David H. Meyer

The paper identifies molecular mechanisms that integrate environmental cues to trigger diapause exit in killifish embryos using transcriptomics and chemical screening.

This study shows that ATG-18 overexpression extends C. elegans lifespan and improves stress resilience through the HLH-30 transcription factor, while also revealing a temporal-specific effect on heat stress survival.

Direct reprogramming of skin fibroblasts into neurons reveals unique gene signatures indicative of HIV infection in the context of viral suppression.

The paper investigates gene expression changes during and after dauer diapause in C. elegans, revealing age deceleration and reversal patterns.

This study shows that DREAM complex activity influences somatic mutation burden, lifespan, and age-related disease, with reduced activity linked to longer lifespan and lower disease risk.

The paper shows that hil-1/H1-0, a nutrient-regulated linker histone, mediates resilience and restoration during fasting-refeeding in C. elegans and human cells.

The paper shows that AFD neuron dysfunction in C. elegans alters transposable element (TE) expression, with Mirage transposase induction being a consistent phenotype, while Tc1 mutagenesis depends on background factors.

The paper shows that temperature perception in C. elegans can drive transgenerational epigenetic inheritance through RNAi factors and small RNAs.

The paper shows ASI sensory neurons control the CEP-1/p53 DNA damage response in PGCs via TGF-beta signaling, reducing inherited mutations.

This paper develops a transcriptome-based aging clock for C. elegans with high accuracy, applicable to human age prediction.