Arabidopsis thaliana serpins AtSRP4 and AtSRP5 negatively regulate stress-induced cell death and effector-triggered immunity induced by bacterial effector AvrRpt2
Arabidopsis thaliana serpins AtSRP4 and AtSRP5 negatively regulate stress-induced cell death and effector-triggered immunity induced by bacterial effector AvrRpt2
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DOI：
10.1111/ppl.12516
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发表时间：
2017-03-01
影响因子：
6.4
通讯作者：
Nandi, Ashis Kumar
中科院分区：
文献类型：
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作者：
Bhattacharjee, Lipika;Singh, Deepjyoti;Nandi, Ashis Kumar
蛋白酶抑制剂及其同源蛋白酶调节生长、发育和防御。丝氨酸蛋白酶抑制剂（Serine protease inhibitors，serpins）是一个广泛存在于后生动物和植物中的基因家族。果蝇NECROTIC（NEC）基因及其同源基因是一种丝氨酸蛋白酶抑制剂，参与调节细胞死亡途径中的蛋白酶。虽然拟南芥基因组中含有几个丝氨酸蛋白酶抑制剂同源物，生物学功能是未知的，其中大部分。在这里，我们发现两个拟南芥丝氨酸蛋白酶抑制剂，AtSRP 4和AtSRP 5，是最接近的序列同源的果蝇NEC蛋白，并参与胁迫诱导的细胞死亡和防御。AtSRP 4和AtSRP 5基因在紫外线（UV）处理和接种无毒病原体后诱导的表达。AtSRP 4和AtSRP 5的敲除突变体和amiRNA系夸大了UV和过敏反应（HR）诱导的细胞死亡。AtSRP 4的过表达减少UV和HR诱导的细胞死亡。AtSRP 4和AtSRP 5的突变体抑制而AtSRP 4的过表达支持细菌病原体假单胞菌的生长。番茄DC 3000携带AvrRpt 2效应子，但不携带其它无毒或有毒病原体。结果共同确定AtSRP 4和AtSRP 5作为应激诱导的细胞死亡和AvrRpt 2触发的免疫的负调节剂;然而，AtSRP 4的影响比AtSRP 5更突出。
Protease inhibitors and their cognate proteases regulate growth, development and defense. Serine protease inhibitors (serpins) constitute a large family of genes in most metazoans and plants. Drosophila NECROTIC (NEC) gene and its homologues in the mammalian system are well-characterized serpins, which play a role in regulating proteases that participate in cell death pathways. Although the Arabidopsis genome contains several serpin homologs, biological function is not known for most of them. Here we show that two Arabidopsis serpins, AtSRP4 and AtSRP5, are closest sequence homologue of DrosophilaNEC protein, and are involved in stress-induced cell death and defense. Expression of both AtSRP4 and AtSRP5 genes induced upon ultra-violet (UV)-treatment and inoculation with avirulent pathogens. The knockout mutants and amiRNA lines of AtSRP4 and AtSRP5 exaggerated UV- and hypersensitive response (HR)-induced cell death. Over-expression of AtSRP4 reduced UV- and HR-induced cell death. Mutants of AtSRP4 and AtSRP5 suppressed whereas over-expression of AtSRP4 supported the growth of bacterial pathogen Pseudomonas syringae pv. tomatoDC3000 carrying the AvrRpt2 effector, but not other avirulent or virulent pathogens. Results altogether identified AtSRP4 and AtSRP5 as negative regulators of stress-induced cell death and AvrRpt2-triggered immunity; however, the influence of AtSRP4 was more prominent than AtSRP5.