Key Laboratory of Bio-Resource and Eco-Environment of Ministry of Education, State Key Laboratory of Hydraulics and Mountain River Engineering, College of Life Sciences, Sichuan University, Chengdu, Sichuan, P. R. China.
Ecological Security and Protection Key Laboratory of Sichuan Province, Mianyang Normal University, Mianyang, Sichuan, P. R. China.
PLoS Genet. 2020 Jul 1;16(7):e1008883. doi: 10.1371/journal.pgen.1008883. eCollection 2020 Jul.
Plant steroid hormones brassinosteroids (BRs) regulate plant growth and development at many levels. While negative regulatory factors that inhibit development and are counteracted by BRs exist in the root meristem, these factors have not been characterized. The functions of UPB1 transcription factor in BR-regulated root growth have not been established, although its role in regulating root are well documented. Here, we found that BIN2 interacts with and phosphorylates the UPB1 transcription factor consequently promoting UPB1 stability and transcriptional activity. Genetic analysis revealed that UPB1 deficiency could partially recover the short-root phenotype of BR-deficient mutants. Expression of a mutated UPB1S37AS41A protein lacking a conserved BIN2 phosphorylation sites can rescue shorter root phenotype of bin2-1 mutant. In addition, UPB1 was repressed by BES1 at the transcriptional level. The paclobutrazol-resistant protein family (PRE2/3) interacts with UPB1 and inhibits its transcriptional activity to promote root meristem development, and BIN2-mediated phosphorylation of UPB1 suppresses its interaction with PRE2/3, and subsequently impairing root meristem development. Taken together, our data elucidate a molecular mechanism by which BR promotes root growth via inhibiting BIN2-UPB1 module.
植物甾体激素油菜素内酯(BRs)在多个层面上调节植物的生长和发育。虽然在根分生组织中存在抑制发育并被 BR 抵消的负调控因子,但这些因子尚未被表征。虽然 UPB1 转录因子在 BR 调节根生长中的作用已有详细记录,但它在 BR 调节中的功能尚未确定。在这里,我们发现 BIN2 与 UPB1 转录因子相互作用并使其磷酸化,从而促进 UPB1 的稳定性和转录活性。遗传分析表明,UPB1 缺陷可部分恢复 BR 缺陷突变体的短根表型。表达一种突变的 UPB1S37AS41A 蛋白,该蛋白缺失一个保守的 BIN2 磷酸化位点,可挽救 bin2-1 突变体较短的根表型。此外,BES1 在转录水平上抑制 UPB1 的表达。对多效唑有抗性的蛋白家族(PRE2/3)与 UPB1 相互作用,并抑制其转录活性,从而促进根分生组织的发育,而 BIN2 介导的 UPB1 磷酸化抑制其与 PRE2/3 的相互作用,进而损害根分生组织的发育。总之,我们的数据阐明了 BR 通过抑制 BIN2-UPB1 模块促进根生长的分子机制。