Sucrose induces flowering by degradation of the floral repressor Ghd7 via K48-linked polyubiquitination in rice.

蔗糖通过 K48 连接的多聚泛素化降解开花抑制因子 Ghd7 来诱导水稻开花

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作者:Cho Lae-Hyeon, Yoon Jinmi, Baek Gibeom, Tun Win, Kwon Hyeok Chan, Lee Dae-Woo, Choi Seok-Hyun, Lee Yang-Seok, Jeon Jong-Seong, An Gynheung
Sucrose functions as a signaling molecule in several metabolic pathways as well as in various developmental processes. However, the molecular mechanisms by which sucrose regulates these processes remain largely unknown. In the present study, we demonstrate that sucrose promotes flowering by mediating the stability of a regulatory protein that represses flowering in rice. Exogenous application of sucrose promoted flowering by inducing florigen gene expression. Reduction of sucrose levels in the phloem through genetic modifications, such as the overexpression of the vacuolar invertase OsVIN2 or the mutation of OsSUT2, a sucrose transporter, delayed flowering. Analysis of relative transcript levels of floral regulatory genes showed that sucrose activated Ehd1 upstream of the florigen, with no significant effect on the expression of other upstream genes. Examination of protein stability after sucrose treatment of major floral repressors revealed that the Ghd7 protein was specifically degraded. The Ghd7 protein interacted with the E3 ligase IPA INTERACTING PROTEIN1 (IPI1), and sucrose-induced K48-linked polyubiquitination of Ghd7 via IPI1, leading to protein degradation. Mutants defective in IPI1 delayed flowering, confirming its role in modulating proteins involved in flowering. We conclude that sucrose acts as a signaling molecule to induce flowering by promoting Ghd7 degradation via IPI1.

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