Wang Pu, Zhao Lin, Hou Haoli, Zhang Hao, Huang Yan, Wang Yapei, Li Hui, Gao Fei, Yan Shihan, Li Lijia
State Key Laboratory of Hybrid Rice, College of Life Sciences, Wuhan University, Wuhan 430072, China.
State Key Laboratory of Hybrid Rice, College of Life Sciences, Wuhan University, Wuhan 430072, China
Plant Cell Physiol. 2015 May;56(5):965-76. doi: 10.1093/pcp/pcv023. Epub 2015 Feb 9.
Histone modification plays a crucial role in regulation of chromatin architecture and function, responding to adverse external stimuli. However, little is known about a possible relationship between epigenetic modification and programmed cell death (PCD) in response to environmental stress. Here, we found that heat stress induced PCD in maize seedling leaves which was characterized by chromatin DNA laddering and DNA strand breaks detected by a terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling (TUNEL) test. The activities of the reactive oxygen species (ROS)-related enzymes superoxide dismutase (SOD), peroxidase (POD) and catalase (CAT) were progressively increased over time in the heat-treated seedlings. However, the concentration of H2O2 remained at relatively lower levels, while the concentration of superoxide anion ([Formula: see text]) was increased, accompanied by the occurrence of higher ion leakage rates after heat treatment. The total acetylation levels of histones H3K9, H4K5 and H3 were significantly increased, whereas the di-methylation level of histone H3K4 was unchanged and the di-methylation level of histone H3K9 was decreased in the seedling leaves exposed to heat stress compared with the control seedlings, accompanied by increased nucleolus size indicative of chromatin decondensation. Furthermore, treatment of seedlings with trichostatin A (TSA), which always results in genomic histone hyperacetylation, caused an increase in the [Formula: see text] level within the cells. The results suggested that heat stress persistently induced [Formula: see text], leading to PCD in association with histone modification changes in the maize leaves.
组蛋白修饰在染色质结构和功能的调节中起着关键作用，以应对不利的外部刺激。然而，关于表观遗传修饰与响应环境胁迫的程序性细胞死亡（PCD）之间的可能关系，人们知之甚少。在这里，我们发现热胁迫诱导玉米幼苗叶片发生PCD，其特征是通过末端脱氧核苷酸转移酶介导的dUTP缺口末端标记（TUNEL）试验检测到染色质DNA梯状条带和DNA链断裂。在热处理的幼苗中，活性氧（ROS）相关酶超氧化物歧化酶（SOD）、过氧化物酶（POD）和过氧化氢酶（CAT）的活性随时间逐渐增加。然而，H2O2的浓度保持在相对较低的水平，而过氧阴离子（[公式：见正文]）的浓度增加，同时热处理后离子渗漏率升高。与对照幼苗相比，热胁迫下幼苗叶片中组蛋白H3K9、H4K5和H3的总乙酰化水平显著增加，而组蛋白H3K4的二甲基化水平不变，组蛋白H3K9的二甲基化水平降低，同时核仁大小增加，表明染色质解聚。此外，用曲古抑菌素A（TSA）处理幼苗，TSA总是导致基因组组蛋白高度乙酰化，导致细胞内[公式：见正文]水平升高。结果表明，热胁迫持续诱导[公式：见正文]，导致玉米叶片中与组蛋白修饰变化相关的PCD。
