Evidence map›Paper›PMID 16077099›Full record

ArticleJournal of bacteriology2005

Methanol-dependent gene expression demonstrates that methyl-coenzyme M reductase is essential in Methanosarcina acetivorans C2A and allows isolation of mutants with defects in regulation of the methanol utilization pathway.

Michael Rother, Paolo Boccazzi, Arpita Bose, Matthew A Pritchett, W W Metcalf

Open access · greenAbstract read
In one paragraph

Article in Journal of bacteriology, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
2.7field-weighted citation impact, top 11% of its field
1 · What the graph read from it

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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

19 citing papers in PubMed, 40 citations in OpenAlex.

  1. Review
  2. A promoter-RBS library for fine-tuning gene expression inApplied and environmental microbiology · 2024
    Article
  3. Review
  4. Article
  5. Cas9-mediated genome editing in the methanogenic archaeonProceedings of the National Academy of Sciences of the United States of America · 2017
    Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. Genetic manipulation of Methanosarcina spp.Frontiers in microbiology · 2012
    Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Article
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  18. Article
  19. The evolutionary history of Cys-tRNACys formation.Proceedings of the National Academy of Sciences of the United States of America · 2005
    Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

5 authors at 1 institution in 1 country.

Michael RotherDepartment of Microbiology, University of Illinois at Urbana-Champaign, 601 South Goodwin Avenue, Urbana, IL 61801, USA.
Paolo Boccazzi
Arpita Bose
Matthew A Pritchett
W W Metcalf
University of Illinois Urbana-Champaign · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Methanosarcina acetivorans C2A is able to convert several substrates to methane via at least four distinct methanogenic pathways. A common step in each of these pathways is the reduction of methyl-coenzyme M (CoM) to methane catalyzed by methyl-CoM reductase (MCR). Because this enzyme is used in each of the known pathways, the mcrBDCGA operon, which encodes MCR, is expected to be essential. To validate this prediction, a system for conditional gene inactivation was developed. A heterologous copy of the mcrBDCGA operon was placed under the control of the highly regulated mtaC1 promoter, which directs the expression of genes involved in methanol utilization, and recombined onto the M. acetivorans chromosome. This allowed for disruption of the endogenous mcr operon in the presence of methanol. Because the PmtaC1 promoter is transcribed only during growth on methanol, mcrBDCGA was rendered methanol dependent and the strain was unable to grow in trimethylamine media, strongly suggesting that mcrBDCGA is essential. Upon prolonged incubation, suppressed mutants which expressed mcrBDCGA constitutively could be selected. Expression analysis of PmtaC1::uidA gene fusions in several isolated suppressed mutants suggests that they carry trans-active mutations leading to deregulation of all genes under control of this promoter. Subsequently, proteome analysis of one such suppressed mutant revealed that all known proteins derived from mtaC1 promoter-dependent expression were constitutively expressed in this mutant. This genetic system can therefore be employed for the testing of essential genes and for the identification of genes under a common regulatory mechanism by making regulatory mutations phenotypically selectable.

Indexed as

Gene DeletionGene Expression Regulation, ArchaealGene Expression Regulation, EnzymologicGenes, ReporterMethanolMethanosarcinaMethylaminesMutagenesisOxidoreductasesPhenotypePromoter Regions, GeneticRecombinant Fusion ProteinsMethanolMethylaminesmethyl coenzyme M reductaseOxidoreductasesRecombinant Fusion Proteinstrimethylamine

Identifiers

PMID16077099
PMCPMC1196066
OpenAlexW2115901152

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

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.