scholarly journals Author response: The genetic basis of aneuploidy tolerance in wild yeast

2019 ◽  
Author(s):  
James Hose ◽  
Leah E Escalante ◽  
Katie J Clowers ◽  
H Auguste Dutcher ◽  
DeElegant Robinson ◽  
...  
Keyword(s):  
Genetic Basis ◽  
Author Response ◽  
Wild Yeast

scholarly journals Author response: Dosage compensation can buffer copy-number variation in wild yeast

2015 ◽  
Author(s):  
James Hose ◽  
Chris Mun Yong ◽  
Maria Sardi ◽  
Zhishi Wang ◽  
Michael A Newton ◽  
...  
Keyword(s):  
Copy Number Variation ◽  
Dosage Compensation ◽  
Copy Number ◽  
Author Response ◽  
Wild Yeast ◽  
Number Variation

scholarly journals The genetic basis of aneuploidy tolerance in wild yeast

eLife ◽  
2020 ◽  
Vol 9 ◽  
Author(s):  
James Hose ◽  
Leah E Escalante ◽  
Katie J Clowers ◽  
H Auguste Dutcher ◽  
DeElegant Robinson ◽  
...  
Keyword(s):  
Saccharomyces Cerevisiae ◽  
Drug Treatment ◽  
Genetic Basis ◽  
Rna Binding ◽  
Laboratory Strain ◽  
Pathogenic Fungi ◽  
Wild Type ◽  
Wild Yeast ◽  
Mechanistic Understanding

Aneuploidy is highly detrimental during development yet common in cancers and pathogenic fungi – what gives rise to differences in aneuploidy tolerance remains unclear. We previously showed that wild isolates of Saccharomyces cerevisiae tolerate chromosome amplification while laboratory strains used as a model for aneuploid syndromes do not. Here, we mapped the genetic basis to Ssd1, an RNA-binding translational regulator that is functional in wild aneuploids but defective in laboratory strain W303. Loss of SSD1 recapitulates myriad aneuploidy signatures previously taken as eukaryotic responses. We show that aneuploidy tolerance is enabled via a role for Ssd1 in mitochondrial physiology, including binding and regulating nuclear-encoded mitochondrial mRNAs, coupled with a role in mitigating proteostasis stress. Recapitulating ssd1Δ defects with combinatorial drug treatment selectively blocked proliferation of wild-type aneuploids compared to euploids. Our work adds to elegant studies in the sensitized laboratory strain to present a mechanistic understanding of eukaryotic aneuploidy tolerance.

Author response for "The genetic basis of oral leukoplakia and its key role in understanding oral carcinogenesis"

2020 ◽  
Author(s):  
Letícia Martins Guimarães ◽  
Marina Gonçalves Diniz ◽  
Sílvia Regina Rogatto ◽  
Ricardo Santiago Gomez ◽  
Carolina Cavalieri Gomes
Keyword(s):  
Genetic Basis ◽  
Oral Leukoplakia ◽  
Author Response ◽  
Oral Carcinogenesis

scholarly journals Author response: A genetic basis for molecular asymmetry at vertebrate electrical synapses

2017 ◽  
Author(s):  
Adam C Miller ◽  
Alex C Whitebirch ◽  
Arish N Shah ◽  
Kurt C Marsden ◽  
Michael Granato ◽  
...  
Keyword(s):  
Genetic Basis ◽  
Author Response ◽  
Electrical Synapses ◽  
Molecular Asymmetry

scholarly journals Author response: DNA methylation in Arabidopsis has a genetic basis and shows evidence of local adaptation

2015 ◽  
Author(s):  
Manu J Dubin ◽  
Pei Zhang ◽  
Dazhe Meng ◽  
Marie-Stanislas Remigereau ◽  
Edward J Osborne ◽  
...  
Keyword(s):  
Dna Methylation ◽  
Local Adaptation ◽  
Genetic Basis ◽  
Author Response

scholarly journals Evolution of Natural Lifespan Variation and Molecular Strategies of Extended Lifespan

2021 ◽  
Vol 5 (Supplement_1) ◽  
pp. 32-33
Author(s):  
Alaattin Kaya
Keyword(s):  
Caloric Restriction ◽  
Genetic Basis ◽  
Epigenetic Landscape ◽  
Intermediary Metabolites ◽  
Replicative Lifespan ◽  
Nad Metabolism ◽  
Wild Yeast ◽  
Lifespan Variation ◽  
Extended Lifespan ◽  
Selective Forces

Abstract To understand the genetic basis and the selective forces acting on longevity, it is useful to employ ecologically diverse individuals of the same species, widely different in lifespan. This way, we may capture the experiment of Nature that modifies the genotype arriving at different lifespans. Here, we analyzed 76 ecologically diverse wild yeast isolates and discovered wide diversity of lifespan. We sequenced the genomes of these organisms and analyzed how their replicative lifespan is shaped by nutrients and transcriptional and metabolite patterns. By identifying genes, proteins and metabolites that correlate with longevity across these isolates, we found that long-lived strains elevate intermediary metabolites, differentially regulate genes involved in NAD metabolism and adjust control of epigenetic landscape through conserved, rare histone modifier. Our data further offer insights into the evolution and mechanisms by which caloric restriction regulates lifespan by modulating the availability of nutrients without decreasing fitness.

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