G. I. Lang

This study uses experimental evolution in yeast to identify compensatory mutations that alleviate the effects of human disease-associated PMM2 mutations.

The paper identifies adaptive mutations in diploid yeast by analyzing fitness effects of evolved mutations and finds that overdominant and partially dominant mutations contribute to short-term adaptation.

The paper shows that overdominant mutations limit loss of heterozygosity at linked loci in yeast, leading to varied evolutionary outcomes.

The paper uses evolutionary replay experiments to identify and validate positive genetic interactions involving KEL1 mutations in yeast, showing these interactions are not detected by loss-of-function methods.

The paper studies nontransitive fitness evolution in yeast, showing that adaptive mutations in nuclear and viral genomes lead to nontransitive interactions where evolved clones outcompete ancestors but lose to distant ancestors.

This study shows that genome duplication in haploid yeast provides immediate fitness benefits but reduces long-term adaptability.

This study shows that diploid yeast adaptation is slower and biased towards dominant mutations due to restricted access to beneficial mutations.

The paper identifies non-adaptive mutations and synergistic epistasis in yeast populations using bulk-segregant analysis of 11 lineages.