The function of the Saccharomyces cerevisiae iso-1-cytochrome c gene is independent of the codon at invariant residue Phe82 when the gene is present on a low-copy-number vector

1991 ◽  
Vol 4 (5) ◽  
pp. 575-578 ◽  
Author(s):  
S.E. Hilgen ◽  
G.J. Pielak
Keyword(s):  
Saccharomyces Cerevisiae ◽  
Cytochrome C ◽  
Copy Number ◽  
Low Copy Number ◽  
Invariant Residue

Genes that can bypass the CLN requirement for Saccharomyces cerevisiae cell cycle START

1994 ◽  
Vol 14 (3) ◽  
pp. 2041-2047
Author(s):  
C B Epstein ◽  
F R Cross
Keyword(s):  
Saccharomyces Cerevisiae ◽  
Cell Cycle ◽  
Transcription Factor ◽  
Copy Number ◽  
Single Gene ◽  
Low Copy Number ◽  
Synthetically Lethal ◽  
Low Expression

Cell cycle START in Saccharomyces cerevisiae requires at least one of the three CLN genes (CLN1, CLN2, or CLN3). A total of 12 mutations bypassing this requirement were found to be dominant mutations in a single gene that we named BYC1 (for bypass of CLN requirement). We also isolated a plasmid that had cln bypass activity at a low copy number; the gene responsible was distinct from BYC1 and was identical to the recently described BCK2 gene. Strains carrying bck2::ARG4 disruption alleles were fully viable, but bck2::ARG4 completely suppressed the cln bypass activity of BYC1. swi4 and swi6 deletion alleles also efficiently suppressed BYC1 cln bypass activity; Swi4 and Swi6 are components of a transcription factor previously implicated in control of CLN1 and CLN2 expression. bck2::ARG4 was synthetically lethal with cln3 deletion, suggesting that CLN1 and CLN2 cannot function in the simultaneous absence of BCK2 and CLN3; this observation correlates with low expression of CLN1 and CLN2 in bck2 strains deprived of CLN3 function. Thus, factors implicated in CLN1 and CLN2 expression and/or function are also required for BYC1 function in the absence of all three CLN genes; this may suggest the involvement of other targets of Swi4, Swi6, and Bck2 in START.

scholarly journals Reversion analysis of [psi−] mutations in Saccharomyces cerevisiae

1981 ◽  
Vol 37 (2) ◽  
pp. 173-182 ◽  
Author(s):  
P. M. Lund ◽  
B. S. Cox
Keyword(s):  
Saccharomyces Cerevisiae ◽  
Copy Number ◽  
Guanidine Hydrochloride ◽  
Copy Number Variants ◽  
Dimethyl Sulphoxide ◽  
High Frequencies ◽  
Low Copy Number

SUMMARYMutants of [psi] a cytoplasmically inherited factor in the yeast Saccharomyces cerevisiae were isolated after treatment with a variety of agents including conventional mutagens and a number of compounds which cause loss of [psi] at high frequencies, namely methanol, KCl, dimethyl sulphoxide and guanidine hydrochloride. In [psi−] mutants the suppressor SUQ5 does not suppress ochre mutations such as ade.2.1.Reversion analysis of the [psi−] mutants revealed three classes: (1) a class of agents producing [psi−] mutations which could readily revert to [psi+] (methanol, KCl and dimethyl sulphoxide belong to this class), (2) those which could not be shown to revert (GuHCl) and (3) the conventional mutagens which produced both revertible and apparently non-revertible [psi−] mutations. We conclude that GuHCl causes a deletion or loss of the [psi] factor. Methanol may cause an alteration of ‘state’ for example, of a promoter, and KCl may be selecting or inducing low copy number variants of [psi+] strains. It is possible that DMSO may be involved in regulation of [psi].

scholarly journals Genes that can bypass the CLN requirement for Saccharomyces cerevisiae cell cycle START.

1994 ◽  
Vol 14 (3) ◽  
pp. 2041-2047 ◽  
Author(s):  
C B Epstein ◽  
F R Cross
Keyword(s):  
Saccharomyces Cerevisiae ◽  
Cell Cycle ◽  
Transcription Factor ◽  
Copy Number ◽  
Single Gene ◽  
Low Copy Number ◽  
Synthetically Lethal ◽  
Low Expression

Cell cycle START in Saccharomyces cerevisiae requires at least one of the three CLN genes (CLN1, CLN2, or CLN3). A total of 12 mutations bypassing this requirement were found to be dominant mutations in a single gene that we named BYC1 (for bypass of CLN requirement). We also isolated a plasmid that had cln bypass activity at a low copy number; the gene responsible was distinct from BYC1 and was identical to the recently described BCK2 gene. Strains carrying bck2::ARG4 disruption alleles were fully viable, but bck2::ARG4 completely suppressed the cln bypass activity of BYC1. swi4 and swi6 deletion alleles also efficiently suppressed BYC1 cln bypass activity; Swi4 and Swi6 are components of a transcription factor previously implicated in control of CLN1 and CLN2 expression. bck2::ARG4 was synthetically lethal with cln3 deletion, suggesting that CLN1 and CLN2 cannot function in the simultaneous absence of BCK2 and CLN3; this observation correlates with low expression of CLN1 and CLN2 in bck2 strains deprived of CLN3 function. Thus, factors implicated in CLN1 and CLN2 expression and/or function are also required for BYC1 function in the absence of all three CLN genes; this may suggest the involvement of other targets of Swi4, Swi6, and Bck2 in START.

scholarly journals Whole-genome sequencing from the New Zealand Saccharomyces cerevisiae population reveals the genomic impacts of novel microbial range expansion

2020 ◽  
Vol 11 (1) ◽  
Author(s):  
Peter Higgins ◽  
Cooper A Grace ◽  
Soon A Lee ◽  
Matthew R Goddard
Keyword(s):  
Saccharomyces Cerevisiae ◽  
New Zealand ◽  
Whole Genome Sequencing ◽  
Genome Sequencing ◽  
Range Expansion ◽  
Copy Number ◽  
Small Scale ◽  
Whole Genome ◽  
Copy Number Changes ◽  
The Impact

Abstract Saccharomyces cerevisiae is extensively utilized for commercial fermentation, and is also an important biological model; however, its ecology has only recently begun to be understood. Through the use of whole-genome sequencing, the species has been characterized into a number of distinct subpopulations, defined by geographical ranges and industrial uses. Here, the whole-genome sequences of 104 New Zealand (NZ) S. cerevisiae strains, including 52 novel genomes, are analyzed alongside 450 published sequences derived from various global locations. The impact of S. cerevisiae novel range expansion into NZ was investigated and these analyses reveal the positioning of NZ strains as a subgroup to the predominantly European/wine clade. A number of genomic differences with the European group correlate with range expansion into NZ, including 18 highly enriched single-nucleotide polymorphism (SNPs) and novel Ty1/2 insertions. While it is not possible to categorically determine if any genetic differences are due to stochastic process or the operations of natural selection, we suggest that the observation of NZ-specific copy number increases of four sugar transporter genes in the HXT family may reasonably represent an adaptation in the NZ S. cerevisiae subpopulation, and this correlates with the observations of copy number changes during adaptation in small-scale experimental evolution studies.

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