Effector gene silencing mediated by histone methylation underpins host adaptation in an oomycete plant pathogen
Effector gene silencing mediated by histone methylation underpins host adaptation in an oomycete plant pathogen
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组蛋白甲基化介导的效应基因沉默支持卵菌植物病原体的宿主适应
DOI：
10.1093/nar/gkz1160
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发表时间：
2019-12
影响因子：
14.9
通讯作者：
Dong Suomeng
中科院分区：
文献类型：
--
作者：
Wang Liyuan;Chen Han;Li JiangJiang;Shu Haidong;Zhang Xiangxue;Wang Yuanchao;Tyler Brett M.;Dong Suomeng
病原菌种群的不断适应性是实施有效疾病控制措施的主要障碍。越来越多的证据表明，基因转录多态性是病原体规避宿主免疫的一种策略。然而，转录可塑性的潜在机制在很大程度上仍然难以捉摸。本研究发现，大豆根腐病病原菌大豆疫霉（Phytophthora sojae）通过效应基因Avr1b的转录多态性（在没有任何序列变异的情况下发生）逃避大豆抗性基因Rps1b。在自然发生的Avr1b沉默菌株中，在Avr1b位点观察到组蛋白H3赖氨酸27三甲基化（H3K27me3）水平升高，而在Avr1b表达菌株中则没有，这表明这种表观遗传修饰与Avr1b沉默之间存在相关性。为了从遗传学上验证这一假设，我们使用CRISPR/Cas9编辑了编码H3K27me3甲基转移酶复合物核心亚基的基因PsSu(z)12，并获得了三个缺失突变体。在这些突变体中，Avr1b基因组区域的H3K27me3缺失与Avr1b基因沉默受损相关。重要的是，这些突变体失去了逃避携带Rps1b的大豆免疫识别的能力。这些数据支持病原体效应转录多态性与染色质表观遗传标记变化相关的模型，强调表观遗传变异是病原体适应可塑性的一种机制。
Abstract The relentless adaptability of pathogen populations is a major obstacle to effective disease control measures. Increasing evidence suggests that gene transcriptional polymorphisms are a strategy deployed by pathogens to evade host immunity. However, the underlying mechanisms of transcriptional plasticity remain largely elusive. Here we found that the soybean root rot pathogen Phytophthora sojae evades the soybean Resistance gene Rps1b through transcriptional polymorphisms in the effector gene Avr1b that occur in the absence of any sequence variation. Elevated levels of histone H3 Lysine27 tri-methylation (H3K27me3) were observed at the Avr1b locus in a naturally occurring Avr1b-silenced strain but not in an Avr1b-expressing strain, suggesting a correlation between this epigenetic modification and silencing of Avr1b. To genetically test this hypothesis, we edited the gene, PsSu(z)12, encoding a core subunit of the H3K27me3 methyltransferase complex by using CRISPR/Cas9, and obtained three deletion mutants. H3K27me3 depletion within the Avr1b genomic region correlated with impaired Avr1b gene silencing in these mutants. Importantly, these mutants lost the ability to evade immune recognition by soybeans carrying Rps1b. These data support a model in which pathogen effector transcriptional polymorphisms are associated with changes in chromatin epigenetic marks, highlighting epigenetic variation as a mechanism of pathogen adaptive plasticity.
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影响因子：
12.3
作者：
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影响因子：
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作者：
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影响因子：
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