AtSKIP functions as a mediator between cytokinin and light signaling pathway in Arabidopsis thaliana |
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Authors: | Xia Zhang Ji-Hee Min Ping Huang Jung-Sung Chung Kyeong-Hwan Lee Cheol Soo Kim |
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Affiliation: | 1. Xinjiang Key Laboratory of Biological Resources and Genetic Engineering, College of Life Science and Technology, Xinjiang University, 14 Sheng li Road, Urumqi, 830046, China 2. Department of Plant Biotechnology, Chonnam National University, Gwangju, 500-757, South Korea 3. Department of Agronomy, Gyeongsang National University, Jinju, 660-701, South Korea 4. Department of Rural and Biosystems Engineering, Chonnam National University, Gwangju, 500-757, South Korea
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Abstract: | Key message AtSKIP participated in cytokinin-regulated leaf initiation. Putative phosphorylated AtSKIP (AtSKIP DD ) displayed the opposite function in the leaf development from AtSKIP transgenic seedlings. Abstract AtSKIP, as a multiple protein, is involved in many physiological processes, such as flowering, cell cycle regulator, photomorphogenesis and stress tolerance. However, the mechanism of AtSKIP in these processes is unclear. Here, we identify one gene, AtSKIP, which is associated with cytokinin-regulated leaf growth process in Arabidopsis. The expression of AtSKIP was regulated by cytokinin. Leaf development in AtSKIP overproduced seedlings was independent of light, but promoted by cytokinin, and phosphorylation of AtSKIP (AtSKIPDD) partially interfered with AtSKIP function as a positive regulator in cytokinin signaling, indicative of true leaf formation, and the defects of AtSKIPDD in the true leaf formation could be recovered to some extent by the addition of cytokinin. Moreover, different cytokinin-responsive gene Authentic Response Regulator 7 (ARR7) promoter-GUS activity further proved that expression of AtSKIP or AtSKIPDD altered endogenous cytokinin signaling in plants. Together, these data indicate that AtSKIP participates in cytokinin-regulated promotion of leaf growth in photomorphogenesis, and that phosphorylation interferes with AtSKIP normal function. |
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