ArticleOpen biology2016
Characterization of DicB by partially masking its potent inhibitory activity of cell division.
Article in Open biology, 2016. 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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Who cites it
6 citing papers in PubMed.
- A transcription factor from the cryptic Escherichia coli Rac prophage controls both phage and host operons.Nucleic acids research · 2025Article
- A Cryptic Prophage Transcription Factor Drives Phenotypic Changes via Host Gene Regulation.bioRxiv : the preprint server for biology · 2024Article
- YdfD, a Lysis Protein of the Qin Prophage, Is a Specific Inhibitor of the IspG-Catalyzed Step in the MEP Pathway ofInternational journal of molecular sciences · 2022Article
- The Association of Cell Division Regulated by DicC With the Formation of Viable but Non-culturableFrontiers in microbiology · 2019Article
- Expression of Phi11 Gp07 Causes Filamentation inThe open microbiology journal · 2018Article
- Interaction of Type IV Toxin/Antitoxin Systems in Cryptic Prophages of Escherichia coli K-12.Toxins · 2017Article
Corrections and comments
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Authors and funding
7 authors.
Funding
Abstract
DicB, a protein encoded by the Kim (Qin) prophage in Escherichia coli, inhibits cell division through interaction with MinC. Thus far, characterization of DicB has been severely hampered owing to its potent activity which ceases cell division and leads to cell death. In this work, through fusing maltose-binding protein to the N-terminus of DicB (MBP-DicB), we successfully expressed and purified recombinant DicB that enabled in vitro analysis for the first time. More importantly, taking advantage of the reduced inhibitory activity of MBP-DicB, we were able to study its effects on cell growth and morphology. Inhibition of cell growth by MBP-DicB was systematically evaluated using various DicB constructs, and their corresponding effects on cell morphology were also investigated. Our results revealed that the N-terminal segment of DicB plays an essential functional role, in contrast to its C-terminal tail. The N-terminus of DicB is of critical importance as even the first amino acid (following the initial Met) could not be removed, although it could be mutated. This study provides the first glimpse of the molecular determinants underlying DicB's function.
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Registered trials
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