Body of Abstract: Peroxisomes are critical organelles that house fatty acid ꞵ-oxidation and antioxidative enzymes that detoxify reactive oxygen and nitrogen species. Impairment of peroxisome function can impact many physiological processes in plants and humans. The primary mechanism for organelle turnover is autophagy, and stress-inducing conditions, including nutrient starvation and oxidative stress, and adaptor proteins, such as NBR1, promote general autophagy. The selective autophagy of peroxisomes is termed pexophagy. Although pexophagy maintains peroxisomal proteostasis by recycling damaged or excess peroxisomes, the conditions and proteins that trigger and execute pexophagy in plants remain to be identified. We are optimizing literature-described autophagy-inducing conditions and monitoring both autophagy and pexophagy by using immunoblotting analysis of reporters that are cleaved upon vacuolar delivery. As expected, wild-type seedlings display only low levels of autophagy under control conditions and robustly induce autophagy following nutrient starvation. We also detect cleavage of a reporter targeted to the peroxisome membrane upon nutrient starvation that is diminished in an autophagy mutant, indicating that our peroxisomal reporter can report pexophagy. Comparing the extents of cleavage of the two reporters suggest that pexophagy is a minor component of autophagy during nutrient starvation, perhaps because peroxisomal fatty acid β-oxidation is needed to mobilize lipids freed from the membranes of other organelles undergoing autophagy. We are currently developing a pH-sensitive di-fluorescent reporter to separately mark peroxisomal and autophagic membranes. This system will allow us to simultaneously monitor pexophagy and autophagy under stress conditions and in various mutant backgrounds, including mutants lacking NBR1 or various peroxisomal proteins.