Costs, benefits and redundant mechanisms of adaption to chronic low-dose stress in yeast

Markiewicz-Potoczny, Marta; Lydall, David

doi:10.1080/15384101.2016.1218104

Cited by 9 publications

(7 citation statements)

References 81 publications

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“…Consistent with this we recently reported that cdc13-1 mutants lacking RAD9 or EXO1 retain the ability to adapt to low level telomere damage (Markiewicz-Potoczny and Lydall, 2016).…”

Section: Discussionsupporting

confidence: 81%

Systematic analysis of the effects of the DNA damage response network in telomere defective budding yeast

Holstein¹,

Ngo

Lawless³

et al. 2017

Preprint

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Functional telomeres are critically important to eukaryotic genetic stability. Budding yeast is a powerful model organism for genetic analysis and yeast telomeres are maintained by very similar mechanisms to human telomeres. Scores of proteins and pathways are known to affect telomere function. Here, we report a series of related genome-wide genetic interaction screens performed on budding yeast cells with acute or chronic telomere defects. We examined genetic interactions in cells defective in Cdc13 and Stn1, affecting two components of CST, a single stranded DNA (ssDNA) binding complex that binds telomeric DNA. We investigated genetic interactions in cells with defects in Rfa3, affecting the major ssDNA binding protein, RPA, which has overlapping functions with CST at telomeres. We also examined genetic interactions in cells lacking EXO1 or RAD9, affecting different aspects of the DNA damage response in a cdc13-1 background. Comparing fitness profiles across the data sets allows us build up a picture of the specific responses to different types of dysfunctional telomeres. Our results show that there is no universal response to telomere defects. To help others engage with the large volumes of data we make the data available via two interactive web-based tools: Profilyzer and DIXY. Among numerous genetic interactions we found the chk1∆ mutation improved fitness of cdc13-1 exo1∆ cells more than other checkpoint mutations (ddc1∆, rad9∆, rad17∆, rad24∆), whereas in cdc13-1 cells the effects of all checkpoint mutations were similar. We find that Chk1 stimulates resection at defective telomeres, revealing a new role for Chk1 in the eukaryotic DNA damage response network.

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“…Consistent with this we recently reported that cdc13-1 mutants lacking RAD9 or EXO1 retain the ability to adapt to low level telomere damage (Markiewicz-Potoczny and Lydall, 2016).…”

Section: Discussionsupporting

confidence: 81%

Systematic analysis of the effects of the DNA damage response network in telomere defective budding yeast

Holstein¹,

Ngo

Lawless³

et al. 2017

Preprint

Self Cite

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show abstract

“…Furthermore, elevating the basal levels of expression for certain stress factors can have a negative impact on other virulence traits [6]. Therefore, the expression of stress functions in the absence of stress does incur a fitness cost [6,7]. Nevertheless, clear examples of microbial stress priming have been reported, as summarised in this review and elsewhere [8], indicating that the fitness advantage conferred by some anticipatory responses outweighs their fitness cost.…”

Section: Microbial Memorymentioning

confidence: 85%

Memory in Fungal Pathogens Promotes Immune Evasion, Colonisation, and Infection

Brown

Gow

Warris

et al. 2019

Trends in Microbiology

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By analogy with Pavlov's dogs, certain pathogens have evolved anticipatory behaviours that exploit specific signals in the human host to prepare themselves against imminent host challenges. This adaptive prediction, a type of history-dependent microbial behaviour, represents a primitive form of microbial memory. For fungal pathogens, adaptive prediction helps them circumvent nutritional immunity, protects them against phagocytic killing, and activates immune evasion strategies. We describe how these anticipatory responses, and the contrasting lifestyles and evolutionary trajectories of fungal pathogens, have influenced the evolution of such adaptive behaviours, and how these behaviours affect host colonisation and infection.

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“…, RAD9 and EXO1 ), changes the effects of other genes in the network. Consistent with this, cdc13-1 mutants lacking RAD9 or EXO1 retain the ability to adapt to low-level telomere damage ( Markiewicz-Potoczny and Lydall 2016 ).…”

Section: Discussionmentioning

confidence: 59%

Systematic Analysis of the DNA Damage Response Network in Telomere Defective Budding Yeast

Holstein

Ngo

Lawless

et al. 2017

G3 Genes|Genomes|Genetics

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Functional telomeres are critically important to eukaryotic genetic stability. Scores of proteins and pathways are known to affect telomere function. Here, we report a series of related genome-wide genetic interaction screens performed on budding yeast cells with acute or chronic telomere defects. Genetic interactions were examined in cells defective in Cdc13 and Stn1, affecting two components of CST, a single stranded DNA (ssDNA) binding complex that binds telomeric DNA. For comparison, genetic interactions were also examined in cells with defects in Rfa3, affecting the major ssDNA binding protein, RPA, which has overlapping functions with CST at telomeres. In more complex experiments, genetic interactions were measured in cells lacking EXO1 or RAD9, affecting different aspects of the DNA damage response, and containing a cdc13-1 induced telomere defect. Comparing fitness profiles across these data sets helps build a picture of the specific responses to different types of dysfunctional telomeres. The experiments show that each context reveals different genetic interactions, consistent with the idea that each genetic defect causes distinct molecular defects. To help others engage with the large volumes of data, the data are made available via two interactive web-based tools: Profilyzer and DIXY. One particularly striking genetic interaction observed was that the chk1∆ mutation improved fitness of cdc13-1 exo1∆ cells more than other checkpoint mutations (ddc1∆, rad9∆, rad17∆, and rad24∆), whereas, in cdc13-1 cells, the effects of all checkpoint mutations were similar. We show that this can be explained by Chk1 stimulating resection—a new function for Chk1 in the eukaryotic DNA damage response network.

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Costs, benefits and redundant mechanisms of adaption to chronic low-dose stress in yeast

Cited by 9 publications

References 81 publications

Systematic analysis of the effects of the DNA damage response network in telomere defective budding yeast

Systematic analysis of the effects of the DNA damage response network in telomere defective budding yeast

Memory in Fungal Pathogens Promotes Immune Evasion, Colonisation, and Infection

Systematic Analysis of the DNA Damage Response Network in Telomere Defective Budding Yeast

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