Ferreira Marco Aurélio, Teixeira Ruan M, Brustolini Otávio J B, Saia Thainá F F, Jean-Baptiste James, Ribeiro Nathalia G A, Breves Sâmera S, Sampaio Fellipe R, Santos Eulálio G D, Leon Borys A, Oliveira Celio C, Duarte Christiane E M, Lima Lucas L, Oliveira Leandro L, Ramos Humberto J O, Reis Pedro A B, Fontes Elizabeth P B
Department of Biochemistry and Molecular Biology, Universidade Federal de Viçosa, Viçosa, Minas Gerais, Brazil.
National Institute of Science and Technology in Plant-Pest Interactions, Bioagro, Universidade Federal de Viçosa, Viçosa, Minas Gerais, Brazil.
Nat Commun. 2025 May 13;16(1):4433. doi: 10.1038/s41467-025-59571-y.
Photosynthesis and translation are targets of metabolic control and development in plants, yet how stress signals coordinately regulate these opposing energy-producing and consuming processes remains enigmatic. Here, we unravel a growth control circuit that ties photosynthesis to translational control in response to biotic and abiotic signals. Our findings reveal that the L10-INTERACTING MYB DOMAIN-CONTAINING PROTEIN (LIMYB), a key player of the NUCLEAR SHUTTLE PROTEIN-INTERACTING KINASE 1 (NIK1)/ RIBOSOMAL PROTEIN L10 (RPL10) antiviral signaling pathway, not only downregulates translation genes, but also represses photosynthesis-related genes and photosynthesis itself. LIMYB repressor activity, regulated by phosphorylation, is crucial for the decline in photosynthesis under stress. NIK1 activation by PAMPs or the phosphomimetic NIK1-T474D represses photosynthesis-related genes and photosynthesis in control but not in limyb lines. Furthermore, heat and osmotic stress also activate the NIK1/RPL10/LIMYB signaling circuit in wild type. These stresses induce NIK1 phosphorylation, but not marker gene repression, in limyb, indicating that LIMYB connects NIK1 activation to stress-mediated downregulation of translation- and photosynthesis-related genes. This coordinated repression via the NIK1/RPL10/LIMYB module may help plants adapt to changing environments.
光合作用和翻译是植物代谢控制和发育的靶点，然而应激信号如何协调调节这些相反的能量产生和消耗过程仍然是个谜。在这里，我们揭示了一个生长控制回路，该回路将光合作用与响应生物和非生物信号的翻译控制联系起来。我们的研究结果表明，L10相互作用含MYB结构域蛋白（LIMYB）是核穿梭蛋白相互作用激酶1（NIK1）/核糖体蛋白L10（RPL10）抗病毒信号通路的关键参与者，它不仅下调翻译基因，还抑制光合作用相关基因和光合作用本身。受磷酸化调节的LIMYB阻遏活性对于应激下光合作用的下降至关重要。PAMPs或磷酸模拟物NIK1-T474D激活NIK1会抑制对照中但不抑制limyb系中的光合作用相关基因和光合作用。此外，热胁迫和渗透胁迫也会在野生型中激活NIK1/RPL10/LIMYB信号回路。这些胁迫在limyb中诱导NIK1磷酸化，但不诱导标记基因抑制，这表明LIMYB将NIK1激活与应激介导的翻译和光合作用相关基因的下调联系起来。通过NIK1/RPL10/LIMYB模块的这种协同抑制可能有助于植物适应不断变化的环境。
