ArticleMolecular microbiology2010
Nitric oxide-sensitive and -insensitive interaction of Bacillus subtilis NsrR with a ResDE-controlled promoter.
Article in Molecular microbiology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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Who cites it
17 citing papers in PubMed, 37 citations in OpenAlex.
- Val43 residue of NsrR is crucial for the nitric oxide response ofMicrobiology spectrum · 2024Article
- Mechanisms and biotechnological applications of transcription factors.Synthetic and systems biotechnology · 2023Review
- Distinct Interaction Mechanism of RNA Polymerase and ResD at Proximal and Distal Subsites for Transcription Activation of Nitrite Reductase in Bacillus subtilis.Journal of bacteriology · 2022Article
- Native Mass Spectrometry of Iron-Sulfur Proteins.Methods in molecular biology (Clifton, N.J.) · 2021Article
- Sensing iron availabilityChemical science · 2017Article
- Genome-Wide Analysis of ResD, NsrR, and Fur Binding in Bacillus subtilis during Anaerobic Fermentative Growth byJournal of bacteriology · 2017Article
- Crystal structures of the NO sensor NsrR reveal how its iron-sulfur cluster modulates DNA binding.Nature communications · 2017Article
- Fe-S proteins that regulate gene expression.Biochimica et biophysica acta · 2015Review
- NsrR from Streptomyces coelicolor is a nitric oxide-sensing [4Fe-4S] cluster protein with a specialized regulatory function.The Journal of biological chemistry · 2015Article
- spxA2, encoding a regulator of stress resistance in Bacillus anthracis, is controlled by SaiR, a new member of the Rrf2 protein family.Molecular microbiology · 2014Article
- Transcriptional regulation of bacterial virulence gene expression by molecular oxygen and nitric oxide.Virulence · 2014Review
- Corynebacterium glutamicum ArnR controls expression of nitrate reductase operon narKGHJI and nitric oxide (NO)-detoxifying enzyme gene hmp in an NO-responsive manner.Journal of bacteriology · 2014Article
- The ResD response regulator, through functional interaction with NsrR and fur, plays three distinct roles in Bacillus subtilis transcriptional control.Journal of bacteriology · 2014Article
- The global response regulator RegR controls expression of denitrification genes in Bradyrhizobium japonicum.PloS one · 2014Article
- Bacterial iron-sulfur regulatory proteins as biological sensor-switches.Antioxidants & redox signaling · 2012Review
- Bacterial adaptation of respiration from oxic to microoxic and anoxic conditions: redox control.Antioxidants & redox signaling · 2012Review
- Global transcriptional control by NsrR in Bacillus subtilis.Journal of bacteriology · 2012Article
Corrections and comments
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
Abstract
NsrR is a nitric oxide (NO)-sensitive transcription repressor that controls NO metabolism in a wide range of bacteria. In Bacillus subtilis, NsrR represses transcription of the nitrite reductase (nasDEF) genes that are under positive control of the ResD-ResE two-component signal transduction system. Derepression is achieved by reaction of NO with NsrR. Unlike some NsrR orthologues that were shown to contain a NO-sensitive [2Fe-2S] cluster, B. subtilis NsrR, when purified anaerobically either from aerobic or from anaerobic Escherichia coli and B. subtilis cultures, contains a [4Fe-4S] cluster. [4Fe-4S]-NsrR binds around the -35 element of the nasD promoter with much higher affinity than apo-NsrR and binding of [4Fe-4S]-NsrR, but not apo-protein, is sensitive to NO. RNA polymerase and phosphorylated ResD make a ternary complex at the nasD promoter and NsrR dissociates the preformed ternary complex. In addition to the -35 region, NsrR binds to two distinct sites of the upstream regulatory region where ResD also binds. These interactions, unlike the high-affinity site binding, do not depend on the NsrR [4Fe-4S] cluster and binding is not sensitive to NO, suggesting a role for apo-NsrR in transcriptional regulation.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.