乙烯对酰基转移酶的调控机制和BAHD酰基转移酶对盐胁迫的响应，到目前为止仍不清楚。本实验室在前期研究中，根据RNA-Seq、ChIP-Seq和microarray的结果，推测出一个新的BAHD酰基转移酶AT5G01210(BAT2)受乙烯的诱导，且位于EIN3转录因子的下游。初步分析显示BAT2调控溶血磷脂酰胆碱的生成，并且还能够响应盐胁迫。本研究在此基础上，检测乙烯对BAT2表达的诱导、EIN3和BAT2启动子的靶标关系和遗传上的上下游关系；利用BAT2的不同遗传操作株系(RNAi基因沉默、CRISPR-Cas9基因敲除、T-DNA插入和基因过表达)，检测盐胁迫相关表型性状、基因表达和生理指标的变化；检测溶血磷脂酰胆碱处理后bat2突变体耐盐性的变化，证明乙烯通过调控BAHD酰基转移酶BAT2响应盐胁迫，从而深入了解乙烯通过调控BAT2响应盐胁迫的分子调控机制。

The mechanism of ethylene regulating the expression of BAHD acyltransferase, and the responses of BAHD acyltransferase to salt stress are still unclear. In previous research of our lab, a novel BAHD acyltransferase gene, AT5G01210(BAT2), was detected according to results of RNA-Seq, ChIP-Seq and microarray experiments. The novel BAHD acyltransferase gene BAT2 was induced by ethylene and activated by EIN3 transcription factor in the ethylene signaling. The previous results also showed BAT2 regulates the production of hemolytic phosphatidyl choline and responses to salt stress. In this research, the inducing expression of BAT2 by ethylene, the target relationship of EIN3 to the BAT2 promote, and the genetic relationship of EIN3 and BAT2 in the ethylene signaling will be proved. The salt stress related phenotypic traits, genes expression and physiological indicators will be detected in lines by different genetic approaches (RNAi gene silencing, CRISPR-Cas9 gene knockout, T-DNA insertion mutations, and genes overexpression). The salt response phenotypes of bat2 mutant treated with hemolytic phosphatidyl choline will be compared with untreated bat2 mutant and wild type plants. In the end, the molecular mechanism of BAT2 responding to salt stress will be uncovered. These studies will undoubtedly provide new materials for understanding molecular regulation mechanism of ethylene responding to salt stress.