State Key Laboratory for Conservation and Utilization of Subtropical Agro-Bioresources, South China Agricultural University, Guangzhou, 510642, China.
Guangzhou City Academy of Agricultural Sciences, Key Laboratory of Biology, Genetics and Breeding, Guangzhou, 510000, China.
Adv Biol (Weinh). 2023 Dec;7(12):e2300106. doi: 10.1002/adbi.202300106. Epub 2023 Jul 6.
Phosphorus (Pi) starvation prevents a good match between light energy absorption and photosynthetic carbon metabolism, generating photo-reactive oxygen species (photo-ROS) in chloroplasts. Plants have evolved to withstand photo-oxidative stress, but the key regulatory mechanism underlying it remains unclear. In rice (Oryza sativa), DEEP GREEN PANICLE1 (DGP1) is robustly up-regulated in response to Pi deficiency. DGP1 decreases the DNA-binding capacities of the transcriptional activators GLK1/2 on the photosynthetic genes involved in chlorophyll biosynthesis, light harvesting, and electron transport. This Pi-starvation-induced mechanism dampens both electron transport rates through photosystem I and II (ETRI and ETRII) and thus mitigates the electron-excessive stress in mesophyll cells. Meanwhile, DGP1 hijacks glycolytic enzymes GAPC1/2/3, redirecting glucose metabolism toward the pentose phosphate pathway with superfluous NADPH production. Phenotypically, light irradiation induces O production in Pi-starved WT leaves but is observably accelerated in dgp1 mutant and impaired in GAPCs and glk1glk2 lines. Interestingly, overexpressed DGP1 in rice caused hyposensitivity to ROS-inducers (catechin and methyl viologen), but the dgp1 mutant shows a similar inhibitory phenotype with the WT seedlings. Overall, the DGP1 gene serves as a specific antagonizer against photo-ROS in Pi-starved rice plants, which coordinates light-absorbing and anti-oxidative systems by orchestrating transcriptional and metabolic regulations, respectively.
磷（Pi）饥饿会阻止光能吸收和光合作用碳代谢之间的良好匹配，从而在叶绿体中产生光反应性氧物种（photo-ROS）。植物已经进化到能够耐受光氧化应激，但其中的关键调节机制仍不清楚。在水稻（Oryza sativa）中，深绿穗 1 （DGP1）在响应 Pi 缺乏时强烈上调。DGP1 降低了参与叶绿素生物合成、光捕获和电子传递的光合作用基因的转录激活因子 GLK1/2 的 DNA 结合能力。这种由 Pi 饥饿诱导的机制抑制了通过光系统 I 和 II（ETRI 和 ETRII）的电子传递速率，从而减轻了叶肉细胞中的电子过剩应激。同时，DGP1劫持糖酵解酶 GAPC1/2/3，将葡萄糖代谢转向戊糖磷酸途径，产生多余的 NADPH。表型上，光照诱导 Pi 饥饿 WT 叶片中 O 的产生，但在 dgp1 突变体中明显加速，在 GAPCs 和 glk1glk2 系中受损。有趣的是，在水稻中过表达 DGP1 导致对 ROS 诱导剂（儿茶素和甲基紫精）的低敏感性，但 dgp1 突变体与 WT 幼苗表现出相似的抑制表型。总的来说，DGP1 基因在 Pi 饥饿的水稻植物中充当特定的 photo-ROS 拮抗剂，通过协调转录和代谢调节分别协调光吸收和抗氧化系统。
