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Title: | Controller protein of restriction-modification system Kpn2I affects transcription of its gene by acting as a transcription elongation roadblock | Authors: | Klimuk, Evgeny Bogdanova, Ekaterina Nagornykh, Max Rodić, Anđela Đorđević, Marko Medvedeva, Sofia Pavlova, Olga Severinov, Konstantin |
Issue Date: | 1-Jan-2018 | Rank: | M21a | Journal: | Nucleic Acids Research | Abstract: | © 2018 The Author(s). Published by Oxford University Press on behalf of Nucleic Acids Research. C-proteins control restriction-modification (R-M) systems' genes transcription to ensure sufficient levels of restriction endonuclease to allow protection from foreign DNA while avoiding itsmodification by excess methyltransferase. Here, we characterize transcription regulation in C-protein dependent R-M system Kpn2I. The Kpn2I restriction endonuclease gene is transcribed from a constitutive, weak promoter, which, atypically, is C-protein independent. Kpn2I C-protein (C.Kpn2I) binds upstream of the strong methyltransferase gene promoter and inhibits it, likely by preventing the interaction of the RNA polymerase sigma subunit with the-35 consensus element. Diminished transcription from the methyltransferase promoter increases transcription from overlapping divergent C-protein gene promoters. All known C-proteins affect transcription initiation from R-M genes promoters. Uniquely, the C.Kpn2I binding site is located within the coding region of its gene. C.Kpn2I acts as a roadblock stalling elongating RNA polymerase and decreasing production of full-length C.Kpn2I mRNA. Mathematical modeling shows that this unusual mode of regulation leads to the same dynamics of accumulation of R-M gene transcripts as observed in systems where C-proteins act at transcription initiation stage only. Bioinformatics analyses suggest that transcription regulation through binding of C.Kpn2I-like proteins within the coding regions of their genes may be widespread. |
URI: | https://biore.bio.bg.ac.rs/handle/123456789/371 | ISSN: | 0305-1048 | DOI: | 10.1093/nar/gky880 |
Appears in Collections: | Journal Article |
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