细胞外ATP参与调节抗霉素A诱导的植物细胞死亡

王建荷1,王娟娟1,庞海龙1,贾凌云1,孙坤1,张继1,2,冯汉青1,*
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

通信作者:冯汉青;E-mail: fenghanq@nwnu.edu.cn

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eATP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, Ca2+AA诱导的细胞死亡和ROS水平的影响与eATP的行为相似, AA处理下的Ca2+水平受到了eATP的调控; 更为重要的是, 质膜Ca2+通道抑制剂或Ca2+螯合剂均可消除eATPAA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eATPROS的影响且依赖于Ca2+作为其下游信号。

关键词:细胞外ATP; 抗霉素A; 细胞死亡; ROS; Ca2+

收稿:2021-01-22   修定:2021-03-04

资助: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和西北师范大学青年创新团队项目。

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

WANG Jianhe1, WANG Juanjuan1, PANG Hailong1, JIA Lingyun1, SUN Kun1, ZHANG Ji11,2, FENG Hanqing1,*
1College of Life Sciences, Northwest Normal University, Lanzhou 730070, China; 2New Rural Development Research Institute, Northwest Normal University, Lanzhou 730070, China

Corresponding author: FENG Hanqing; E-mail: fenghanq@nwnu.edu.cn

Abstract:

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 eATP 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 Ca2+ levels under AA treatment. More importantly, plasma membrane Ca2+ channel inhibitor or Ca2+ 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 Ca2+ as its downstream signal.

Key words: extracellular ATP; antimycin A; cell death; ROS; Ca2+

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