细胞外ATP参与调节抗霉素A诱导的植物细胞死亡  

Extracellular ATP is involved in the regulation of antimycin A-induced plant cell death

作　　者：王建荷 王娟娟[1] 庞海龙[1] 贾凌云[1] 孙坤[1] 张继[1,2] 冯汉青[1] WANG Jianhe;WANG Juanjuan;PANG Hailong;JIA Lingyun;SUN Kun;ZHANG Ji;FENG Hanqing(College of Life Sciences,Northwest Normal University,Lanzhou 730070,China;New Rural Development Research Institute,Northwest Normal University,Lanzhou 730070,China)

机构地区：[1]西北师范大学生命科学学院,兰州730070 [2]西北师范大学新农村发展研究院,兰州730070

出　　处：《植物生理学报》2021年第4期838-846,共9页Plant Physiology Journal

基　　金：国家自然科学基金(31870246和31560070);甘肃省重点研发计划(18YF1NA051);甘肃省引导科技创新发展专项资金(2019ZX-05);甘肃省高等学校科研项目(2015A-007);甘肃省高校基本科研业务费;西北师范大学青年创新团队项目。

摘　　要：选用烟草悬浮细胞(Nicotiana tabacum ‘Bright Yellow-2’)为试验材料,研究细胞外ATP (extracellular ATP, eATP)对抗霉素A (antimycin A, AA)所诱导的细胞死亡的影响及可能的调节机制。结果表明, AA可引起细胞死亡和细胞活性氧(reactive oxygen species, ROS)水平的上升,外源施加ROS清除剂DMTU(N,N′-dimethylthiourea)可缓解AA诱导的细胞死亡水平的上升。另外, AA导致细胞eATP水平的下降;而用外源ATP缓解AA诱导的e ATP下降的同时, AA诱导的细胞死亡和ROS水平的上升也被缓解。进一步试验发现, Ca^(2+)对AA诱导的细胞死亡和ROS水平的影响与eATP的行为相似,且AA处理下的Ca^(2+)水平受到了eATP的调控;更为重要的是,质膜Ca^(2+)通道抑制剂或Ca^(2+)螯合剂均可消除eATP对AA诱导的细胞死亡上升的缓解作用。上述观察表明, eATP能够调节AA诱导的细胞死亡,这种作用很可能联系着eATP对ROS的影响且依赖于Ca^(2+)作为其下游信号。Tobacco suspension cells(Nicotiana tabacum ‘Bright Yellow-2’) were used as experimental materials to study the effects and possible adjustment mechanisms of extracellular ATP(eATP) on cell death induced by antimycin A(AA). The results showed that AA could cause an increase in cell death and reactive oxygen species(ROS) levels, and the application of ROS scavenger DMTU(N,N′-dimethylthiourea) could effectively alleviate the increase of AA-induced cell death. In addition, AA induced a decrease in cell e ATP levels. Exogenous ATP was used to alleviate AA-induced eATP decrease, meanwhile AA-induced cell death and increase in ROS levels were also alleviated. Further experiments found that the effect of Ca^(2+) on AA-induced cell death and ROS levels was similar to the behavior of eATP, and eATP could regulate the Ca^(2+) levels under AA treatment. More importantly, plasma membrane Ca^(2+) channel inhibitor or Ca^(2+) chelator could eliminate the alleviating effect of eATP on the increase in cell death induced by AA. The above observations indicate that eATP can regulate AA-induced cell death, and this regulation is probably related to the effect of eATP on ROS and depends on Ca^(2+) as its downstream signal.

关 键 词：细胞外ATP 抗霉素A 细胞死亡 ROS CA^(2+) 

分 类 号：Q942[生物学—植物学]