Mapping of the Saccharomyces cerevisiae CDC3, CDC25, and CDC42 genes to chromosome XII by chromosome blotting and tetrad analysis

Johnson, Douglas I.; Jacobs, Charles W.; Pringle, John R.; Robinson, Lucy C.; Carle, Georges F.; Olson, Maynard V.

doi:10.1002/yea.320030405

Cited by 29 publications

(16 citation statements)

References 27 publications

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“…Another series of tetrad analyses showed that mhrl had a linkage with cdc25 (38 cM) on chromosome XII and a very weak linkage with ilv5 on the same chromosome (Table V). Since ilv5 is located 32 cM distal to cdc25 (Johnson et al, 1987), the locus for mhrl is 38 cM towards the centromere from cdc25 on chromosome XII. The nearest mutation to mhrl would be cdc42, but cdc42 is located 54 cM distant from cdc25 (Johnson et al, 1987).…”

Section: Resultsmentioning

confidence: 99%

A nuclear mutation defective in mitochondrial recombination in yeast.

et al. 1995

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Homologous recombination (crossing over and gene conversion) is generally essential for heritage and DNA repair, and occasionally causes DNA aberrations, in nuclei of eukaryotes. However, little is known about the roles of homologous recombination in the inheritance and stability of mitochondrial DNA which is continuously damaged by reactive oxygen species, by‐products of respiration. Here, we report the first example of a nuclear recessive mutation which suggests an essential role for homologous recombination in the stable inheritance of mitochondrial DNA. For the detection of this class of mutants, we devised a novel procedure, ‘mitochondrial crossing in haploid’, which has enabled us to examine many mutant clones. Using this procedure, we examined mutants of Saccharomyces cerevisiae that showed an elevated UV induction of respiration‐deficient mutations. We obtained a mutant that was defective in both the omega‐intron homing and Endo.SceI‐induced homologous gene conversion. We found that the mutant cells are temperature sensitive in the maintenance of mitochondrial DNA. A tetrad analysis indicated that elevated UV induction of respiration‐deficient mutations, recombination deficiency and temperature sensitivity are all caused by a single nuclear mutation (mhr1) on chromosome XII. The pleiotropic characteristics of the mutant suggest an essential role for the MHR1 gene in DNA repair, recombination and the maintenance of DNA in mitochondria.

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Section: Resultsmentioning

confidence: 99%

A nuclear mutation defective in mitochondrial recombination in yeast.

et al. 1995

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“…The -201 leu2-3,112 ura3-52). The gcd7-201 allele was identified in ascospore clones by its phenotypes of slow growth and resistance to 0.5 mM 5-fluoro-DL-tryptophan (40), and the exgl and cdc42 alleles were identified as described previously (7,28).…”

Section: Resultsmentioning

confidence: 99%

Evidence that GCD6 and GCD7, translational regulators of GCN4, are subunits of the guanine nucleotide exchange factor for eIF-2 in Saccharomyces cerevisiae.

Bushman¹,

Asuru²,

Matts³

et al. 1993

Mol. Cell. Biol.

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Starvation of the yeast Saccharomyces cerevisiae for an amino acid signals increased translation of GCN4, a transcriptional activator of amino acid biosynthetic genes. We have isolated and characterized the GCD6 and GCD7 genes and shown that their products are required to repress GCN4 translation under nonstarvation conditions. We find that both GCD6 and GCD7 show sequence similarities to components of a high-molecularweight complex (the GCD complex) that appears to be the yeast equivalent of translation initiation factor 2B (eIF-2B), which catalyzes GDP-GTP exchange on eIF-2. Furthermore, we show that GCD6 is 30%o identical to the largest subunit of eIF-2B isolated from rabbit reticulocytes. Deletion of either GCD6 or GCD7 is lethal, and nonlethal mutations in these genes increase GCN4 translation in the same fashion described for defects in known subunits of eIF-2 or the GCD complex; derepression of GCN4 is dependent on short open reading frames in the GCN4 mRNA leader and occurs independently of eIF-2i phosphorylation by protein kinase GCN2, which is normally required to stimulate GCN4 translation. Together, our results provide evidence that GCD6 and GCD7 are subunits of eIF-2B in S. cerevisiae and further implicate this GDP-GTP exchange factor in gene-specific translational control.In response to starvation for an amino acid, the budding yeast Saccharomyces cerevisiae increases expression of the GCN4 protein, which in turn activates transcription of more than 30 genes encoding enzymes involved in amino acid biosynthesis (general amino acid control). The increase in GCN4 expression occurs primarily at the level of translation initiation (for a review, see references 22, 24, and 25) and involves a pathway of positive and negative regulatory factors, some of which have general functions in translation initiation (Fig. 1).A reduction in the activity of eukaryotic translation initiation factor 2 (eIF-2) appears to be responsible for increasing GCN4 translation in amino acid-starved cells (25 Exchange factor eIF-2B isolated from rabbit reticulocytes is composed of five subunits and copurifies with a fraction of eIF-2 (29, 36). A complex associated with eIF-2 that contains GCD1, GCD2, and GCN3 was postulated to be the GTP-GDP exchange factor for eIF-2 in S. cerevisiae (6,15). The GCD1 and GCD2 subunits of this "GCD complex" have essential functions in translation initiation in S. cerevisiae (6,15,56). Nonlethal mutations in these factors lead to increased GCN4 expression under nonstarvation conditions, as would be expected of mutations in subunits of eIF-2B that reduce guanine nucleotide exchange on eIF-2 and thereby lower eIF-2 activity.Four upstream open reading frames (uORFs) in the leader of GCN4 mRNA couple GCN4 translation to the level of eIF-2 activity (22,23). Under nonstarvation conditions, it appears that ribosomes scanning from the 5' end of GCN4 mRNA translate the first ORF (uORF1) and reinitiate at one of the remaining uORFs, -2, -3, or -4, instead of at GCN4.Because of the low level of eIF-2. GTP. tRN...

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“…Mutant alleles were introduced into the JC482 background by at least seven serial backcrosses or by transformation. The cdc3-1 allele in YLK271 was derived from SLTD3-6B (Johnson et al, 1987). The cla4::TRP1 allele in JRL55 was derived from strain TRY-1D (Richman et al, 1999).…”

Section: Yeast Strains Media and Reagentsmentioning

confidence: 99%

Role of the Septin Ring in the Asymmetric Localization of Proteins at the Mother-Bud Neck inSaccharomyces cerevisiae

Kozubowski

Larson

Tatchell

2005

MBoC

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In the yeast Saccharomyces cerevisiae, septins form a scaffold in the shape of a ring at the future budding site that rearranges into a collar at the mother-bud neck. Many proteins bind asymmetrically to the septin collar. We found that the protein Bni4-CFP was located on the exterior of the septin ring before budding and on the mother side of the collar after budding, whereas the protein kinase Kcc4-YFP was located on the interior of the septin ring before budding and moved into the bud during the formation of the septin collar. Unbudded cells treated with the actin inhibitor latrunculin-A assembled cortical caps of septins on which Bni4-CFP and Kcc4-YFP colocalized. Bni4-CFP and Kcc4-YFP also colocalized on cortical caps of septins found in strains deleted for the genes encoding the GTPase activating proteins of Cdc42 (RGA1, RGA2, and BEM3). However, Bni4-CFP and Kcc4-YFP were still partially separated in mutants (gin4, elm1, cla4, and cdc3-1) in which septin morphology was severely disrupted in other ways. These observations provide clues to the mechanisms for the asymmetric localization of septin-associated proteins.

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Mapping of the Saccharomyces cerevisiae CDC3, CDC25, and CDC42 genes to chromosome XII by chromosome blotting and tetrad analysis

Cited by 29 publications

References 27 publications

A nuclear mutation defective in mitochondrial recombination in yeast.

A nuclear mutation defective in mitochondrial recombination in yeast.

Evidence that GCD6 and GCD7, translational regulators of GCN4, are subunits of the guanine nucleotide exchange factor for eIF-2 in Saccharomyces cerevisiae.

Role of the Septin Ring in the Asymmetric Localization of Proteins at the Mother-Bud Neck inSaccharomyces cerevisiae

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