Differential RNA-seq of Vibrio cholerae identifies the VqmR small RNA as a regulator of biofilm formation.

TitleDifferential RNA-seq of Vibrio cholerae identifies the VqmR small RNA as a regulator of biofilm formation.
Publication TypeJournal Article
Year of Publication2015
AuthorsPapenfort, K, Förstner, KU, Cong, J-P, Sharma, CM, Bassler, BL
JournalProc Natl Acad Sci U S A
Volume112
Issue7
PaginationE766-75
Date Published2015 Feb 17
ISSN1091-6490
KeywordsBase Sequence, Biofilms, Gene Expression Profiling, Genes, Bacterial, Molecular Sequence Data, Mutagenesis, Oligonucleotide Array Sequence Analysis, Promoter Regions, Genetic, RNA, Viral, Sequence Analysis, RNA, Sequence Homology, Nucleic Acid, Transcription, Genetic, Vibrio cholerae
Abstract

<p>Quorum sensing (QS) is a process of cell-to-cell communication that enables bacteria to transition between individual and collective lifestyles. QS controls virulence and biofilm formation in Vibrio cholerae, the causative agent of cholera disease. Differential RNA sequencing (RNA-seq) of wild-type V. cholerae and a locked low-cell-density QS-mutant strain identified 7,240 transcriptional start sites with ∼ 47% initiated in the antisense direction. A total of 107 of the transcripts do not appear to encode proteins, suggesting they specify regulatory RNAs. We focused on one such transcript that we name VqmR. vqmR is located upstream of the vqmA gene encoding a DNA-binding transcription factor. Mutagenesis and microarray analyses demonstrate that VqmA activates vqmR transcription, that vqmR encodes a regulatory RNA, and VqmR directly controls at least eight mRNA targets including the rtx (repeats in toxin) toxin genes and the vpsT transcriptional regulator of biofilm production. We show that VqmR inhibits biofilm formation through repression of vpsT. Together, these data provide to our knowledege the first global annotation of the transcriptional start sites in V. cholerae and highlight the importance of posttranscriptional regulation for collective behaviors in this human pathogen.</p>

DOI10.1073/pnas.1500203112
Alternate JournalProc. Natl. Acad. Sci. U.S.A.
PubMed ID25646441
PubMed Central IDPMC4343088
Grant List5R01GM065859 / GM / NIGMS NIH HHS / United States
R01 GM065859 / GM / NIGMS NIH HHS / United States
/ / Howard Hughes Medical Institute / United States