English (United Kingdom)

https://curated-unify.zendy.io/wp-json/zendy-region/v1/featured_content/oa?rat=en

https://curated-unify.zendy.io/wp-json/zendy-region/v1/highlighted_journal/

Global: Zendy Plus annual

Presents the access of premium content as premium feature

Premium Content

Presents the keyphrase highlighting as premium feature

Keyphrase Highlighting

Presents the summarisation as premium feature

Summarisation

Insights

Presents the pdf analysis as premium feature

PDF Analysis

Presents the zaia usage as premium feature

ZAIA

Global: Zendy Tools annual

Global: Zendy Free Plan

Global: Zendy Tools monthly

Global: Zendy Plus monthly

Alkylating agents introduce cytotoxic and/or mutagenic lesions to DNA bases leading to induction of adaptive (Ada) response, a mechanism protecting cells against deleterious effects of environmental chemicals. In  Escherichia coli , the Ada response involves expression of four genes:  ada ,  alkA ,  alkB , and  aidB . In  Pseudomonas putida , the organization of Ada regulon is different, raising questions regarding regulation of Ada gene expression. The aim of the presented studies was to analyze the role of AlkA glycosylase and AlkB dioxygenase in protecting  P. putida  cells against damage to DNA caused by alkylating agents. The results of bioinformatic analysis, of survival and mutagenesis of methyl methanesulfonate (MMS) or  N -methyl-N’-nitro- N -nitrosoguanidine (MNNG) treated  P. putida  mutants in  ada ,  alkA  and  alkB  genes as well as assay of promoter activity revealed diverse roles of Ada, AlkA and AlkB proteins in protecting cellular DNA against alkylating agents. We found AlkA protein crucial to abolish the cytotoxic but not the mutagenic effects of alkylans since: (i) the mutation in the  alkA  gene was the most deleterious for MMS/MNNG treated  P. putida  cells, (ii) the activity of the  alkA  promoter was Ada-dependent and the highest among the tested genes.  P. putida  AlkB (PpAlkB), characterized by optimal conditions for  in vitro  repair of specific substrates, complementation assay, and M13/MS2 survival test, allowed to establish conservation of enzymatic function of  P. putida  and  E. coli  AlkB protein. We found that the organization of  P. putida  Ada regulon differs from that of  E. coli . AlkA protein induced within the Ada response is crucial for protecting  P. putida  against cytotoxicity, whereas Ada prevents the mutagenic action of alkylating agents. In contrast to  E. coli  AlkB (EcAlkB), PpAlkB remains beyond the Ada regulon and is expressed constitutively. It probably creates a backup system that protects  P. putida  strains defective in other DNA repair systems against alkylating agents of exo- and endogenous origin.

plos one

Pseudomonas putida AlkA and AlkB Proteins Comprise Different Defense Systems for the Repair of Alkylation Damage to DNA – In Vivo, In Vitro, and In Silico Studies