ArticleGenetics2009
Epistatic effects of the protease/chaperone HflB on some damaged forms of 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 8 papers.
What it found
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Who cites it
8 citing papers in PubMed, 11 citations in OpenAlex.
- Yeast filamentation signaling is connected to a specific substrate translocation mechanism of the Mep2 transceptor.PLoS genetics · 2020Article
- Nitrogen assimilation in Escherichia coli: putting molecular data into a systems perspective.Microbiology and molecular biology reviews : MMBR · 2013Review
- 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 molecular basis of K+ exclusion by the Escherichia coli ammonium channel AmtB.The Journal of biological chemistry · 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 Rut pathway for pyrimidine degradation: novel chemistry and toxicity problems.Journal of bacteriology · 2010Article
- Genetic evidence for an essential oscillation of transmembrane-spanning segment 5 in the Escherichia coli ammonium channel AmtB.Genetics · 2009Article
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
Abstract
The Escherichia coli ammonium channel AmtB is a trimer in which each monomer carries a pore for substrate conduction and a cytoplasmic C-terminal extension of approximately 25 residues. Deletion of the entire extension leaves the protein with intermediate activity, but some smaller lesions in this region completely inactivate AmtB, as do some lesions in its cytoplasmic loops. We here provide genetic evidence that inactivation depends on the essential protease HflB, which appears to cause inactivation not as a protease but as a chaperone. Selection for restored function of AmtB is a positive selection for loss of the ATPase/chaperone activity of HflB and reveals that the conditional lethal phenotype for hflB is cold sensitivity. Deletion of only a few residues from the C terminus of damaged AmtB proteins seems to prevent HflB from acting on them. Either yields the intermediate activity of a complete C-terminal deletion. HflB apparently "tacks" damaged AmtB tails to the adjacent monomers. Knowing that HflB has intervened is prerequisite to determining the functional basis for AmtB inactivation.
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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.