The Saccharomyces cerevisiae TRT2 tRNAThr gene upstream of STE6 is a barrier to repression in MAT  cells and exerts a potential tRNA position effect in MATa cells

Simms, Tiffany A.; Miller, Elsy C.; Buisson, Nicolas P.; Jambunathan, Nithya; Donze, David

doi:10.1093/nar/gkh858

Cited by 38 publications

(49 citation statements)

References 47 publications

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“…Three (ACO1, ARO8 and YEL033W) of the six genes showed a consistent but modest modification in transcript level by Northern blot analysis (Conesa et al, 2005). A similar tRNA position effect was also reported initially for the tRNA-Thr(CGU) gene upstream of CBT1 in the native chromosomal locus (Simms et al, 2004). However, more detail subsequent analysis demonstrated that tRNA-Thr(CGU) gene in its natural context serves as an insulator between STE6, an upstream gene, and CBT1, preventing the STE6 regulatory elements from affecting CBT1 transcription (Simms et al, 2008).…”

Section: Accepted M Manuscriptsupporting

confidence: 77%

Maf1, repressor of tRNA transcription, is involved in the control of gluconeogenetic genes in Saccharomyces cerevisiae

Morawiec

Wichtowska

Graczyk

et al. 2013

Gene

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Section: Accepted M Manuscriptsupporting

confidence: 77%

Maf1, repressor of tRNA transcription, is involved in the control of gluconeogenetic genes in Saccharomyces cerevisiae

Morawiec

Wichtowska

Graczyk

et al. 2013

Gene

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“…on adjacent transcription units (Simms et al 2004). In particular, the tRNA gene located adjacent to HMR acts as a barrier to protect nearby genes from the spread of heterochromatin (Donze et al 1999;Donze and Kamakaka 2001).…”

Section: Discussionmentioning

confidence: 99%

A Cis-Acting tRNA Gene Imposes the Cell Cycle Progression Requirement for Establishing Silencing at the HMR Locus in Yeast

Lazarus

Holmes

2011

Genetics

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Numerous studies have determined that the establishment of Sir protein-dependent transcriptional silencing in yeast requires progression through the cell cycle. In our study we examined the cell cycle requirement for the establishment of silencing at the HML and HMR loci using strains bearing conditional or inducible SIR3 alleles. Consistent with prior reports, we observed that establishing silencing at HMR required progression through the cell cycle. Unexpectedly, we found that the HML locus is far less dependent on cell cycle progression to establish silencing. Seeking cis-acting elements that could account for this difference, we found that deletion of a tRNA gene that serves as a chromatin boundary at HMR abolishes the cell cycle progression requirement at this locus, while insertion of sequences containing this tRNA gene adjacent to HML imposes dependence on cell cycle progression for the full establishment of silencing. Our results indicate that the cell cycle progression requirement is not a property intrinsic to the formation of heterochromatin in yeast, but is instead a cis-limited, locus-specific phenomenon. We show that inactivation of the Scc1 cohesin also abolishes the requirement for cell cycle progression and test models based on a possible link between the tRNA gene and cohesin association.

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“…Alternatively, SUP4-o may be specifically acting as an initiator or terminator of gene-conversion tracts. In yeast, tRNA genes can cause replication fork pausing (Deshpande and Newlon 1996;Dubarry et al 2011), and can act as chromatin silencing barriers or insulators (Simms et al 2004;Simms et al 2008). tRNA gene sites are weakly recombinogenic when RNAP III collides with DNA polymerase (de la Loza et al 2009); and when essential replication genes are downregulated, Ty retrotransposons and tRNA genes are frequently found together at the breakpoints of chromosome rearrangements -indicates no replication stress, + indicates a low level of replication stress, and +++ indicates high levels of replication stress.…”

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confidence: 99%

Remarkably Long-Tract Gene Conversion Induced by Fragile Site Instability inSaccharomyces cerevisiae

Chumki¹,

Dunn²,

Coates³

et al. 2016

Genetics

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Replication stress causes breaks at chromosomal locations called common fragile sites. Deletions causing loss of heterozygosity (LOH) in human tumors are strongly correlated with common fragile sites, but the role of gene conversion in LOH at fragile sites in tumors is less well studied. Here, we investigated gene conversion stimulated by instability at fragile site FS2 in the yeast Saccharomyces cerevisiae. In our screening system, mitotic LOH events near FS2 are identified by production of red/white sectored colonies. We analyzed single nucleotide polymorphisms between homologs to determine the cause and extent of LOH. Instability at FS2 increases gene conversion 48-to 62-fold, and conversions unassociated with crossover represent 6-7% of LOH events. Gene conversion can result from repair of mismatches in heteroduplex DNA during synthesis-dependent strand annealing (SDSA), double-strand break repair (DSBR), and from break-induced replication (BIR) that switches templates [double BIR (dBIR)]. It has been proposed that SDSA and DSBR typically result in shorter gene-conversion tracts than dBIR. In cells under replication stress, we found that bidirectional tracts at FS2 have a median length of 40.8 kb and a wide distribution of lengths; most of these tracts are not crossover-associated. Tracts that begin at the fragile site FS2 and extend only distally are significantly shorter. The high abundance and long length of noncrossover, bidirectional gene-conversion tracts suggests that dBIR is a prominent mechanism for repair of lesions at FS2, thus this mechanism is likely to be a driver of common fragile site-stimulated LOH in human tumors.KEYWORDS loss of heterozygosity; gene conversion; BIR; fragile site; homologous recombination D NA integrity is frequently challenged by chemical, environmental, and physical agents, as well as by endogenous factors. Common fragile sites are one source of endogenous damage, causing DNA instability and breaks under conditions of replication stress when DNA replication is partially inhibited (Durkin and Glover 2007;Sarni and Kerem 2016). Replication stress has typically been induced experimentally by treating cells with the polymerase inhibitor aphidicolin (Glover et al. 1984) or by genetically lowering the levels of DNA polymerases Lemoine et al. 2008). In vivo, replication stress has been observed early in the process of tumor development as a result of alteration of replication fork progression and nucleotide deficiency caused by activation of oncogenes (Di Micco et al. 2006;Bester et al. 2011). In cancer cells, human common fragile sites are hotspots for chromosomal deletions, amplifications, and rearrangements (Burrow et al. 2009;Drusco et al. 2011; OzeriGalai et al. 2011 OzeriGalai et al. , 2012, and a large-scale screen of deletions in 746 cancer cell lines reported that many areas of unexplained deletions are in fragile sites (Bignell et al. 2010).The alterations at human common fragile sites in cancer cells are proposed to result from the processes of DNA repair at...

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The Saccharomyces cerevisiae TRT2 tRNAThr gene upstream of STE6 is a barrier to repression in MAT cells and exerts a potential tRNA position effect in MATa cells

Cited by 38 publications

References 47 publications

Maf1, repressor of tRNA transcription, is involved in the control of gluconeogenetic genes in Saccharomyces cerevisiae

Maf1, repressor of tRNA transcription, is involved in the control of gluconeogenetic genes in Saccharomyces cerevisiae

A Cis-Acting tRNA Gene Imposes the Cell Cycle Progression Requirement for Establishing Silencing at the HMR Locus in Yeast

Remarkably Long-Tract Gene Conversion Induced by Fragile Site Instability inSaccharomyces cerevisiae

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