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揭示srbA小RNA通过调控铜绿假单胞菌中的algU、mucA、rhlA和rsmA在生物膜形成中的作用。

Unveiling the role of srbA sRNA in biofilm formation by regulating algU, mucA, rhlA, and rsmA in Pseudomonas aeruginosa.

作者信息

Saha Piyali, Mukherjee Samir Kumar, Hossain Sk Tofajjen

机构信息

Department of Microbiology, University of Kalyani, Kalyani 741235, India.

出版信息

Biochem J. 2025 May 7;482(11):621-37. doi: 10.1042/BCJ20240650.

DOI:10.1042/BCJ20240650
PMID:40331940
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC12203948/
Abstract

The survival and increasing antimicrobial resistance of various bacteria, including clinically relevant opportunistic pathogen, Pseudomonas aeruginosa, largely depends on their biofilm architectural strength, that makes a challenge to eradicate it. Small RNAs (sRNAs) have been identified as the key modulators in regulating the expression and function of different transcriptional regulators, and the components of regulatory networks involved in bacterial biofilm formation. This study was focused to identify the regulatory role of the srbA sRNA in controlling biofilm formation in P. aeruginosa. srbA was found to be upregulated in both substratum-attached and colony biofilms compared to planktonic growth conditions. Further analysis revealed that srbA overexpressing strain produced more biofilm, whereas a significant reduction in biofilm formation was noted due to srbA deletion. Interestingly, it was also predicted from the study that srbA might regulate the expression of AlgU/MucA, the sigma and anti-sigma factor, involved in biofilm developmental network. Additionally, srbA showed possible interference on the expression of two other important biofilm regulatory genes, rhlA and rsmA. Overall, this research highlights the critical role of srbA sRNA as a central regulator of biofilm formation, and possibly the pathogenicity of P. aeruginosa. These findings might offer potential avenues for developing targeted therapeutic strategies to mitigate biofilm-related infections caused by P. aeruginosa.

摘要

包括临床相关的机会致病菌铜绿假单胞菌在内的各种细菌的存活及不断增加的抗微生物耐药性,很大程度上取决于它们生物膜的结构强度,这使得根除生物膜具有挑战性。小RNA(sRNA)已被确定为调节不同转录调节因子的表达和功能以及参与细菌生物膜形成的调控网络组成部分的关键调节因子。本研究的重点是确定srbA sRNA在控制铜绿假单胞菌生物膜形成中的调节作用。与浮游生长条件相比,发现srbA在附着于基质的生物膜和菌落生物膜中均上调。进一步分析表明,过表达srbA的菌株产生更多生物膜,而由于srbA缺失,生物膜形成显著减少。有趣地是,该研究还预测srbA可能调节参与生物膜发育网络的σ因子和抗σ因子AlgU/MucA的表达。此外,srbA对另外两个重要的生物膜调节基因rhlA和rsmA的表达显示出可能的干扰。总体而言,本研究突出了srbA sRNA作为生物膜形成的核心调节因子以及可能作为铜绿假单胞菌致病性调节因子的关键作用。这些发现可能为开发有针对性的治疗策略以减轻由铜绿假单胞菌引起的生物膜相关感染提供潜在途径。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a0c4/12203948/7daeef191f2c/BCJ-482-11-BCJ20240650-g009.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a0c4/12203948/889c7d950c11/BCJ-482-11-BCJ20240650-g001.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a0c4/12203948/66a8cbb00e4d/BCJ-482-11-BCJ20240650-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a0c4/12203948/d2e3eeac3fa4/BCJ-482-11-BCJ20240650-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a0c4/12203948/1322d4c06834/BCJ-482-11-BCJ20240650-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a0c4/12203948/6efc0fa8d771/BCJ-482-11-BCJ20240650-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a0c4/12203948/a51a1423dbcb/BCJ-482-11-BCJ20240650-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a0c4/12203948/e64cc58b8a72/BCJ-482-11-BCJ20240650-g008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a0c4/12203948/7daeef191f2c/BCJ-482-11-BCJ20240650-g009.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a0c4/12203948/889c7d950c11/BCJ-482-11-BCJ20240650-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a0c4/12203948/3a2cc05cd28c/BCJ-482-11-BCJ20240650-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a0c4/12203948/66a8cbb00e4d/BCJ-482-11-BCJ20240650-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a0c4/12203948/d2e3eeac3fa4/BCJ-482-11-BCJ20240650-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a0c4/12203948/1322d4c06834/BCJ-482-11-BCJ20240650-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a0c4/12203948/6efc0fa8d771/BCJ-482-11-BCJ20240650-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a0c4/12203948/a51a1423dbcb/BCJ-482-11-BCJ20240650-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a0c4/12203948/e64cc58b8a72/BCJ-482-11-BCJ20240650-g008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a0c4/12203948/7daeef191f2c/BCJ-482-11-BCJ20240650-g009.jpg

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