HDA6 represses the histone acetylation modification and expression of WRKY18/40 to inhibit camalexin biosynthesis in Arabidopsis

期刊论文
发表日期：

2026年6月2日

查看全文

Lei He,
Yizhong Wang,
Zhenjiang Wu,
Jingjing Liu,
Wannian Yang

摘要

Key message

As a general gene repressor, HDA6 inhibits camalexin biosynthesis through decreasing histone acetylation and H3K4me3 modification of biosynthesis genes and repressing the accumulation of SA and SA-induced expression of WRKY18 and WRKY40, two regulators in camalexin biosynthesis.

Abstract

Camalexin, a major phytoalexin in cruciferous plants, is induced by biotic and abiotic stresses. However, it is not clear how plants maintain its biosynthesis in a silenced state. In this work, the role of HDA6 in repressing camalexin biosynthesis was investigated. We found that in the shi5 mutant, camalexin biosynthesis was constitutively activated, accompanied by the constitutive expression of camalexin biosynthesis genes CYP71A13, PAD3, and GSTF6, as well as increased histone acetylation and H3K4me3 levels on their promoters. Furthermore, the activation of camalexin biosynthesis in shi5 is also dependent on the constitutive accumulation of salicylic acid (SA) caused by the previously reported constitutive expression of SID2. Moreover, the camalexin biosynthesis regulators WRKY18 and WRKY40 are also upregulated in shi5 due to the constitutive accumulation of SA. Introducing wrky18 or wrky40 mutations into shi5 reduced camalexin content to wild-type levels, accompanied by decreased expression of CYP71A13, PAD3, and GSTF6. Taken together, both the camalexin biosynthesis genes and WRKY18/40 are direct targets of HDA6. In shi5, loss of HDA6 leads to constitutive SA accumulation, which activates WRKYs’ expression; both the activated WRKY18/40 proteins and increased histone acetylation and H3K4me3 levels are required for the constitutive expression of camalexin biosynthesis genes. It is proposed that HDA6 represses camalexin biosynthesis through decreasing histone acetylation and H3K4me3 modification and repressing SA accumulation and the subsequent SA-induced expression of WRKYs.