The toxic metalloid arsenic (As), is a major pollutant of soil and water, imposing severe health concerns on human lives. It enters the food chain mainly through As-contaminated crops. The uptake, translocation and accumulation of As in plant tissue are often controlled by certain soil-inhabiting microbial communities. Among them, indigenous, free-living As-resistant plant growth-promoting rhizobacteria (PGPR) plays a pivotal role in As-immobilization. Besides, the plant’s inability to withstand As after a threshold level is actively managed by these PGPR increasing As-tolerance in host plants by a synergistic plant-microbe interaction. The dual functionality of As-resistant PGPR i.e., phytostimulation and minimization of As-induced phytotoxic damages are one of the main focal points of this review article. It is known that such PGPR having the functional arsenic-resistant genes (in ars operon) including As-transporters, As-transforming genes contributed to the As accumulation and detoxification/transformation respectively. Apart from assisting in nutrient acquisition and modulating phytohormone levels, As-resistant PGPR also influences the antioxidative defense system in plants by maneuvering multiple enzymatic and non-enzymatic antioxidants. Furthermore, they are effective in reducing membrane damage and electrolyte leakage in plant cells. As-induced photosynthetic damage is also found to be salvaged by As-resistant PGPR. Briefly, the eco-physiological, biochemical and molecular mechanisms of As-resistant PGPR are thus elaborated here with regard to the As-exposed crops.

有毒的准金属砷 (As) 是土壤和水的主要污染物，对人类生活造成严重的健康问题。它主要通过受砷污染的作物进入食物链。植物组织中砷的吸收、易位和积累通常受某些土壤栖息微生物群落的控制。其中，本土的、自由生活的抗砷植物生长促进根际细菌 (PGPR) 在固定砷中起着关键作用。此外，植物在阈值水平后无法承受 As 是由这些 PGPR 通过协同植物-微生物相互作用增加宿主植物中的 As 耐受性来积极管理的。As 抗性 PGPR 的双重功能，即植物刺激和 As 引起的植物毒性损害的最小化是这篇评论文章的主要焦点之一。ars操纵子）包括 As 转运蛋白，As 转化基因分别有助于 As 积累和解毒/转化。除了协助营养获取和调节植物激素水平外，As 抗性 PGPR 还通过操纵多种酶促和非酶促抗氧化剂来影响植物的抗氧化防御系统。此外，它们可有效减少植物细胞中的膜损伤和电解质泄漏。还发现 As 抗性 PGPR 可以挽救 As 诱导的光合损伤。简而言之，本文就砷暴露的作物详细阐述了抗砷 PGPR 的生态生理、生化和分子机制。