Comparative Integrated Omics Analysis of the Hfq Regulon in Bordetella pertussis

0517771 - MBÚ 2020 RIV CH eng J - Journal Article
Dienstbier, Ana - Amman, F. - Štipl, Daniel - Petráčková, Denisa - Večerek, Branislav
Comparative Integrated Omics Analysis of the Hfq Regulon in Bordetella pertussis.
International Journal of Molecular Sciences. Roč. 20, č. 12 (2019), č. článku 3073. E-ISSN 1422-0067
R&D Projects: GA ČR(CZ) GA19-12338S; GA MŠMT(CZ) LQ1604
Grant - others:AV ČR(CZ) MSM200201702
Program: Program na podporu mezinárodní spolupráce začínajících výzkumných pracovníků
Institutional support: RVO:61388971
Keywords : Bordetella pertussis * Hfq * T3SS
OECD category: Microbiology
Impact factor: 4.556, year: 2019
Method of publishing: Open access
https://www.mdpi.com/1422-0067/20/12/3073

Bordetella pertussis is a Gram-negative strictly human pathogen of the respiratory tract and the etiological agent of whooping cough (pertussis). Previously, we have shown that RNA chaperone Hfq is required for virulence of B. pertussis. Furthermore, microarray analysis revealed that a large number of genes are affected by the lack of Hfq. This study represents the first attempt to characterize the Hfq regulon in bacterial pathogen using an integrative omics approach. Gene expression profiles were analyzed by RNA-seq and protein amounts in cell-associated and cell-free fractions were determined by LC-MS/MS technique. Comparative analysis of transcriptomic and proteomic data revealed solid correlation (r(2) = 0.4) considering the role of Hfq in post-transcriptional control of gene expression. Importantly, our study confirms and further enlightens the role of Hfq in pathogenicity of B. pertussis as it shows that Delta hfq strain displays strongly impaired secretion of substrates of Type III secretion system (T3SS) and substantially reduced resistance to serum killing. On the other hand, significantly increased production of proteins implicated in transport of important metabolites and essential nutrients observed in the mutant seems to compensate for the physiological defect introduced by the deletion of the hfq gene.
Permanent Link: http://hdl.handle.net/11104/0303053