Histone acetyltransferase plays a critical role in transcriptional regulation by increasing accessibility of target genes to transcriptional activators. Botrytis cinerea is an important necrotrophic fungal pathogen with worldwide distribution and a very wide host range, but little is known of how the fungus regulates the transition from saprophytic growth to infectious growth. Here, the function of BcSas2, a histone acetyltransferase of B. cinerea, was investigated. Deletion of the BcSAS2 gene resulted in significantly reduced acetylation levels of histone H4, particularly of H4K16ac. The deletion mutant ΔBcSas2.1 was not only less pathogenic but also more sensitive to oxidative stress than the wild-type strain. RNA-Seq analysis revealed that a total of 13 B. cinerea genes associated with pathogenicity were down-regulated in the ΔBcSas2.1 mutant. Independent knockouts of two of these genes, BcXYGA (xyloglucanase) and BcCAT (catalase), led to dramatically decreased virulence and hypersensitivity to oxidative stress, respectively. Chromatin immunoprecipitation followed by quantitative PCR confirmed that BcSas2 bound directly to the promoter regions of both these pathogenicity-related genes. These observations indicated that BcSas2 regulated the transcription of pathogenicity-related genes by controlling the acetylation level of H4K16, thereby affecting the virulence and oxidative sensitivity of B. cinerea.

组蛋白乙酰转移酶通过增加靶基因对转录激活因子的可及性，在转录调控中起关键作用。灰葡萄孢（Botrytis cinerea）是重要的坏死性真菌病原体，在世界范围内分布并且具有广泛的宿主范围，但是对于真菌如何调节从腐生性生长到传染性生长的转变知之甚少。在这里，BcSas2，一个组蛋白乙酰转移的功能灰霉病，进行了调查。BcSAS2基因的删除导致组蛋白H4，特别是H4K16ac的乙酰化水平大大降低。缺失突变体ΔBcSas2.1不仅比野生型菌株致病力小，而且对氧化应激更敏感。RNA-Seq分析显示总共13与致病性相关的灰质芽孢杆菌基因在ΔBcSas2.1突变体中被下调。这些基因中的两个基因BcXYGA（木葡聚糖酶）和BcCAT（过氧化氢酶）的独立敲除分别导致毒力和对氧化应激的超敏性大大降低。染色质免疫沉淀后进行定量PCR证实BcSas2直接与这两个致病性相关基因的启动子区域结合。这些观察结果表明，BcSas2通过控制H4K16的乙酰化水平，进而影响毒力和氧化灵敏度调节的致病相关基因的转录灰霉病。