Investigating the heterochromatin model of C. elegans aging using ChromID proximity labeling

Loss of heterochromatin, a transcriptionally repressive chromatin state, is believed to be a major contributor to organismal aging in both human and C. elegans models. However, the underlying mechanisms are not fully understood. To identify candidate proteins that may play a role in this proposed epigenetic aging mechanism, I utilize ChromID, an in vivo proximity labeling technique specific to chromatin marks. The overall goal of my thesis project is to identify and characterize changes in the heterochromatin histone mark interactome during C. elegans aging using ChromID and functionally analyze the impact of the candidate proteins on organismal aging. The major aims of the project are to perform ChromID on H3K9me3 (constitutive heterochromatin) and H3K27me3 (facultative heterochromatin) at different timepoints, which would identify proteins that have a positive or negative correlation with lifespan. These ChromID hits will form the basis of experiments that seek to determine if these candidate proteins play a functional role in lifespan and heterochromatin silencing.