The activation of the stress response pathway mediated by PERK has different outcomes in different contexts: in some ophthalomogical disorders such as retinitis pigmentosa where vision degrades with age, the activation of PERK has a protective effect as evidence by studies in mouse models (PMC6583901); in other pathological contexts, e.g. amyotrophic lateral sclerosis (PMC3033190), atherosclerosis(PMC3967405), neurodegenerative disorders (PMC5010237), inhibition of PERK leads to better outcomes in terms of cell viability. This contrasting effect of PERK activation is recapitulated by the translation regulators downstream of PERK, suggesting that mRNA translation regulation may set up the context for the outcome of PERK activation. The fly eye is a great platform to study this because both protective and degenerative effects can be modeled in the same tissue: mild stress where PERK is protective as seen in adRP can be modeled with the ninaE^G69D allele, and chronic stress where PERK is degenerative can be modeled by overexpression of Rh1^G69D protein specifically in the eye. We're hoping to make a dent in our understanding of the dual nature of PERK activation using this set up.