Over-expression of Arabidopsis Bax inhibitor-1 delays methyl jasmonate-induced leaf senescence by suppressing the activation of MAP kinase 6

被引:36
作者
Yue, Haiyun
Nie, Shengjun
Xing, Da [1 ]
机构
[1] S China Normal Univ, MOE Key Lab Laser Life Sci, Guangzhou 510631, Guangdong, Peoples R China
基金
国家高技术研究发展计划(863计划);
关键词
Arabidopsis; Bax inhibitor-1; calcium; methyl jasmonate; mitogen-activated protein kinase 6; senescence; PROGRAMMED CELL-DEATH; PROTEIN-KINASE; SIGNAL-TRANSDUCTION; HYDROGEN-PEROXIDE; PLANT DEFENSE; MOLECULAR ANALYSIS; NITRIC-OXIDE; CALCIUM; ACID; CA2+;
D O I
10.1093/jxb/ers122
中图分类号
Q94 [植物学];
学科分类号
071001 ;
摘要
Methyl jasmonate (MeJA) is an important signalling molecule that has been reported to be able to promote plant senescence. The cell death suppressor Bax inhibitor-1 (BI1) has been found to suppress stress factor-mediated cell death in yeast and Arabidopsis. However, the effect and the genetic mechanism of Arabidopsis thaliana BI1 (AtBI1) on leaf senescence remain unclear. It was found here that the AtBI1 mutant, atbi1-2 (a gene knock-out), showed accelerated progression of MeJA-induced leaf senescence, while the AtBI1 complementation lines displayed similar symptoms as the WT during the senescence process. In addition, over-expression of the AtBI1 gene delayed the onset of MeJA-induced leaf senescence. Further analyses showed that during the process of MeJA-induced senescence, the activity of MPK6, a mitogen-activated protein kinase (MAPK), increased in WT plants, whereas it was significantly suppressed in AtBI1-overexpressing plants. Under the MeJA treatment, cytosolic calcium ([Ca2+](cyt)) functioned upstream of MPK6 activation and the elevation of [Ca2+](cyt) was reduced in AtBI1-overexpressing leaves. These results suggested a role of AtBI1 over-expression in delaying MeJA-induced leaf senescence by suppressing the [Ca2+](cyt)-dependent activation of MPK6, thus providing a new insight into the function and mechanism of AtBI1 in plant senescence.
引用
收藏
页码:4463 / 4474
页数:12
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