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作 者:支添添[1,2] 周舟 韩成云[1,2] 任春梅 Tiantian Zhi;Zhou Zhou;Chengyun Han;Chunmei Ren(College of Bioscience and Biotechnology,Hunan Agricultural University,Changsha 410128,China;Yichun University,Yichun 336000,China)
机构地区:[1]湖南农业大学生物科学技术学院,长沙410128 [2]宜春学院,宜春336000
出 处:《植物学报》2022年第3期288-298,共11页Chinese Bulletin of Botany
基 金:国家自然科学基金(No.31760301);江西省教育厅科技项目(No.GJJ190872)。
摘 要:程序性细胞死亡(PCD)对于植物生长发育和防御反应均极为重要。拟南芥(Arabidopsisthaliana)酪氨酸降解途径延胡索酰乙酰乙酸水解酶(FAH)缺失突变体sscd1(short-day sensitive cell death 1)在短日照下(8小时光照/16小时黑暗)发生PCD。前期研究发现,sscd1突变体的PCD与茉莉素(JAs)信号转导有关,而与水杨酸(SA)信号转导无关。PAD4(Phytoalexin deficient4)参与SA和JAs信号转导之间的相互拮抗。该研究发现sscd1突变体PCD伴随着PAD4表达上调;而PAD4突变导致sscd1突变体PCD加速,同时上调JAs信号转导途径下游响应基因vegetative storage protein 2、thionin2.1和defensin1.2的表达;sscd1/pad4/coil三突变体中JAs信号转导受阻导致PCD加速现象消失。PAD4突变上调sscd1突变体酪氨酸降解基因homogentisate dioxygenase和maleylacetoacetate isomerase以及单线态氧特异性诱导基因bonzai1-associated protein 1和a putative c2h2 zinc finger transcription factor的表达,并且上调均依赖JAs信号转导受体COI1。综上所述,PAD4突变通过增强JAs信号转导加速酪氨酸降解,增加单线态氧的积累,从而促进sscd1突变体的PCD。Programmed cell death(PCD)is extremely important for plant growth and defense.Fumarylacetoacetate hydrolase(FAH)deficient mutant short-day sensitive cell death 1(sscd1)displayed PCD under short day condition(8 h light/16 h darkness).Our previous study found PCD in sscd1 was related to jasmonates(JAs)signal transduction but not to salicylic acid(SA).Phytoalexin deficient 4(PAD4)is involved in mutual antagonism between SA and JAs signaling.In this study,PCD was accompanied by up-regulation of PAD4;while mutation of PAD4 accelerated the sscd1 PCD and induced JAs signaling pathway downstream response genes vegetative storage protein 2、thionin2.1 and defensin1.2.In triple mutant sscd1/pad4/coil,JAs signal transduction was blocked,resulting in the disappearance of PCD acceleration.PAD4 mutation induce the expression of Tyr degradation gene homogentisate dioxygenase and maleylacetoacetate isomerase,singlet oxygen specific induced genes bonzai1-associated protein 1 and a putative c2h2 zinc finger transcription factor in sscd1,the induction is dependent on JAs signaling receptor COI1.In conclusion,PAD4 mutation increase JAs signaling,then accelerate tyrosine degradation and singlet oxygen accumulation,thereby promoting PCD in the sscd1 mutant.
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