Functional analysis of epigenetic regulation in Drosophilaintestinal homeostasis

为了确定调节肠道免疫或体内平衡的新的、进化保守的表观遗传机制，我们利用果蝇模型系统探索了参与肠道病理的染色质修饰剂。我们发现，在肠干细胞(ISC)/肠母细胞（EB）中强制去除组蛋白H3 lysine36甲基化（H3K36me）可增加对铜绿假单胞菌感染的抵抗力。然而，进一步的分析表明，ISC/EB中强迫H3K36me去甲基化导致氧化应激反应基因过度激活，缩短寿命。这些结果表明，H3K36me可能有助于果蝇肠道应激反应的适当调节和/或维持稳态。

To identify novel, evolutionally conserved epigenetic mechanisms that regulate gut immunity or homeostasis, we explored chromatin modifiers involved in intestinal pathology using the Drosophila model system. We found that forced removal of histone H3 lysine36 methylation (H3K36me) in intestinal stem cell (ISC)/enteroblast (EB) increases the resistance to Pseudomonas aeruginosa infection. However, further analyses indicated that the forced H3K36me demethylation in ISC/EB causes over-activation of oxidative stress response genes and shortens lifespan. These results suggest that H3K36me might contribute to appropriate regulation of stress responses and/or the maintenance of homeostasis in Drosophila intestine.