叶片衰老伴随黄化和Rubisco降解而过早发生,以应对各种胁迫。然而,应激感知和衰老反应之间的信号通路尚未完全理解,尽管以前的研究表明参与活性氧(ROS)。在使用野生型(WT)和自噬缺陷型atg5菌株研究Physcomitriumpatens中自噬的生理功能时,我们发现Physcomitrium菌落在黑暗或氮缺乏的条件下过早地衰老,ATG5比WT更早。在本研究中,我们测量了细胞H2O2,并检查了H2O2是否介导了Physcomitrium菌落的过早衰老。甲基紫精,ROS发生器,细胞H2O2水平升高并引起衰老样症状。在黑暗或氮缺乏条件下,WT和atg5中的H2O2水平也升高至相同的平台水平。ROS清除剂N-乙酰半胱氨酸和ROS源抑制剂羰基氰化物间氯苯腙抑制H2O2水平的增加以及衰老。转移到贫氮培养基后,ATG5中的H2O2水平比WT中的升高更早约18h,而atg5在2天之前变黄。我们得出的结论是,在黑暗或氮缺乏条件下,H2O2水平的升高可介导Physcomitrium的过早衰老,但不能解释WT和atg5细胞的不同衰老反应。
Leaf senescence accompanied by yellowing and Rubisco degradation occurs prematurely in response to various stresses. However, signaling pathways between stress perception and senescence responses are not understood fully, although previous studies suggest the involvement of reactive oxygen species (ROS). While investigating the physiological functions of autophagy in
Physcomitrium patens using wild-type (WT) and autophagy-deficient atg5 strains, we found that
Physcomitrium colonies senesce prematurely under dark or nitrogen-deficient conditions, with atg5 senescing earlier than WT. In the present study, we measured cellular H2O2, and examined whether H2O2 mediates premature senescence in
Physcomitrium colonies. Methyl viologen, an ROS generator, increased cellular H2O2 levels and caused senescence-like symptoms. H2O2 levels were also elevated to the same plateau levels in WT and atg5 under dark or nitrogen-deficient conditions. The ROS scavenger N-acetylcysteine and the ROS source inhibitor carbonyl cyanide m-chlorophenylhydrazone inhibited the increase in H2O2 levels as well as senescence. Upon transfer to a nitrogen-deficient medium, H2O2 levels increased earlier in atg5 than in WT by ~18 h, whereas atg5 yellowed earlier by >2 days. We conclude that the increased H2O2 levels under dark or nitrogen-deficient conditions mediate premature senescence in
Physcomitrium but do not explain the different senescence responses of WT and atg5 cells.