atg-16.2

1. atg-16.2 is required for lifespan in worms.

   “is required for the increased exopher biogenesis, reduction in polyQ aggregate load, and lifespan extension induced by neuronal inhibition of early-acting autophagy genes.”

   Model organismsneuronal inhibition of early-acting autophagy genesneuron

   Neuronal waste management: new roles for autophagy genes in the extrusion of protein aggregates and in longevity

   Autophagy·Feb 27, 2024

2. atg-16.2 is required for lifespan in worms.

   “Lifespan extension, reduction in PolyQ aggregates and increase in exophers were absent in atg-16.2 null mutants”

   Model organismslifespan extension by inhibiting neuronal early-acting autophagy genes

   Autophagy protein ATG-16.2 and its WD40 domain mediate the beneficial effects of inhibiting early-acting autophagy genes in C. elegans neurons

   Nature aging·Jan 4, 2024

3. atg-16.2 is required for lifespan in worms.

   “atg-16.2 was required for the effects of early autophagy gene reduction on neuronal PolyQ aggregation, exopher formation, and lifespan.”

   Model organismsrequired for lifespan extension following early autophagy gene reductionneuron

   Inhibition of early-acting autophagy genes in C. elegans neurons improves protein homeostasis, promotes exopher production, and extends lifespan via the ATG-16.2 WD40 domain

   bioRxiv (Cold Spring Harbor Laboratory)·Dec 14, 2022Preprint

1. atg-16.2 is required for thermotolerance in worms.

   “found the WD40 domain to be selectively required for thermotolerance induced by germline removal”

   Model organismsthermotolerance induced by germline removal; shown by deletion of the WD40 domain

   Protein segment supports cellular waste breakdown in worms

   bioRxiv·Oct 20, 2026Preprint

1. atg-16.2 decreases lysosomal membrane damage in worms.

   “the ATG-16.2 WD40 domain was also critical in limiting lysosomal membrane damage after acute heat stress.”

   Model organismsafter acute heat stress; shown by deletion of the WD40 domain

   Protein segment supports cellular waste breakdown in worms

   bioRxiv·Oct 20, 2026Preprint

1. atg-16.2 is required for autophagy in worms.

   “but was required for autophagic flux across all major tissues examined.”

   Model organismsshown by endogenous deletion of the WD40 domainall major tissues examined

   Protein segment supports cellular waste breakdown in worms

   bioRxiv·Oct 20, 2026Preprint

More on Autophagy

1. atg-16.2 has no effect on healthspan measures in worms.

   “The ATG-16.2 WD40 domain was dispensable for healthspan measures”

   Model organismsshown by endogenous deletion of the WD40 domain

   Protein segment supports cellular waste breakdown in worms

   bioRxiv·Oct 20, 2026Preprint

1. atg-16.2 is required for exopher biogenesis in worms.

   “ATG-16.2 WD40 domain, a conserved domain critical for at least some noncanonical autophagy functions of ATG16L1 in mammalian cells, is required for the increased exopher biogenesis”

   Model organismsneuronal inhibition of early-acting autophagy genesneuron

   Neuronal waste management: new roles for autophagy genes in the extrusion of protein aggregates and in longevity

   Autophagy·Feb 27, 2024

More on Exopher biogenesis

1. atg-16.2 is required for exopher formation in worms.

   “atg-16.2 was required for the effects of early autophagy gene reduction on neuronal PolyQ aggregation, exopher formation, and lifespan.”

   Model organismsrequired for increased exopher formation following early autophagy gene reductionneuron

   Inhibition of early-acting autophagy genes in C. elegans neurons improves protein homeostasis, promotes exopher production, and extends lifespan via the ATG-16.2 WD40 domain

   bioRxiv (Cold Spring Harbor Laboratory)·Dec 14, 2022Preprint

1. atg-16.2 is required for neuronal PolyQ aggregation in worms.

   “atg-16.2 was required for the effects of early autophagy gene reduction on neuronal PolyQ aggregation, exopher formation, and lifespan.”

   Model organismsrequired for the reduction in aggregation following early autophagy gene reductionneuron

   Inhibition of early-acting autophagy genes in C. elegans neurons improves protein homeostasis, promotes exopher production, and extends lifespan via the ATG-16.2 WD40 domain

   bioRxiv (Cold Spring Harbor Laboratory)·Dec 14, 2022Preprint

1. atg-16.2 is associated with neuronal lysosomal pH in worms.

   “loss of the ATG-16.2 WD40 domain reduced nuclear TFEB/HLH-30, reduced neuronal autophagic degradation, altered neuronal lysosomal pH”

   Model organismsgermline-less animals; shown by deletion of the WD40 domainneuron

   Protein segment supports cellular waste breakdown in worms

   bioRxiv·Oct 20, 2026Preprint

More on Neuronal lysosomal pH