ArticleCurrent genetics2012
Use of a ura5+-lys7+ cassette to construct unmarked gene knock-ins in Schizosaccharomyces pombe.
Article in Current genetics, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 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
14 citing papers in PubMed.
- Article
- Creating Meiotic Recombination-Regulating DNA Sites byBiomolecules · 2024Article
- Gene duplication and deletion caused by over-replication at a fork barrier.Nature communications · 2023Article
- A marker-free genome editing method inmicroPublication biology · 2023Article
- Targeted Forward Genetics: Population-Scale Analyses of Allele Replacements Spanning Thousands of Base Pairs in Fission Yeast.G3 (Bethesda, Md.) · 2019Article
- Metabolic engineering ofMetabolic engineering communications · 2017Article
- Relative contributions of the structural and catalytic roles of Rrp6 in exosomal degradation of individual mRNAs.RNA (New York, N.Y.) · 2016Article
- A Tool for Multiple Targeted Genome Deletions that Is Precise, Scar-Free, and Suitable for Automation.PloS one · 2015Article
- Role of Ccr4-Not complex in heterochromatin formation at meiotic genes and subtelomeres in fission yeast.Epigenetics & chromatin · 2015Article
- Implementation of the CRISPR-Cas9 system in fission yeast.Nature communications · 2014Article
- Multifaceted genome control by Set1 Dependent and Independent of H3K4 methylation and the Set1C/COMPASS complex.PLoS genetics · 2014Article
- Rapid, efficient and precise allele replacement in the fission yeast Schizosaccharomyces pombe.Current genetics · 2014Article
- Sck1 negatively regulates Gpa2-mediated glucose signaling in Schizosaccharomyces pombe.Eukaryotic cell · 2014Article
- Binding of the transcription factor Atf1 to promoters serves as a barrier to phase nucleosome arrays and avoid cryptic transcription.Nucleic acids research · 2014Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
While the counterselectable Schizosaccharomyces pombe ura4(+) gene can be used to prepare a site in the S. pombe genome to receive an unmarked mutant allele (loss of ura4(+) confers 5FOA-resistant (5FOA(R)) growth), the desired unmarked knock-in strains are generally outnumbered by spontaneously arising 5FOA(R) mutants. Relative to the same approach using the homologous URA3(+) gene in Saccharomyces cerevisiae, knock-ins in S. pombe are harder to identify due to a lower efficiency of homologous recombination and a relatively high background of spontaneous 5FOA(R) colonies. To develop an improved method for identifying cells receiving unmarked mutant alleles, we first determined that 5FOA(R) strains carry mutations in either of two genes; ura4(+) and ura5(+). We then cloned the S. pombe ura5(+) orotate phosphoribosyltransferase gene and constructed a 2.1 kb cassette containing ura5(+) together with the S. pombe lys7(+) gene. Using this doubly marked cassette to disrupt the sck1(+) kinase gene, we can distinguish between strains created by homologous knock-in of unmarked wild-type or kinase-dead alleles and spontaneously arising ura4(-) and ura5(-) mutants by screening 5FOA(R) colonies for the loss of the lys7(+) marker. The utility of this system, especially when the phenotype for the strain carrying the knock-in allele is indistinguishable from that of the disruption strain, is borne out by the fact that ~95% of 5FOA(R) colonies in our studies arose from background ura4(-) and ura5(-) mutations.
Indexed as
Identifiers
22198627What 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.