The effect of zygotic bud position on the transmission of mitochondrial genes in Saccharomyces cerevisiae

1978 ◽  
Vol 163 (2) ◽  
pp. 131-144 ◽  
Author(s):  
Robert L. Strausberg ◽  
Philip S. Perlman
Keyword(s):  
Saccharomyces Cerevisiae ◽  
Mitochondrial Genes ◽  
Bud Position

Transcriptional analysis of the Saccharomyces cerevisiae mitochondrial var1 gene: anomalous hybridization of RNA from AT-rich regions

1983 ◽  
Vol 3 (9) ◽  
pp. 1615-1624
Author(s):  
H P Zassenhaus ◽  
F Farrelly ◽  
M E Hudspeth ◽  
L I Grossman ◽  
R A Butow
Keyword(s):  
Saccharomyces Cerevisiae ◽  
Mitochondrial Genes ◽  
Transcriptional Analysis ◽  
Asymmetric Distribution ◽  
Direct Function ◽  
Important Conclusion ◽  
The Family ◽  
Var1 Gene ◽  
Flanking Sequences ◽  
Transcription Map

A family of mitochondrial RNAs hybridizes specifically to the var1 region on Saccharomyces cerevisiae mitochondrial DNA (Farrelly et al., J. Biol. Chem. 257:6581-6587, 1982). We constructed a fine-structure transcription map of this region by hybridizing DNA probes containing different portions of the var1 region and some flanking sequences to mitochondrial RNAs isolated from var1-containing petites. We also report the nucleotide sequence of more than 1.2 kilobases of DNA flanking the var1 gene. Our primary findings are: (i) The family of RNAs we detect with homology to var1 DNA is colinear with the var1 gene. Their direction of transcription is olil to cap, as it is for most other mitochondrial genes. (ii) Extensive hybridization anomalies are present, most likely due to the high A-T (A-U) content of the hybridizing species and to the asymmetric distribution of their G-C residues. An important conclusion is that failure to detect transcripts from A-T-rich regions of the yeast mitochondrial genome by standard blot transfer hybridizations cannot be interpreted to mean that such sequences, which are commonly supposed to be spacer DNA, are noncoding or lack direct function in the expression of mitochondrial genes.

scholarly journals Bud8p and Bud9p, Proteins That May Mark the Sites for Bipolar Budding in Yeast

2001 ◽  
Vol 12 (8) ◽  
pp. 2497-2518 ◽  
Author(s):  
Heidi A. Harkins ◽  
Nicolas Pagé ◽  
Laura R. Schenkman ◽  
Claudio De Virgilio ◽  
Sidney Shaw ◽  
...  
Keyword(s):  
Saccharomyces Cerevisiae ◽  
Double Mutant ◽  
Previous Analysis ◽  
Integral Membrane Proteins ◽  
Cell Cortex ◽  
Daughter Cells ◽  
Distal Pole ◽  
Bud Position ◽  
Bud Site ◽  
Hydrophilic Domain

The bipolar budding pattern of a /α Saccharomyces cerevisiae cells appears to depend on persistent spatial markers in the cell cortex at the two poles of the cell. Previous analysis of mutants with specific defects in bipolar budding identifiedBUD8 and BUD9 as potentially encoding components of the markers at the poles distal and proximal to the birth scar, respectively. Further genetic analysis reported here supports this hypothesis. Mutants deleted for BUD8 orBUD9 grow normally but bud exclusively from the proximal and distal poles, respectively, and the double-mutant phenotype suggests that the bipolar budding pathway has been totally disabled. Moreover, overexpression of these genes can cause either an increased bias for budding at the distal (BUD8) or proximal (BUD9) pole or a randomization of bud position, depending on the level of expression. The structures and localizations of Bud8p and Bud9p are also consistent with their postulated roles as cortical markers. Both proteins appear to be integral membrane proteins of the plasma membrane, and they have very similar overall structures, with long N-terminal domains that are both N- andO-glycosylated followed by a pair of putative transmembrane domains surrounding a short hydrophilic domain that is presumably cytoplasmic. The putative transmembrane and cytoplasmic domains of the two proteins are very similar in sequence. When Bud8p and Bud9p were localized by immunofluorescence and tagging with GFP, each protein was found predominantly in the expected location, with Bud8p at presumptive bud sites, bud tips, and the distal poles of daughter cells and Bud9p at the necks of large-budded cells and the proximal poles of daughter cells. Bud8p localized approximately normally in several mutants in which daughter cells are competent to form their first buds at the distal pole, but it was not detected in abni1 mutant, in which such distal-pole budding is lost. Surprisingly, Bud8p localization to the presumptive bud site and bud tip also depends on actin but is independent of the septins.

scholarly journals Transcriptional analysis of the Saccharomyces cerevisiae mitochondrial var1 gene: anomalous hybridization of RNA from AT-rich regions.

1983 ◽  
Vol 3 (9) ◽  
pp. 1615-1624 ◽  
Author(s):  
H P Zassenhaus ◽  
F Farrelly ◽  
M E Hudspeth ◽  
L I Grossman ◽  
R A Butow
Keyword(s):  
Saccharomyces Cerevisiae ◽  
Mitochondrial Genes ◽  
Transcriptional Analysis ◽  
Asymmetric Distribution ◽  
Direct Function ◽  
Important Conclusion ◽  
The Family ◽  
Var1 Gene ◽  
Flanking Sequences ◽  
Transcription Map

A family of mitochondrial RNAs hybridizes specifically to the var1 region on Saccharomyces cerevisiae mitochondrial DNA (Farrelly et al., J. Biol. Chem. 257:6581-6587, 1982). We constructed a fine-structure transcription map of this region by hybridizing DNA probes containing different portions of the var1 region and some flanking sequences to mitochondrial RNAs isolated from var1-containing petites. We also report the nucleotide sequence of more than 1.2 kilobases of DNA flanking the var1 gene. Our primary findings are: (i) The family of RNAs we detect with homology to var1 DNA is colinear with the var1 gene. Their direction of transcription is olil to cap, as it is for most other mitochondrial genes. (ii) Extensive hybridization anomalies are present, most likely due to the high A-T (A-U) content of the hybridizing species and to the asymmetric distribution of their G-C residues. An important conclusion is that failure to detect transcripts from A-T-rich regions of the yeast mitochondrial genome by standard blot transfer hybridizations cannot be interpreted to mean that such sequences, which are commonly supposed to be spacer DNA, are noncoding or lack direct function in the expression of mitochondrial genes.

scholarly journals Product of Saccharomyces cerevisiae nuclear gene PET494 activates translation of a specific mitochondrial mRNA.

1986 ◽  
Vol 6 (11) ◽  
pp. 3694-3703 ◽  
Author(s):  
M C Costanzo ◽  
T D Fox
Keyword(s):  
Saccharomyces Cerevisiae ◽  
Fusion Protein ◽  
Mitochondrial Gene ◽  
Nuclear Gene ◽  
Mitochondrial Genes ◽  
Wild Type ◽  
Site Of Action ◽  
Flanking Sequences ◽  
Untranslated Leaders ◽  
Beta Galactosidase

The product of Saccharomyces cerevisiae nuclear gene PET494 is known to be required for a posttranscriptional step in the accumulation of one mitochondrial gene product, subunit III of cytochrome c oxidase (coxIII). Here we show that the PET494 protein probably acts in mitochondria by demonstrating that both a PET494-beta-galactosidase fusion protein and unmodified PET494 are specifically associated with mitochondria. To define the PET494 site of action, we isolated mutations that suppress a pet494 deletion. These mutations were rearrangements of the mitochondrial gene oxi2 that encodes coxIII. The suppressor oxi2 genes had acquired the 5'-flanking sequences of other mitochondrial genes and gave rise to oxi2 transcripts carrying the 5'-untranslated leaders of their mRNAs. These results demonstrate that in wild-type cells PET494 specifically promotes coxIII translation, probably by interacting with the 5'-untranslated leader of the oxi2 mRNA.

scholarly journals Influence of the nuclear gene tmp3 on the loss of mitochondrial genes in Saccharomyces cerevisiae.

1982 ◽  
Vol 2 (4) ◽  
pp. 457-466 ◽  
Author(s):  
R Zelikson ◽  
M Luzzati
Keyword(s):  
Saccharomyces Cerevisiae ◽  
Mitochondrial Genome ◽  
Dihydrofolate Reductase ◽  
Nuclear Gene ◽  
Mitochondrial Genes ◽  
Enzyme Complex ◽  
Mitochondrial Enzyme ◽  
High Concentration ◽  
Rapid Loss ◽  
Specific Loss

The Saccharomyces cerevisiae tmp3 mutant is deficient in the mitochondrial enzyme complex that participates in the formation of one-carbon-group-tetrahydrofolate coenzymes, serine transhydroxymethylase, dihydrofolate reductase, and thymidylate synthetase, thus leading to multiple nutritional requirements of dTMP, adenine, histidine, and methionine. The tmp3 mutant quickly loses its mitochondrial genome even when grown on fully supplemented medium or on a high concentration of 5-formyl tetrahydrofolate, which replaces all the four requirements. A study of the loss of the mitochondrial genome by following several mitochondrial genetic markers showed that there was a preferential specific loss of a large region of the mitochondrial genome, covering mit ts983, Er, Cr, and mit ts982 up to OrI, and retention of the region of Pr and mit tscs1297. A kinetic study showed that there was a preferentially rapid loss of the region covering the mit+ alleles ts983 to tscs902 at the rate of 10% per generation.

Mapping of mitochondrial genes in Saccharomyces cerevisiae

1976 ◽  
Vol 146 (2) ◽  
pp. 117-132 ◽  
Author(s):  
R. J. Schweyen ◽  
U. Steyrer ◽  
F. Kaudewitz ◽  
B. Dujon ◽  
P. P. Slonimski
Keyword(s):  
Saccharomyces Cerevisiae ◽  
Mitochondrial Genes

Influence of the nuclear gene tmp3 on the loss of mitochondrial genes in Saccharomyces cerevisiae

1982 ◽  
Vol 2 (4) ◽  
pp. 457-466
Author(s):  
R Zelikson ◽  
M Luzzati
Keyword(s):  
Saccharomyces Cerevisiae ◽  
Mitochondrial Genome ◽  
Dihydrofolate Reductase ◽  
Nuclear Gene ◽  
Mitochondrial Genes ◽  
Enzyme Complex ◽  
Mitochondrial Enzyme ◽  
High Concentration ◽  
Rapid Loss ◽  
Specific Loss

The Saccharomyces cerevisiae tmp3 mutant is deficient in the mitochondrial enzyme complex that participates in the formation of one-carbon-group-tetrahydrofolate coenzymes, serine transhydroxymethylase, dihydrofolate reductase, and thymidylate synthetase, thus leading to multiple nutritional requirements of dTMP, adenine, histidine, and methionine. The tmp3 mutant quickly loses its mitochondrial genome even when grown on fully supplemented medium or on a high concentration of 5-formyl tetrahydrofolate, which replaces all the four requirements. A study of the loss of the mitochondrial genome by following several mitochondrial genetic markers showed that there was a preferential specific loss of a large region of the mitochondrial genome, covering mit ts983, Er, Cr, and mit ts982 up to OrI, and retention of the region of Pr and mit tscs1297. A kinetic study showed that there was a preferentially rapid loss of the region covering the mit+ alleles ts983 to tscs902 at the rate of 10% per generation.

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