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自促使细胞死亡诱导过氧化在Physcomitrium patens中的细胞死亡
Md Arif Sakil1,2, Kyosuke Mukae1,3, Junyu Bao1
1Graduate School of Science and Engineering, Saitama University, Saitama, 338-8570 Japan.
Plant & cell physiology
|November 29, 2023
概括
Physcomitrium patens的自缺陷突变体显示出对过氧化 (H2O2) 压力的增强生存能力. 自促进H2O2诱导的细胞死亡,通过提供产生反应性氧物种 (ROS) 的氨基酸.
科学领域:
- 植物生物学 植物生物学
- 细胞应激反应的应激反应
- 自学研究 自学研究
背景情况:
- 自是一种细胞回收过程.
- 干燥应激可以诱导反应性氧物种 (ROS).
- 在Physcomitrium patens中的自缺陷突变 (atg5, atg7) 显示出显著的干燥耐受性.
研究的目的:
- 为了研究氧化 (H2O2) 诱导的细胞死亡中自的作用在Physcomitrium patens.
- 确定自,ROS生成和在H2O2压力下细胞活力之间的关系.
主要方法:
- 野生类型 (WT) 和自缺陷 (atg5, atg7) P. 病原体的治疗用H2O2.2.
- 测量细胞内H2O2水平.
- 细胞死亡和真空球完整性的评估.
- 使用ROS清除剂 (N-乙半氨酸) 和电子运输链 (ETC) 分离器 (碳酸化物m-chlorophenylhydrazone).
- 抑制自 (3-甲基氨酸) 和补充氨基酸来源 (牛血清白蛋白).
主要成果:
- 自缺陷突变体在H2O2治疗中幸存下来,这种治疗对WT是致命的.
- 与突变细胞相比,WT细胞表现出更高的细胞内H2O2平原水平和细胞死亡.
- ROS清理剂和ETC解剂降低了WT中的H2O2水平和细胞死亡.
- 自抑制降低了WT中的H2O2平原和细胞死亡.
- 用氨基酸补充剂 (通过BSA) 在突变者中增加了H2O2平原.
结论:
- 自活跃地促进P. patens中H2O2诱导的细胞死亡.
- 自衍生的氨基酸通过线粒体/质体ETCs被分解,产生导致细胞死亡的ROS.
- 空腔体崩是H2O2诱导的细胞死亡的特征,由自介导.
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