Iniguez A Leonardo, Dong Yuemei, Carter Heather D, Ahmer Brian M M, Stone Julie M, Triplett Eric W
University of Wisconsin-Madison, Department of Agronomy, Madison 53706, USA.
Mol Plant Microbe Interact. 2005 Feb;18(2):169-78. doi: 10.1094/MPMI-18-0169.
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.
细菌内生菌存在于植物内部，不会引发疾病或形成共生结构。一些内生菌，如肺炎克雷伯菌342（Kp342），可促进植物生长和营养吸收。其他内生菌，如鼠伤寒沙门氏菌（S. typhimurium），则是污染生鲜农产品的人类病原体。本文提供了多条证据来支持植物防御反应途径调控内生细菌定殖这一假说。与亲本基因型相比，蒺藜苜蓿的乙烯不敏感突变体被Kp342过度定殖。乙烯是植物诱导系统抗性的信号分子，添加乙烯会减少苜蓿属植物中的内生菌定殖。添加乙烯作用抑制剂1-甲基环丙烯可逆转这种乙烯介导的内生菌定殖抑制作用。鼠伤寒沙门氏菌对苜蓿属植物的定殖也受到外源乙烯的影响。缺乏鞭毛或鼠伤寒沙门氏菌致病岛1（TTSS-SPI1）III型分泌系统组分的突变体在苜蓿属植物内部的定殖数量高于野生型。拟南芥防御反应相关基因型表明，只有不依赖水杨酸（SA）的防御反应有助于限制Kp342的定殖。相比之下，鼠伤寒沙门氏菌的定殖受到依赖SA和不依赖SA反应的影响。鼠伤寒沙门氏菌突变体进一步明确了这些反应，表明鞭毛和TTSS-SPI1效应器均可被识别。鞭毛主要通过不依赖SA的反应起作用（在没有鞭毛的情况下，SA积累受损仍会影响定殖）。无论基因型在依赖SA或不依赖SA的反应中是否受到影响，去除TTSS-SPI1效应器都会导致过度定殖。与这些结果一致，鼠伤寒沙门氏菌激活了PR1（一个依赖SA的病程相关基因）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。这些观察结果提示了减少人类肠道病原体对生鲜农产品污染以及增加植物中促生长细菌数量的方法。
