ArticleGenetics2009
Genetic evidence for an essential oscillation of transmembrane-spanning segment 5 in the Escherichia coli ammonium channel AmtB.
Article in Genetics, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 18 citations in OpenAlex.
- Exaggerated trans-membrane charge of ammonium transporters in nutrient-poor marine environments.Open biology · 2022Article
- Signaling ammonium across membranes through an ammonium sensor histidine kinase.Nature communications · 2018Article
- Direct observation of electrogenic NH4(+) transport in ammonium transport (Amt) proteins.Proceedings of the National Academy of Sciences of the United States of America · 2014Article
- Nitrogen assimilation in Escherichia coli: putting molecular data into a systems perspective.Microbiology and molecular biology reviews : MMBR · 2013Review
- Article
- Mechanism for nitrogen isotope fractionation during ammonium assimilation by Escherichia coli K12.Proceedings of the National Academy of Sciences of the United States of America · 2013Article
- The pivotal twin histidines and aromatic triad of the Escherichia coli ammonium channel AmtB can be replaced.Proceedings of the National Academy of Sciences of the United States of America · 2011Article
- Article
- The Rh protein family: gene evolution, membrane biology, and disease association.Cellular and molecular life sciences : CMLS · 2010Review
- Epistatic effects of the protease/chaperone HflB on some damaged forms of the Escherichia coli ammonium channel AmtB.Genetics · 2009Article
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
Ammonium channels, called Amt or Mep, concentrate NH(4)(+) against a gradient. Each monomer of the trimer has a pore through which substrate passes and a C-terminal cytoplasmic extension. The importance of the C-terminal extension to AmtB activity remains unclear. We have described lesions in conserved C-terminal residues that inactivate AmtB and here characterize 38 intragenic suppressors upstream of the C terminus ( approximately 1/3 of total suppressors). Three that occurred repeatedly, including the previously characterized W148L at the pore entry, restored growth at low NH(3) to nearly wild-type levels and hence restored high activity. V116L completely restored function to two of the mutant proteins and, when separated from other lesions, did not damage wild-type AmtB. A179E notably altered folding of AmtB, compensated for all inactivating C-terminal lesions, and damaged wild-type AmtB. V116L and A179E lie at the cytoplasmic end of transmembrane-spanning segments (TM) 3 and 5, respectively, and the proximal part of the C-terminal tail makes intimate contacts with the loops following them before crossing to the adjacent monomer. Collectively, the properties of intragenic suppressor strains lead us to postulate that the C-terminal tail facilitates an oscillation of TM 5 that is required for coordinated pore function and high AmtB activity. Movement of TM 5 appears to control the opening of both the periplasmic entry and the cytoplasmic exit to the pore.
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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.