The Key Laboratory of Plant Molecular Physiology, Institute of Botany, Chinese Academy of Sciences, Beijing 100093, China.
The Key Laboratory of Plant Molecular Physiology, Institute of Botany, Chinese Academy of Sciences, Beijing 100093, China; University of Chinese Academy of Sciences, Beijing 100049, China.
Dev Cell. 2017 Dec 18;43(6):731-743.e5. doi: 10.1016/j.devcel.2017.11.016.
Improvement of chilling tolerance is a major target in rice breeding. The signaling pathways regulating chilling consist of complex networks, including key transcription factors and their targets. However, it remains largely unknown how transcription factors are activated by chilling stress. Here, we report that the transcription factor OsbHLH002/OsICE1 is phosphorylated by OsMAPK3 under chilling stress. The osbhlh002-1 knockout mutant and antisense transgenic plants showed chilling hypersensitivity, whereas OsbHLH002-overexpressing plants exhibited enhanced chilling tolerance. OsbHLH002 can directly target OsTPP1, which encodes a key enzyme for trehalose biosynthesis. OsMAPK3 interacts with OsbHLH002 to prevent its ubiquitination by the E3 ligase OsHOS1. Under chilling stress, active OsMAPK3 phosphorylates OsbHLH002, leading to accumulation of phospho-OsbHLH002, which promotes OsTPP1 expression and increases trehalose content and resistance to chilling damage. Taken together, these results indicate that OsbHLH002 is phosphorylated by OsMAPK3, which enhances OsbHLH002 activation to its target OsTPP1 during chilling stress.
提高水稻的抗冷性是水稻育种的主要目标。调控冷胁迫的信号通路包括复杂的网络，包括关键转录因子及其靶标。然而，转录因子如何被冷胁迫激活在很大程度上仍然未知。在这里，我们报告说转录因子 OsbHLH002/OsICE1 在冷胁迫下被 OsMAPK3 磷酸化。osbhlh002-1 敲除突变体和反义转基因植物表现出冷敏感，而 OsbHLH002 过表达植物表现出增强的抗冷性。OsbHLH002 可以直接靶向 OsTPP1，它编码海藻糖生物合成的关键酶。OsMAPK3 与 OsbHLH002 相互作用，以防止其被 E3 连接酶 OsHOS1 泛素化。在冷胁迫下，活性 OsMAPK3 磷酸化 OsbHLH002，导致磷酸化 OsbHLH002 的积累，促进 OsTPP1 的表达，增加海藻糖含量并提高对冷害的抗性。综上所述，这些结果表明 OsbHLH002 被 OsMAPK3 磷酸化，在冷胁迫期间增强 OsbHLH002 对其靶标 OsTPP1 的激活。
