Autophagy is a homeostatic process strategically positioned at the intersection of metabolism and intracellular quality control, with broad physiological and medical manifestations ranging from metabolic imbalance to neurodegeneration, infections, immune disorders, cancer and aging. In yeast, the formation and organization of the autophagosomal apparatus follows a highly prescribed sequence, starting with the pre-autophagosomal structure and ending in autophagosomal fusion with the yeast vacuole. However, in other model organisms, as well as in mammals, the autophagy machinery and its regulators show both similarities and notable differences relative to yeast.

The goals/aims of this ePanel are:

1. Compare and contrast autophagy in yeast and higher organisms with a focus on both the shared regulators and on those factors that have no counterparts in yeast
2. Cover the intersection of autophagy with energy metabolism, innate immune signaling and endomembrane damage
3. Cover how signaling cascades regulate the process of selective autophagy whereby substrates are recruited to forming autophagosomes by receptors and molecular tags such as ubiquitin, galectins, or through other modalities

The conference will cover fundamental principles as outlined above and how they apply to basic and translational aspects of human disease. Intersections with several other stress response processes will be addressed.

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The views expressed in this ePanel are those of the participants and not necessarily of the participants’ organizations or of Keystone Symposia.

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