Pexophagy articles from across Nature Portfolio

Gross et al. show that Atg13 and Atg17 are dispensable for pexophagy during phosphate starvation in yeast. Instead, the metabolite sensor Pho81 binds the Atg1 kinase complex via Atg11 to promote Atg11 phosphorylation by Atg1 and pexophagy.

An accumulation of one substrate of selective autophagy can lead to autophagic degradation deficiencies. Here, the authors show that a pathogenic increase in a single autophagy pathway restricts another by consuming the cell’s autophagy capacity.

Pexophagy plays a pivotal role in the selective removal of ROS-generating peroxisomes, which protects plants from oxidative damage during photosynthesis under high-intensity light.

Pexophagy removes damaged peroxisomes, which are particularly prone to ROS formation. Here, the authors use light to induce peroxisome turnover by local ROS generation, showing STUB1 translocation is critical and might contribute to human disease.

How do metabolic stresses trigger catabolic autophagy for cell survival? A study now reveals that the metabolite sensor Pho81 integrates into and activates the kinase activity of the Atg1 complex for pexophagy triggered by phosphate starvation. This demonstrates the plasticity of the autophagy-initiating Atg1 complex.

This study identifies Atg36 as the selective receptor for pexophagy.