Li Yuanyuan, Cheng Shuyang, Jin Xu, Wu Ruoxuan, Guo Yiyi, Wu Dezhi, Dong Jie
Institute of Crop Science, College of Agriculture and Biotechnology, Zhejiang University, Hangzhou, 310058, China.
College of Agronomy, Hunan Agricultural University, Changsha, 410128, China.
EMBO Rep. 2025 May 30. doi: 10.1038/s44319-025-00491-9.
Plants have evolved intricate strategies to cope with various abiotic stresses. Ubiquitin-mediated protein degradation plays a key role in plant development as well as abiotic stress tolerance. In this study, we identify LAO1, an F-box protein with unknown function, as a negative regulator of plant fitness during nitrogen starvation. DOMINANT SUPPRESSOR OF KAR 2 (DSK2) interacts with and mediates the autophagic degradation of LAO1 protein during nitrogen starvation. The loss of LAO1 improves the fitness of an autophagy-deficient mutant, atg5-1, under nitrogen starvation. Intriguingly, mutations in DSK2 facilitate rather than reduce plant growth after nitrogen starvation. This unexpected effect of DSK2 knockout led us to discover that DSK2 also interacts with and degrades a group of class I TCP transcription factors. Phenotypic observations demonstrate that class I TCPs are crucial for plant adaptation to nitrogen starvation. Moreover, genetic analyses indicate that class I TCPs function downstream of LAO1 and counteract its negative effects. Collectively, our findings unveil a previously undescribed regulatory network governing plant fitness during nitrogen starvation.
植物已经进化出复杂的策略来应对各种非生物胁迫。泛素介导的蛋白质降解在植物发育以及非生物胁迫耐受性中起着关键作用。在本研究中，我们鉴定出LAO1，一种功能未知的F-box蛋白，作为氮饥饿期间植物适应性的负调节因子。在氮饥饿期间，KAR 2的显性抑制因子（DSK2）与LAO1蛋白相互作用并介导其自噬降解。LAO1的缺失提高了自噬缺陷突变体atg5-1在氮饥饿条件下的适应性。有趣的是，DSK2的突变促进而非降低氮饥饿后植物的生长。DSK2敲除的这种意外效应使我们发现DSK2还与一组I类TCP转录因子相互作用并使其降解。表型观察表明，I类TCPs对植物适应氮饥饿至关重要。此外，遗传分析表明，I类TCPs在LAO1下游起作用并抵消其负面影响。总的来说，我们的研究结果揭示了一个以前未描述的调控网络，该网络在氮饥饿期间控制植物的适应性。
