Reduced OxyR positively regulates the prodigiosin biosynthesis in Serratia marcescens FS14

Copyright © 2024 Elsevier Inc. All rights reserved..

OxyR, a LysR family transcriptional regulator, plays vital roles in bacterial oxidative stress response. In this study, we found that the deletion of oxyR not only inhibited the antioxidant capacity of S. marcescens FS14, but also decreased the production of prodigiosin. Further study revealed that OxyR activated the prodigiosin biosynthesis at the transcriptional level. Complementary results showed that not only the wild-type OxyR but also the reduced form OxyRC199S could activate the prodigiosin biosynthesis. We further demonstrated that reduced form of wild type OxyR could bind to the promoter of pig gene cluster, and identified the binding sites which is different from oxidized OxyR binding sites in E. coli. Our results demonstrated that OxyR in FS14 uses oxidized form to regulate the expression of the antioxidant related genes and utilizes reduced form to activate prodigiosin production. Further in silico analysis suggested that the activation of prodigiosin biosynthesis by reduced OxyR should be general in S. marcesencs. To our knowledge, this is the first report to show that OxyR uses the reduced form to activate the gene's expression, therefore, our results provide a novel regulation mechanism of OxyR.

Medienart:

E-Artikel

Erscheinungsjahr:

2024

Erschienen:

2024

Enthalten in:

Zur Gesamtaufnahme - volume:710

Enthalten in:

Biochemical and biophysical research communications - 710(2024) vom: 28. Apr., Seite 149877

Sprache:

Englisch

Beteiligte Personen:

Liu, Hong [VerfasserIn]
Chu, Fenglian [VerfasserIn]
Wu, Yi [VerfasserIn]
Gu, Xiaochen [VerfasserIn]
Ran, Tingting [VerfasserIn]
Wang, Weiwu [VerfasserIn]
Xu, Dongqing [VerfasserIn]

Links:

Volltext

Themen:

Antioxidants
Bacterial Proteins
DNA binding site
Journal Article
OL369FU7CJ
OxyR
Prodigiosin
Serratia marcescens

Anmerkungen:

Date Completed 22.04.2024

Date Revised 22.04.2024

published: Print-Electronic

Citation Status MEDLINE

doi:

10.1016/j.bbrc.2024.149877

funding:

Förderinstitution / Projekttitel:

PPN (Katalog-ID):

NLM370713591