Daniel F. Jarosz

This study shows that a yeast prion domain can induce a heritable state in C. elegans that persists across generations and is reversible.

This study shows that the Ies6 subunit of the INO80 complex exhibits prion-like behavior, which influences metabolic gene expression by altering chromatin structure.

eSIG-Net predicts how single mutations affect protein interactions using a sequence-based interaction language model, outperforming existing methods.

This paper develops a method to edit mitochondrial DNA in yeast using CRISPR by identifying an RNA import motif that enables sgRNA delivery into mitochondria.

The paper shows that protein structure predicts genetic variation and de novo adaptation by analyzing yeast, plants, and humans, and validates predictions with experimental evolution.

The paper identifies ZNF-236 as a key factor maintaining quiescence of stress-induced genes in C. elegans, showing that this silencing is an active genomic state, not passive.

The paper presents a theory predicting which longevity interventions compress relative sickspan by steepening the survival curve, supported by evidence from mice, C. elegans, and Drosophila.

The paper identifies a non-genetic, heritable mechanism of drug resistance in Candida albicans triggered by subtherapeutic fluconazole exposure, which can be reversed and involves prion-like epigenetic processes.

The paper assesses fitness effects of 9,000 natural variants in yeast signaling pathways, finding that many non-neutral variants show signs of local adaptation.

The paper links genome to proteome in yeast progeny to identify variants controlling proteome diversity and predict their fitness effects under stress.

The paper identifies buffer genes in yeast that influence the phenotypic effects of mutations by modulating genetic variation's impact on fitness.

This study profiles protein aggregation in seven tissues of aging killifish, revealing tissue-specific patterns linked to protein biophysics and quality control.

The paper identifies prion-like and phase-separated protein aggregates in aging vertebrate brains using quantitative proteomics in killifish and validates their propagation and functional properties.

This paper identifies a prion, [MIX+], formed by the DNA helicase Mph1/FANCM, which influences genome diversification through DNA damage resistance and meiotic crossover promotion.

This study shows that the prion [BIG+] in yeast increases proliferation but reduces lifespan by altering protein synthesis and translational programs.

The paper identifies a conserved stress response in yeast and human cancers that mitigates the cost of accumulated mutations, suggesting therapeutic targeting potential.

This study identifies a prion-based epigenetic mechanism mediated by the DNA helicase Mph1/FANCM that influences genome integrity and promotes phenotypic diversification.