Institute of Cell Biology and MOE Key Laboratory of Cell Activities and Stress Adaptations, School of Life Sciences, Lanzhou University, Lanzhou, 730000, China.
BMC Plant Biol. 2021 Jul 3;21(1):320. doi: 10.1186/s12870-021-03090-7.
N-terminal acetylation (NTA) is a highly abundant protein modification catalyzed by N-terminal acetyltransferases (NATs) in eukaryotes. However, the plant NATs and their biological functions have been poorly explored. Here we reveal that loss of function of CKRC3 and NBC-1, the auxiliary subunit (Naa25) and catalytic subunit (Naa20) of Arabidopsis NatB, respectively, led to defects in skotomorphogenesis and triple responses of ethylene. Proteome profiling and WB test revealed that the 1-amincyclopropane-1-carboxylate oxidase (ACO, catalyzing the last step of ethylene biosynthesis pathway) activity was significantly down-regulated in natb mutants, leading to reduced endogenous ethylene content. The defective phenotypes could be fully rescued by application of exogenous ethylene, but less by its precursor ACC. The present results reveal a previously unknown regulation mechanism at the co-translational protein level for ethylene homeostasis, in which the NatB-mediated NTA of ACOs render them an intracellular stability to maintain ethylene homeostasis for normal growth and responses.
N-端乙酰化（NTA）是真核生物中由 N-端乙酰转移酶（NATs）催化的一种高度丰富的蛋白质修饰。然而，植物 NATs 及其生物学功能还没有得到很好的探索。在这里，我们揭示了 CKRC3 和 NBC-1（拟南芥 NatB 的辅助亚基（Naa25）和催化亚基（Naa20））的功能丧失，导致了 skotomorphogenesis 和乙烯的三重反应缺陷。蛋白质组谱分析和 WB 测试显示，natb 突变体中 1-氨基环丙烷-1-羧酸氧化酶（ACO，催化乙烯生物合成途径的最后一步）的活性显著下调，导致内源乙烯含量降低。缺陷表型可以通过施加外源乙烯完全挽救，但通过其前体 ACC 则较少。本研究结果揭示了一个以前未知的乙烯稳态的共翻译蛋白水平的调节机制，其中 NatB 介导的 ACOs 的 NTA 使它们在细胞内保持稳定，以维持正常生长和反应所需的乙烯稳态。
