for phytochrome A for expression of phototropic response. The hp1 mutant that exhibits hypersensitive responses to blue light and red light reverses the impairment of second-positive phototropic response in tomato in phytochrome A-deficient background. Physiological analyses indicate that HP1 functions as a negative regulator of phototropic signal transduction pathway, which is removed via action of phytochrome A. The loss of HP1 gene product in frihp1 double mutant allows the unhindered operation of phototropic signal transduction chain, obviating the need for the phytochrome action. Our results also indicate that the role of phytochrome in regulating phototropism is restricted to low fluence blue light only, and at high fluence blue light, the phytochrome A-deficient fri mutant shows the normal phototropic response.

Article, publication date, and citation information can be found at www.plantphysiol.org/cgi/doi/10.1104/pp.103.030650.

1 This work was supported by University Grants Commission, New Delhi, India (research fellowship support to A.S.), by Council of Scientific and Industrial Research, New Delhi, India (to R.K.B.), by Department of Science and Technology, New Delhi, India (research grant to R.S.), and by a Japanese Society for the Promotion of Science, Tokyo, Japan Senior, Visiting Fellowship (to R.S.).

* Corresponding author; e-mail rpssl{at}uohyd.ernet.in; fax 0091–40–23010120.

Received July 22, 2003; returned for revision September 15, 2003; accepted November 16, 2003.

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