The phytohormone jasmonate(JA)coordinates stress and growth responses to increase plant survival in unfavorable environments.Although JA can enhance plant UV-B stress tolerance,the mechanisms underlying the interactio...The phytohormone jasmonate(JA)coordinates stress and growth responses to increase plant survival in unfavorable environments.Although JA can enhance plant UV-B stress tolerance,the mechanisms underlying the interaction of UV-B and JA in this response remain unknown.In this study,we demonstrate that the UV RESISTANCE LOCUS 8-TEOSINTE BRANCHED1,Cycloidea and PCF 4-LIPOXYGENASE2(UVR8-TCP4-LOX2)module regulates UV-B tolerance dependent on JA signaling pathway in Arabidopsis thaliana.We show that the nucleus-localized UVR8 physically interacts with TCP4 to increase the DNA-binding activity of TCP4 and upregulate the JA biosynthesis gene LOX2.Furthermore,UVR8 activates the expression of LOX2 in a TCP4-dependent manner.Our genetic analysis also provides evidence that TCP4 acts downstream of UVR8 and upstream of LOX2 to mediate plant responses to UV-B stress.Our results illustrate that the UV-B-dependent interaction of UVR8 and TCP4 serves as an important UVR8-TCP4-LOX2 module,which integrates UV-B radiation and JA signaling and represents a new UVR8 signaling mechanism in plants.展开更多
基金supported by the Second Tibetan Plateau Scientific Expedition and Research(STEP)program(2019QZKK0502)the National Natural Science Foundation of China(No.32370405).
文摘The phytohormone jasmonate(JA)coordinates stress and growth responses to increase plant survival in unfavorable environments.Although JA can enhance plant UV-B stress tolerance,the mechanisms underlying the interaction of UV-B and JA in this response remain unknown.In this study,we demonstrate that the UV RESISTANCE LOCUS 8-TEOSINTE BRANCHED1,Cycloidea and PCF 4-LIPOXYGENASE2(UVR8-TCP4-LOX2)module regulates UV-B tolerance dependent on JA signaling pathway in Arabidopsis thaliana.We show that the nucleus-localized UVR8 physically interacts with TCP4 to increase the DNA-binding activity of TCP4 and upregulate the JA biosynthesis gene LOX2.Furthermore,UVR8 activates the expression of LOX2 in a TCP4-dependent manner.Our genetic analysis also provides evidence that TCP4 acts downstream of UVR8 and upstream of LOX2 to mediate plant responses to UV-B stress.Our results illustrate that the UV-B-dependent interaction of UVR8 and TCP4 serves as an important UVR8-TCP4-LOX2 module,which integrates UV-B radiation and JA signaling and represents a new UVR8 signaling mechanism in plants.
