ArticlePloS one2017
The KP1_4563 gene is regulated by the cAMP receptor protein and controls type 3 fimbrial function in Klebsiella pneumoniae NTUH-K2044.
Article in PloS one, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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6 citing papers in PubMed, 13 citations in OpenAlex.
- Comparative genomics of hypervirulent Klebsiella pneumoniae isolates from Brazil.Archives of microbiology · 2026Article
- The dual role of cAMP receptor protein (CRP) in regulating type 3 fimbriae expression in Klebsiella pneumoniae CG43S3 in response to oxygen availability.BMC microbiology · 2026Article
- The effect of a temperature-sensitive prophage on the evolution of virulence in an opportunistic bacterial pathogen.Molecular ecology · 2022Article
- RcsAB and Fur Coregulate the Iron-Acquisition System viaFrontiers in cellular and infection microbiology · 2020Article
- EtcABC, a Putative EII Complex, Regulates Type 3 Fimbriae via CRP-cAMP Signaling inFrontiers in microbiology · 2019Article
- Intestinal carbapenem-resistantGut microbesArticle
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Authors and funding
11 authors at 2 institutions in 1 country.
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Abstract
Klebsiella pneumoniae (K. pneumoniae) is an opportunistic pathogen that can adhere to host cells or extracellular matrix via type 1 and type 3 fimbriae. KP1_4563 is a gene encoding a hypothetical protein in K. pneumoniae NTUH-K2044. KP1_4563 is located between the type 1 and type 3 fimbrial gene clusters and is likely associated with fimbrial function given its putative conserved domains of unknown function (DUF1471). Cyclic AMP receptor protein (CRP) regulates virulence-related gene expression and is a crucial transcriptional regulator in many bacteria. The predicted DNA recognition motif of CRP is present in the KP1_4563 promoter region. This study aimed to investigate the function of KP1_4563 in fimbriae and its transcriptional regulation mechanism by CRP. We generated Kp-Δ4563 mutant and complementation strains. We utilized phenotype and adhesion assays to evaluate the role of KP1_4563 in fimbriae. We conducted quantitative RT-PCR (qRT-PCR), LacZ fusion, electrophoretic mobility shift, and DNase I footprinting assays to study the transcriptional regulation of KP1_4563 gene by CRP. We found that KP1_4563 negatively regulates the function of type 3 fimbriae. Compared with NTUH-K2044, the absence of KP1_4563 enhanced the ability of Kp-Δ4563 to adhere to A549 cells. CRP negatively regulates KP1_4563 by directly binding to its promoter region. KP1_4563 plays an important role in type 3 fimbrial function. This novel insight will assist in the development of strategies for preventing K. pneumoniae infection.
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