Andrew G. Dillin

The paper identifies FMIL-1 as a gene that directs synapse formation in a C. elegans nociceptive circuit by promoting connectivity between PVD neurons and PVC/AVA interneurons.

This study shows that E. faecalis activates the UPRMT in C. elegans through metabolic and oxidative stress, not direct mitochondrial damage.

This study shows that aging reduces 2,6-linked sialic acids on T cells, leading to exhaustion and impaired immune function.

This study shows that macroautophagy-induced lysosomal damage limits quiescent cell re-entry, and reducing this damage can enhance cell cycle re-entry in C. elegans and mammalian cells.

The paper uses CRISPR screens and lectin microarrays to identify TM9SF3 and the CCC complex as novel regulators of high mannose N-glycan synthesis.

The paper shows that germline mitochondria mediate neuron-to-peripheral UPRMT signaling in C. elegans by responding to mitokines like WNT and serotonin and regulating lipid metabolic pathways.

This study shows that the olfactory nervous system in C. elegans regulates mitochondrial function and stress responses through mitophagy and the UPRMT pathway.

This study shows glial cells control autophagy and metabolism in C. elegans through non-autonomous activation of HLH-30 in the intestine.

This study shows glial cells in C. elegans sense mitochondrial stress and signal to neurons to improve protein homeostasis and longevity.

This study identifies SKN-1 as a metabolic surveillance factor that responds to amino acid catabolism to influence stress resistance in C. elegans.

This paper shows that glia in C. elegans can induce a heat shock response in peripheral cells, increasing lifespan and stress resistance, independent of neurons and neurotransmitters.

This study shows that twnk-1 in C. elegans is not the mitochondrial DNA replicative helicase, but instead has alternative mitochondrial functions.

This study shows BBB dysfunction in aging leads to TGF-beta hyperactivation in astrocytes, causing neural dysfunction, which can be reversed by inhibiting TGF-beta signaling.