转录因子BZR1与表观遗传因子HD2C互作调控番茄低温抗性的机制

Tomato plants frequently suffer chilling stress in the greenhouse during spring-winter period. Brassinosteroid (BR)-induced chilling tolerance has been shown to be associated with an increase in the accumulation of abscisic acid (ABA). However, the exact mechanism remains to be further studied. Our previous work found that BZR1, a transcription factor downstream of BR signaling, played an important role in chilling tolerance in tomato. BZR1 interacted with the epigenetic regulator, histone deacetylase HD2C. Silencing of HD2C led to disorders of ABA metabolism and chilling sensitivity. Therefore, BZR1 may regulate histone acetylation of ABA metabolic genes through HD2C to improve tomato chilling tolerance. In this project, we aim to reveal the functions of BZR1 and HD2C in the regulation of tomato chilling tolerance, identify the critical chilling response genes regulated by BZR1 and HD2C and elucidate their functions, and finally dissect the regulation of histone acetylation of ABA metabolic genes by BZR1 and HD2C. The implementation of the project will help elucidate the mechanism by which BR regulates the chilling tolerance of tomato and provide a theoretical basis for the improvement of tomato production efficiency under sub-optimal environmental conditions in the greenhouse.

冬春季节设施番茄频繁遭受低温冷害。油菜素内酯（BR）提高番茄耐冷性与脱落酸（ABA）积累增加有关，但具体机制还有待于进一步研究。我们前期工作发现，BR信号下游的转录因子BZR1在低温抗性中具有重要作用，BZR1能与表观遗传因子组蛋白去乙酰化酶HD2C发生互作，而缺失HD2C导致ABA代谢紊乱及低温抗性下降。因此，BZR1可能通过HD2C调控ABA代谢基因的乙酰化提高番茄耐冷性。申请项目研究BZR1和HD2C在调控番茄耐冷性中的作用，并阐明两者的互作关系；挖掘BZR1和HD2C调控的低温抗性关键基因并阐明其功能；明确BZR1和HD2C对ABA代谢基因的组蛋白乙酰化调控。项目的实施有助于阐明BR调控番茄耐冷性的机制，为实现设施亚适宜环境下番茄生产的提质增效提供理论依据。

番茄设施栽培具有产量高、效益好的优点，近年来设施番茄面积不断扩大，但是面临冬春低温弱光的问题。长期低温弱光会降低光合能力、引起氧化胁迫并抑制植株生长发育，因此迫切需要解决低温弱光抗性调控的问题。油菜素内酯（BR）不仅参与各个植物生长发育过程，而且促进光合作用，提高各种非生物逆境抗性，是增强设施番茄低温弱光抗性的重要途径。本项目主要针对BR信号途径在番茄低温抗性中的生理功能与分子机制展开了系统研究。明确了番茄低温响应中BR含量升高，并通过抑制BR信号通路中的负调控因子BIN2以及促进转录因子BZR1的积累提高番茄低温抗性。揭示了BZR1转录调控NCED1基因促进番茄抗逆激素脱落酸（ABA）合成以及ABA在BR信号增强低温抗性中的关键作用。挖掘到BZR1的互作蛋白组蛋白去乙酰化酶SRT1，通过分子生物学和遗传学证据明确了BZR1与SRT1协同调控番茄低温抗性。进一步通过RNA-seq分析鉴定到BZR1和SRT1共同调控的靶标基因MYB13和bZIP17，两者均为低温抗性的负调控基因，并明确了BZR1与SRT1协同抑制MYB13和bZIP17基因启动子的组蛋白乙酰化及转录表达。此外还发现，提高BR水平有助于增强番茄光合作用以及可溶性糖和淀粉的含量，促进番茄对长期弱光胁迫的抗性。该项研究在分子水平明确了BR调控低温弱光抗性的生理功能，发现了BR信号依赖组蛋白乙酰化修饰调控低温抗性的新机制，并通过揭示BR信号下游低温抗性的负调控基因MYB13和bZIP17为创制耐低温番茄种质奠定了理论基础。