Characterization of a JAZ7 activation-tagged Arabidopsis mutant with increased susceptibility to the fungal pathogen Fusarium oxysporum.
Characterization of a JAZ7 activation-tagged Arabidopsis mutant with increased susceptibility to the fungal pathogen Fusarium oxysporum.
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DOI：
10.1093/jxb/erw040
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发表时间：
2016-04
影响因子：
6.9
通讯作者：
Kazan K
中科院分区：
文献类型：
--
作者：
Thatcher LF;Cevik V;Grant M;Zhai B;Jones JD;Manners JM;Kazan K
JAZ 7 T-DNA激活突变体赋予增加的JA敏感性、上调的防御和JA介导的基因表达，以及增加的对破坏宿主JA应答的两种病原体（尖孢镰刀菌和Pst DC 3000）的易感性。在拟南芥中，茉莉酸（JA）信号在介导尖孢镰刀菌病害的结果中起着关键作用。然而，JASMONATE ZIM结构域（JAZ）蛋白抑制JA信号传导的作用尚未在宿主对该病原体的抗性或易感性中表征。在这里，我们发现大多数JAZ基因是在F.尖孢菌的挑战，并筛选拟南芥JAZ家族成员中的T-DNA插入系，鉴定了高度疾病易感的JAZ 7突变体（jaz 7 -1D）。该突变体表现出组成型JAZ 7表达，并赋予增加的JA敏感性，表明激活的JA信号。与jaz 7功能丧失等位基因不同，jaz 7 -1D还具有增强的JA响应基因表达，改变了发育，并增加了对细菌病原体Pst DC 3000的易感性，该病原体也破坏了宿主的JA响应。我们还证明，JAZ 7与转录因子相互作用，作为激活剂（MYC 3，MYC 4）或抑制剂（JAM 1）的JA信号转导，并包含一个功能性的转录抑制基序介导转录抑制通过辅抑制因子TOPLESS（TPL）。我们建议通过直接TPL招募，在野生型植物JAZ 7功能作为一个阻遏物内的JA反应网络，在jaz 7 -1D植物，失调异位JAZ 7表达超激活JA信号的一部分，通过干扰微调COI 1-JAZ-TPL-TF复合物。
A JAZ7 T-DNA activation mutant confers increased JA-sensitivity, up-regulated defense and JA-mediated gene expression, and increased susceptibility to two pathogens that disrupt host JA-responses, Fusarium oxysporum and Pst DC3000. In Arabidopsis, jasmonate (JA)-signaling plays a key role in mediating Fusarium oxysporum disease outcome. However, the roles of JASMONATE ZIM-domain (JAZ) proteins that repress JA-signaling have not been characterized in host resistance or susceptibility to this pathogen. Here, we found most JAZ genes are induced following F. oxysporum challenge, and screening T-DNA insertion lines in Arabidopsis JAZ family members identified a highly disease-susceptible JAZ7 mutant (jaz7-1D). This mutant exhibited constitutive JAZ7 expression and conferred increased JA-sensitivity, suggesting activation of JA-signaling. Unlike jaz7 loss-of-function alleles, jaz7-1D also had enhanced JA-responsive gene expression, altered development and increased susceptibility to the bacterial pathogen Pst DC3000 that also disrupts host JA-responses. We also demonstrate that JAZ7 interacts with transcription factors functioning as activators (MYC3, MYC4) or repressors (JAM1) of JA-signaling and contains a functional EAR repressor motif mediating transcriptional repression via the co-repressor TOPLESS (TPL). We propose through direct TPL recruitment, in wild-type plants JAZ7 functions as a repressor within the JA-response network and that in jaz7-1D plants, misregulated ectopic JAZ7 expression hyper-activates JA-signaling in part by disturbing finely-tuned COI1-JAZ-TPL-TF complexes.