William B. Mair

The paper identifies redox regulation of ATG5's Cys19 as critical for autophagy initiation under nutrient restriction in human cells and mice.

This paper identifies a conserved interaction between Rheb and GATOR1 subunits that regulates mTORC1 signaling in response to nutrient stress.

This study identifies nutrient-responsive mitochondrial-derived structures in C. elegans muscle cells induced during refeeding, revealing a role in mitochondrial remodeling and metabolic adaptation.

This study shows that peroxisomal dysfunction during aging reduces metabolic flexibility by impairing mitochondrial dynamics and nutrient responses, which can be mitigated by dietary restriction.

The paper introduces novel genetic tools for live imaging of mitochondrial networks in C. elegans and compares them with existing methods, highlighting their advantages and limitations.

The paper shows that YAP-1 coordinates organ growth with body size in C. elegans to maintain uniform proportions, even under tissue-specific growth inhibition.

This study identifies SRSF1 as a rejuvenation factor through transcriptomic reprogramming, showing it improves cellular function and is linked to longevity.

This study identifies CRTC-1's role in balancing histone trimethylation and acetylation to promote longevity in C. elegans.

The paper confirms that set-2 mutants in C. elegans extend lifespan when fed HT115 E. coli, but not OP50-1, suggesting diet-dependent regulation of COMPASS complex effects on aging.

The paper introduces SKI TRIP, a method for profiling cell type-specific translation in C. elegans using single-copy knock-in of a FLAG-tagged ribosomal subunit.

The paper shows that early life activity of RNA splicing factors and lipid metabolism determine the efficacy of longevity interventions in C. elegans.

This study shows that inhibiting mTORC1 specifically in neurons of C. elegans extends lifespan without causing growth or reproductive impairments.

This study shows that AMPK enhances associative learning in C. elegans by promoting neuronal mitochondrial fusion, which is critical for maintaining neuronal function with age and in neurodegenerative conditions.

The paper introduces a CRISPR/Cas9-based system for inserting single-copy transgenes in C. elegans with tissue-specific regulation.