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嗜麦芽窄食单胞菌BII-R7的多系统联合抗铀机制及生物修复潜力:转录组学与微观研究

Multisystem combined uranium resistance mechanisms and bioremediation potential of Stenotrophomonas bentonitica BII-R7: Transcriptomics and microscopic study.

作者信息

Pinel-Cabello M, Jroundi F, López-Fernández M, Geffers R, Jarek M, Jauregui R, Link A, Vílchez-Vargas R, Merroun M L

机构信息

Department of Microbiology, University of Granada, Campus Fuentenueva s/n, 18071, Granada, Spain.

Department of Microbiology, University of Granada, Campus Fuentenueva s/n, 18071, Granada, Spain.

出版信息

J Hazard Mater. 2021 Feb 5;403:123858. doi: 10.1016/j.jhazmat.2020.123858. Epub 2020 Sep 2.

Abstract

The potential use of microorganisms in the bioremediation of U pollution has been extensively described. However, a lack of knowledge on molecular resistance mechanisms has become a challenge for the use of these technologies. We reported on the transcriptomic and microscopic response of Stenotrophomonas bentonitica BII-R7 exposed to 100 and 250 μM of U. Results showed that exposure to 100 μM displayed up-regulation of 185 and 148 genes during the lag and exponential phases, respectively, whereas 143 and 194 were down-regulated, out of 3786 genes (>1.5-fold change). Exposure to 250 μM of U showed up-regulation of 68 genes and down-regulation of 290 during the lag phase. Genes involved in cell wall and membrane protein synthesis, efflux systems and phosphatases were up-regulated under all conditions tested. Microscopic observations evidenced the formation of U-phosphate minerals at membrane and extracellular levels. Thus, a biphasic process is likely to occur: the increased cell wall would promote the biosorption of U to the cell surface and its precipitation as U-phosphate minerals enhanced by phosphatases. Transport systems would prevent U accumulation in the cytoplasm. These findings contribute to an understanding of how microbes cope with U toxicity, thus allowing for the development of efficient bioremediation strategies.

摘要

微生物在铀污染生物修复中的潜在应用已被广泛描述。然而,对分子抗性机制的了解不足已成为这些技术应用的一个挑战。我们报道了嗜麦芽窄食单胞菌BII-R7在暴露于100和250μM铀时的转录组学和微观反应。结果表明,在延迟期和指数期,暴露于100μM铀分别导致185和148个基因上调,而在3786个基因中(变化倍数>1.5倍),143和194个基因下调。暴露于250μM铀在延迟期导致68个基因上调和290个基因下调。在所有测试条件下,参与细胞壁和膜蛋白合成、外排系统和磷酸酶的基因均上调。微观观察证明在膜和细胞外水平形成了铀磷酸盐矿物质。因此,可能会发生一个双相过程:细胞壁增加会促进铀在细胞表面的生物吸附,以及由磷酸酶增强的铀磷酸盐矿物质沉淀。转运系统会阻止铀在细胞质中积累。这些发现有助于理解微生物如何应对铀毒性,从而有助于开发高效的生物修复策略。

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