Kim D. Finley

TL;DR: A set of guidelines for the selection and interpretation of the methods that can be used by investigators who are attempting to examine macroautophagy and related processes, as well as by reviewers who need to provide realistic and reasonable critiques of papers that investigate these processes are presented.

TL;DR: It is demonstrated that expression of several autophagy genes is reduced in Drosophila neural tissues as a normal part of aging, indicating that genetic or age-dependent suppression ofAutophagy is closely associated with the buildup of cellular damage in neurons and a reduced lifespan, while maintaining the expression of a rate-limiting Autophagy gene prevents the age- dependent accumulation of damage in neuron and promotes longevity.

TL;DR: It is demonstrated that Ref(2)P localizes to age-induced protein aggregates as well as to aggregates caused by reduced autophagic or proteasomal activity, and a major role is revealed in the formation of ubiquitin-positive protein aggregation both under physiological conditions and when normal protein turnover is inhibited.

TL;DR: The regulation and mechanism of these selective types of autophagy are just starting to unveil, but what it is already clearly emerging is that structures targeted to destruction are accurately enwrapped by autophagosomes through the action of specific receptors and adaptors.

TL;DR: The high degree of conservation between Drosophila and human bchssuggests that study of the functional pathway of BCHS and associated mutant phenotype may provide useful insights into human neurodegenerative disorders.