A comparative study of the ori sequences from the mitochondrial genomes of twenty wild-type yeast strains

Gene ◽  
1984 ◽  
Vol 32 (3) ◽  
pp. 459-473 ◽  
Author(s):  
Godeleine Faugeron-Fonty ◽  
Caroline Le Van Kim ◽  
Miklos de Zamaroczy ◽  
Regina Goursot ◽  
Giorgio Bernardi
2000 ◽  
Vol 20 (7) ◽  
pp. 2378-2384 ◽  
Author(s):  
Rolf J. Craven ◽  
Thomas D. Petes

ABSTRACT Yeast strains with a mutation in the MEC1 gene are deficient in the cellular checkpoint response to DNA-damaging agents and have short telomeres (K. B. Ritchie, J. C. Mallory, and T. D. Petes, Mol. Cell. Biol. 19:6065–6075, 1999; T. A. Weinert, G. L. Kiser, and L. H. Hartwell, Genes Dev. 8:652–665, 1994). In wild-type yeast cells, genes inserted near the telomeres are transcriptionally silenced (D. E. Gottschling, O. M. Aparichio, B. L. Billington, and V. A. Zakian, Cell 63:751–762, 1990). We show that mec1strains have reduced ability to silence gene expression near the telomere. This deficiency was alleviated by the sml1mutation. Overexpression of Mec1p also resulted in a silencing defect, although this overexpression did not affect the checkpoint function of Mec1p. Telomeric silencing was not affected by mutations in several other genes in the Mec1p checkpoint pathway (null mutations inRAD9 and CHK1 or in several hypomorphicrad53 alleles) but was reduced by a null mutation ofDUN1. In addition, the loss of telomeric silencing inmec1 strains was not a consequence of the slightly shortened telomeres observed in these strains.


2015 ◽  
Vol 43 (3) ◽  
pp. 227-235 ◽  
Author(s):  
Seong Yeol Baek ◽  
You Jung Lee ◽  
Myoung-Dong Kim ◽  
Jae-Hyoung Yi ◽  
Ji-Young Mun ◽  
...  

1998 ◽  
Vol 18 (11) ◽  
pp. 6548-6559 ◽  
Author(s):  
Christine E. Brown ◽  
Alan B. Sachs

ABSTRACT We report that newly synthesized mRNA poly(A) tails are matured to precise lengths by the Pab1p-dependent poly(A) nuclease (PAN) ofSaccharomyces cerevisiae. These results provide evidence for an initial phase of mRNA deadenylation that is required for poly(A) tail length control. In RNA 3′-end processing extracts lacking PAN, transcripts are polyadenylated to lengths exceeding 200 nucleotides. By contrast, in extracts containing PAN, transcripts were produced with the expected wild-type poly(A) tail lengths of 60 to 80 nucleotides. The role for PAN in poly(A) tail length control in vivo was confirmed by the finding that mRNAs are produced with longer poly(A) tails in PAN-deficient yeast strains. Interestingly, wild-type yeast strains were found to produce transcripts which varied in their maximal poly(A) tail length, and this message-specific length control was lost in PAN-deficient strains. Our data support a model whereby mRNAs are polyadenylated by the 3′-end processing machinery with a long tail, possibly of default length, and then in a PAN-dependent manner, the poly(A) tails are rapidly matured to a message-specific length. The ability to control the length of the poly(A) tail for newly expressed mRNAs has the potential to be an important posttranscriptional regulatory step in gene expression.


BMC Genomics ◽  
2008 ◽  
Vol 9 (1) ◽  
pp. 524 ◽  
Author(s):  
Laura Carreto ◽  
Maria F Eiriz ◽  
Ana C Gomes ◽  
Patrícia M Pereira ◽  
Dorit Schuller ◽  
...  

Genetics ◽  
1996 ◽  
Vol 144 (2) ◽  
pp. 495-510 ◽  
Author(s):  
B K Haarer ◽  
A Corbett ◽  
Y Kweon ◽  
A S Petzold ◽  
P Silver ◽  
...  

Abstract Replacement of the wild-type yeast profilin gene (PFY1) with a mutated form (pfy1-111) that has codon 72 changed to encode glutamate rather than arginine results in defects similar to, but less severe than, those that result from complete deletion of the profilin gene. We have used a colony color-sectoring assay to identify mutations that cause pfy1-111, but not wild-type, cells to be inviable. These profilin synthetic lethal (psl) mutations result in various degrees of abnormal growth, morphology, and temperature sensitivity in PFY1 cells. We have examined psl1 strains in the most detail. Interestingly, these strains display a diploid-specific defect in bud-site selection; haploid strains bud normally, while homozygous diploid strains show a dramatic increase in random budding. We discovered that PSL1 is the late secretory gene, SEC3, and have found that mutations in several other late secretory genes are also synthetically lethal with pfy1-111. Our results are likely to reflect an interdependence between the actin cytoskeleton and secretory processes in directing cell polarity and growth. Moreover, they indicate that the secretory pathway is especially crucial for maintaining budding polarity in diploids.


1978 ◽  
Vol 119 (2) ◽  
pp. 213-235 ◽  
Author(s):  
Godeleine Fonty ◽  
Regina Goursot ◽  
David Wilkie ◽  
Giorgio Bernardi

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