ArticleThe EMBO journal2003
Gain-of-function mutations indicate that Escherichia coli Kch forms a functional K+ conduit in vivo.
Article in The EMBO journal, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
24 citing papers in PubMed, 59 citations in OpenAlex.
- Mechanism of Kch activation by ZnPNAS nexus · 2026Article
- Metabolic control of porin permeability influences antibiotic resistance in Escherichia coli.Nature microbiology · 2025Article
- Article
- Electrical Impedance Spectroscopy with Bacterial Biofilms: Neuronal-like Behavior.Nano letters · 2024Article
- Unappreciated Roles for KTrends in microbiology · 2021Review
- The shifting sands of 'gain-of-function' research.Nature · 2021Article
- Molecular Mechanisms for Bacterial Potassium Homeostasis.Journal of molecular biology · 2021Review
- The Voltage-Dependent Deactivation of the KvAP Channel Involves the Breakage of Its S4 Helix.Frontiers in molecular biosciences · 2020Article
- Ru(CO)3Cl(Glycinate) (CORM-3): a carbon monoxide-releasing molecule with broad-spectrum antimicrobial and photosensitive activities against respiration and cation transport in Escherichia coli.Antioxidants & redox signaling · 2013Article
- Functional characterization and determination of the physiological role of a calcium-dependent potassium channel from cyanobacteria.Plant physiology · 2013Article
- Article
- A novel manganese efflux system, YebN, is required for virulence by Xanthomonas oryzae pv. oryzae.PloS one · 2011Article
- Structure of the MthK RCK in complex with cadmium.Journal of structural biology · 2010Article
- Searching for interesting channels: pairing selection and molecular evolution methods to study ion channel structure and function.Molecular bioSystems · 2009Review
- KTN (RCK) domains regulate K+ channels and transporters by controlling the dimer-hinge conformation.Structure (London, England : 1993) · 2009Article
- The desensitization gating of the MthK K+ channel is governed by its cytoplasmic amino terminus.PLoS biology · 2008Article
- Ion channels in microbes.Physiological reviews · 2008Review
- Molecular architecture and divalent cation activation of TvoK, a prokaryotic potassium channel.The Journal of biological chemistry · 2007Article
- Patch clamp and phenotypic analyses of a prokaryotic cyclic nucleotide-gated K+ channel using Escherichia coli as a host.The Journal of biological chemistry · 2007Article
- Transport capabilities of eleven gram-positive bacteria: comparative genomic analyses.Biochimica et biophysica acta · 2007Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Although Kch of Escherichia coli is thought to be a K(+) channel by sequence homology, there is little evidence that it actually conducts K(+) ions in vitro or in vivo. We isolated gain-of-function (GOF) Kch mutations that render bacteria specifically sensitive to K(+) ions. Millimolar added K(+), but not Na(+) or sorbitol, blocks the initiation or continuation of mutant growth in liquid media. The mutations are mapped at the RCK (or KTN) domain, which is considered to be the cytoplasmic sensor controlling the gate. Additional mutations directed to the K(+)-filter sequence rescue the GOF mutant. The apparent K(+)-specific conduction through the 'loose-cannon' mutant channel suggests that the wild-type Kch channel also conducts, albeit in a regulated manner. Changing the internal ATG does not erase the GOF toxicity, but removes kch's short second product, suggesting that it is not required for channel function in vivo. The mutant phenotypes are better explained by a perturbation of membrane potential instead of internal K(+) concentration. Possible implications on the normal function of Kch are discussed.
Indexed as
Identifiers
What OpenQuestion holds
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.