Post-Doctoral Researcher University of Wisconsin Madison, Wisconsin
Autophagy is a cellular recycling pathway that replenishes nutrients by degrading unwanted proteins and organelles coordinately. Autophagy is an essential catabolic pathway in animals but not in plants, which are able to survive even when autophagy is completely blocked. One crucial step of autophagy is the lipidation of the gene ATG8, which is mediated by several ATG proteins including ATG12, and promotes cargo capture, vesicle expansion, and closure. We analyzed two atg12 mutants (atg12-1 and atg12-2) in maize to understand the compensatory catabolic and protective mechanisms that allow plants to survive when autophagy is blocked. The atg12 mutants showed reduced autophagic fluxes and poor growth in nutrient-deficient conditions. We analyzed atg12 mutant gene expression under various nutrient-deficient conditions, such as fixed carbon and nitrogen starvation, and across various leaf developmental stages. We applied the gene regulatory network (GRN) inference algorithm MERLIN to our expression dataset to identify the regulatory programs activated under nutrient-rich and nutrient-poor conditions. We inferred a genome-scale GRN with 911 regulators connecting 7,280 genes and 7,008 predicted regulatory edges using MERLIN. Many MERLIN modules were enriched for relevant biological processes indicative of stress response and were differentially regulated between genotypes and conditions. Interestingly, four gene modules showed significant differential patterns that were conserved across multiple treatments. These modules were associated with the anthocyanin pathway, unfolded protein response, and biosynthetic pathways. Taken together, our network-based analysis identified condition-specific and common gene expression modules in atg12 mutants that can provide insight into the compensatory processes in autophagy-deficient condition.