An ArcA-Modulated Small RNA in Pathogenic Escherichia coli K1

Frontiers in Microbiology

Yangyang Zheng¹  Yajun Song¹  Hao Sun¹  Lu Feng¹  Yu Fan⁴  Fang Chen⁴  Peng Liu⁴  Changhong Zhou⁴  Xuehua Wan⁴ 

[1] College of Life Sciences, Nankai University, Tianjin, China;TEDA Institute of Biological Sciences and Biotechnology, Nankai University, Tianjin, China;The Key Laboratory of Molecular Microbiology and Technology, Ministry of Education, Nankai University, Tianjin, China;Tianjin Key Laboratory of Microbial Functional Genomics, Tianjin, China;

关键词: Escherichia coli K1;    meningitis;    ArcA;    small RNA;    oxygen;   

DOI  :  10.3389/fmicb.2020.574833

来源: DOAJ

【 摘 要 】

Escherichia coli K1 is the leading cause of meningitis in newborns. Understanding the molecular basis of E. coli K1 pathogenicity will help develop treatment of meningitis and prevent neurological sequelae. E. coli K1 replicates in host blood and forms a high level of bacteremia to cause meningitis in human. However, the mechanisms that E. coli K1 employs to sense niche signals for survival in host blood are poorly understood. We identified one intergenic region in E. coli K1 genome that encodes a novel small RNA, sRNA-17. The expression of sRNA-17 was downregulated by ArcA in microaerophilic blood. The ΔsRNA-17 strain grew better in blood than did the wild-type strain and enhanced invasion frequency in human brain microvascular endothelial cells. Transcriptome analyses revealed that sRNA-17 regulates tens of differentially expressed genes. These data indicate that ArcA downregulates the sRNA-17 expression to benefit bacterial survival in blood and penetration of the blood–brain barrier. Our findings reveal a signaling mechanism in E. coli K1 for host adaptation.

【 授权许可】

Unknown