Regulation of enteric endophytic bacterial colonization by plant defenses

Regulation of enteric endophytic bacterial colonization by plant defenses
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DOI:
10.1094/mpmi-18-0169
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发表时间:
2005-02-01
影响因子:
3.5
通讯作者:
Triplett, EW
Triplett, EW
中科院分区:
生物学2区
文献类型:
--
作者:
Iniguez, AL;Dong, YM;Triplett, EW

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细菌内生菌居住在植物内部,不会引起疾病或形成共生结构。一些内生菌,如肺炎克雷伯菌342 (Kp342),促进植物生长和营养。其他的,如肠沙门氏菌血清型鼠伤寒沙门氏菌(S. Typhimurium),是污染生农产品的人类病原体。这里提出了几条证据来支持植物防御反应途径调节内生细菌定植的假设。与亲本基因型相比,一个乙烯不敏感突变体被Kp342超定植。乙烯是诱导植物系统性抗性的信号分子,加入乙烯可以降低紫花苜蓿的内生定殖,这种乙烯介导的内生定殖抑制被加入乙烯作用抑制剂1-甲基环丙烯逆转。鼠伤寒沙门氏菌对紫花苜蓿的定殖也受到外源乙烯的影响。缺乏鞭毛或沙门氏菌致病性岛1 (TTSS-SPI1) III型分泌系统成分的突变体在紫花苜蓿体内的定植数量高于野生型。拟南芥防御反应相关基因型表明,只有水杨酸(SA)独立的防御反应有助于限制Kp342的定植。相比之下,鼠伤寒沙门氏菌的定植受到sa依赖性和非依赖性反应的影响。鼠伤寒沙门氏菌突变体进一步描述了这些反应,表明鞭毛和TTSS-SPI1效应物都可以被识别。鞭毛的作用主要是通过与SA无关的反应(在没有鞭毛的情况下,SA的积累仍会影响定植)。无论基因型在sa依赖性或sa非依赖性应答中是否受到影响,去除TTSS-SPI1效应都会导致过定植。与这些结果一致的是,鼠伤寒沙门氏菌激活了sa依赖性致病相关基因PR1的启动子,而缺乏TTSS-SPI1的鼠伤寒沙门氏菌突变体未能激活该启动子。这些观察结果为减少人类肠道病原体对生农产品的污染和增加植物中促进生长的细菌的数量提供了方法。
Bacterial endophytes reside within the interior of plants without causing disease or forming symbiotic structures. Some endophytes, such as Klebsiella pneumoniae 342 (Kp342), enhance plant growth and nutrition. Others, such as Salmonella enterica serovar Typhimurium (S. typhimurium), are human pathogens that contaminate raw produce. Several lines of evidence are presented here to support the hypothesis that plant defense response pathways regulate colonization by endophytic bacteria. An ethylene-insensitive mutant of Medicago truncatula is hypercolonized by Kp342 compared to the parent genotype. Addition of ethylene, a signal molecule for induced systemic resistance in plants, decreased endophytic colonization in Medicago spp. This ethylene-mediated inhibition of endophytic colonization was reversed by addition of the ethylene action inhibitor, 1-methylcyclopropene. Colonization of Medicago spp. by S. typhimurium also was affected by exogenous ethylene. Mutants lacking flagella or a component of the type III secretion system of Salmonella pathogenicity island 1 (TTSS-SPI1) colonize the interior of Medicago spp. in higher numbers than the wild type. Arabidopsis defense response-related genotypes indicated that only salicylic acid (SA)-independent defense responses contribute to restricting colonization by Kp342. In contrast, colonization by S. typhimurium is affected by both SA-dependent and -independent responses. S. typhimurium mutants further delineated these responses, suggesting that both flagella and TTSS-SPI1 effectors can be recognized. Flagella act primarily through SA-independent responses (compromising SA accumulation still affected colonization in the absence of flagella). Removal of a TTSS-SPI1 effector resulted in hypercolonization regardless of whether the genotype was affected in either SA-dependent or SA-independent responses. Consistent with these results, S. typhimurium activates the promoter of PR1, a SA-dependent pathogenesis-related gene, while S. typhimurium mutants lacking the TTSS-SPI1 failed to activate this promoter. These observations suggest approaches to reduce contamination of raw produce by human enteric pathogens and to increase the number of growth-promoting bacteria in plants.