PNAS Journal Club highlights our work on prions, mutation, and adaptation
A PNAS Journal Club article discusses our 2026 Cell paper and its implications for mutation rates, rapid evolution, and drug resistance.
News from the Jarosz Lab, independent coverage of our research, and selected Stanford features.
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A PNAS Journal Club article discusses our 2026 Cell paper and its implications for mutation rates, rapid evolution, and drug resistance.
A VIB deep dive explains genetic buffering and highlights our finding that Hsp90 changes the effects of thousands of loci, including an unexpectedly large contribution from regulatory variants.
Philip Ball examines how molecular systems buffer the effects of potentially harmful mutations, including our work on how Hsp90 changes the fitness consequences of regulatory variation.
Nature’s daily newsletter highlights the accompanying feature on proteins that buffer mutation effects and their potential relevance to disease.
A feature on discovery-driven basic science discusses our work mapping how molecular variation in unstressed cells can predict responses to future challenges.
Charité coverage of our Science study describes how natural genetic variants remodel the proteome and shape fitness across environments.
How can molecular measurements made in unstressed cells predict what will happen when environments change? In 800 descendants from a cross between two ecologically distinct yeast strains, the team mapped more than 6,400 genetic effects on protein abundance and connected more than 1,600 to individual variants. The resulting genome-to-proteome map revealed pathway-level signatures of natural selection, uncovered coding and regulatory mechanisms that remodel protein levels, and exposed latent variation that was invisible under baseline conditions. Those hidden molecular differences forecasted growth across new environments, including responses to antifungal drugs. The study turns a static catalog of variation into a predictive framework: by measuring how natural variants reorganize the proteome before stress arrives, it becomes possible to anticipate which cellular states will confer fitness when conditions change.
PubMed Stanford Medicine feature Charité coverage Technology Networks Phys.org Publications
Daniel F. Jarosz was appointed the inaugural Senior Associate Dean for Basic Science, a role supporting basic-science faculty and discovery across Stanford Medicine.
A Stanford Medicine feature explores how DNA binding and cell-cycle regulation protect polyglutamine-containing transcription factors from aggregation and suggest ways to counter pathological assemblies.
A Cell Preview by Alexandre P. Magalhaes and Denes Hnisz places our work on DNA binding, mitotic phosphorylation, and polyglutamine assembly in broader context.
Dorothee Dormann and Edward Lemke place our tissue-resolved studies of age-dependent protein aggregation within emerging ideas about intrinsically disordered proteins and biological ageing.
An independent reported feature examines our work mapping age-dependent protein aggregation across tissues and identifying assemblies with prion-like and phase-separation properties.
Coverage of our eLife study explains how a prion can accelerate cellular proliferation while shortening lifespan.
Hiten Madhani’s review includes a dedicated discussion of our chromatin-based prion and its heritable control of transcription.
Stanford Medicine describes how a self-templating protein assembly establishes an active chromatin state that can help cells endure environmental stress.
Iuliia Parfenova and Yves Barral discuss the paired studies defining [SMAUG+] and widespread prion-based control of growth and differentiation strategies.
An invited symposium talk on protein conformational states as durable, non-genetic cellular memories and their roles in disease, development, and evolution.
A Research Highlight covers our single-nucleotide-resolution strategy for identifying causal variants and the biochemical mechanisms that drive phenotypic change.
Stanford Medicine reports how nucleotide-resolution mapping revealed that synonymous and regulatory variants can make unexpectedly large contributions to natural phenotypic diversity.
Shai Slomka and Yitzhak Pilpel discuss our approach for resolving causal natural variants at single-nucleotide resolution.
A feature on our discovery that intrinsically disordered proteins can generate and transmit alternative, sometimes advantageous biological states.
A research summary highlights the bacterial metabolite that induces a heritable, prion-based metabolic state in yeast.
Mick Tuite places our discovery of bacteria-induced [GAR+] formation in the context of microbial communication and prion biology.
Mick Tuite discusses how intrinsically disordered proteins can act as heritable switches without relying on conventional amyloid architecture.
Stanford Medicine reports the discovery of dozens of protein-based switches that can transmit advantageous traits across generations.
German-language coverage describes how bacterial signals can trigger a heritable metabolic state that changes yeast fermentation.
Gemma Staniforth and Mick Tuite discuss the ecological and evolutionary implications of prion-mediated cross-kingdom communication.
A Research Highlight examines evidence that Hsp90-buffered variation contributed to the loss of eyes in cavefish.
Science coverage reports how Hsp90 can conceal genetic variation that becomes phenotypically visible under environmental stress.
Ed Yong explains how environmental change can reveal previously silent variation and help drive rapid morphological evolution.
A feature on how Hsp90 and environmental stress can alter the phenotypic and adaptive consequences of standing genetic variation.
A Nature News Feature examines our evidence that prions are common sources of heritable phenotypic variation in wild yeast.
Science News covers the discovery that wild yeasts frequently use prions to generate heritable traits with context-dependent benefits.
An In Brief highlight covers our work showing how Hsp90 and environmental stress transform the adaptive value of natural genetic variation.
Coverage of work showing how a single amino-acid difference shapes the lesion-bypass activity and fidelity of DinB DNA polymerases.
Earlier lab updates retained with their original publication dates.