We describe here the construction of six deletion mutants and their basic phenotypic analysis in three different backgrounds. The six genes were disrupted in three diploid strains (FY1679, W303 and CEN.PK2) by the long flanking homology (LFH) method (Wach, 1996). Transformants were selected as genet
Gene disruption and basic phenotypic analysis of nine novel yeast genes from chromosome XIV
✍ Scribed by Chiara Capozzo; Francesca Sartorello; Francesca Dal Pero; Michela D'Angelo; Alessandro Vezzi; Stefano Campanaro; Giorgio Valle
- Publisher
- John Wiley and Sons
- Year
- 2000
- Tongue
- English
- Weight
- 324 KB
- Volume
- 16
- Category
- Article
- ISSN
- 0749-503X
No coin nor oath required. For personal study only.
📜 SIMILAR VOLUMES
The European Functional Analysis Network (EUROFAN) is systematically analysing the function of novel Saccharomyces cerevisiae genes revealed by genome sequencing. As part of this effort our consortium has performed a detailed transcript analysis for 250 novel ORFs on chromosome XIV. All transcripts
We report here the construction of six deletion mutants and the analysis of their basic phenotype. Deletion cassettes containing the KanMX4 marker module and long flanking regions homologous to the target locus were constructed for each of the six open reading-frames (ORFs YDL088c, YDL087c, YDL086w,
Within the frame of the EUROFAN project, aimed at the functional analysis of the novel ORFs revealed by the systematic sequencing of the Saccharomyces cerevisiae genome, we have inactivated six ORFs encoding putative proteins with unknown function in the two S. cerevisiae strains FY1679 and W303-1B.
Six open reading frames (ORFs) of unknown function from the left arm of Saccharomyces cerevisiae chromosome XV were deleted in two genetic backgrounds by disruption cassettes with long flanking homology (LFH) , within the frame of the research project EUROFAN. The LFH disruption cassettes, obtained
As a part of the EUROFAN programme, six open reading frames from Saccharomyces cerevisiae (YNL083w, YNL086w, YNL087w, YNL097c, YDL100c and YOR086c) were disrupted in two genetic backgrounds, FY1679 and W303. Individual deletions in diploid strains and tetrad analysis of heterozygous deletants reveal