The molecular mechanisms underlying circadian photoentrainment are complex, comprising several regulatory factors. There is evidence to suggest differential chromatin accessibility in the master clock, SCN, in response to light at different times of the day. Several genes identified close to differential regions of chromatin accessibility are already known to play an important role within the molecular clock and are recognized to be important for entrainment. Previous studies in the lab using ATAC-seq (Assay for Transposase Accessible Chromatin) showed that chromatin near the gene Mafg (MAF BZIP Transcription Factor G) closed following a nocturnal light pulse (LP), indicating repression of the gene. Additionally, the response element to which MAFG binds, which is the AP-1 motif, was highly over-represented in the light regulated accessible chromatin profile, leading us to hypothesise that MAFG, that is part of the AP-1 transcription factor family, regulates photoentrainment through the regulation of AP-1. To investigate this, I conducted in vitro and in vivo analyses to evaluate MAFG function in circadian entrainment. Sections of the Mafg promoter that responded by closing in response to light were cloned into a luciferase reporter plasmid and transfected into U2OS cells. Forskolin (which simulates a LP via the AP-1 pathway) reduced reporter expression, and this was further reduced in cells with siRNA- mediated Mafg knockdown. Furthermore, knockdown of Mafg in BMAL1:Luc U2OS circadian reporter cells showed a reduction in amplitude. In vivo, the baseline circadian phenotype, and photic entrainment phenotype of Mafg knockout mice was studied by housing Mafg+/+ and Mafg-/- mice in strict light/dark cycles. Periodogram analysis showed reduced amplitude of circadian period in knockout mice, suggesting that they have weak & fragmented rhythms. Mafg knockouts also showed slower re- entrainment in a 6-hour phase-advancing jetlag study and reduced phase shifting in response to a nocturnal LP (CT 16), indicating reduced photic responses in Mafg -/- animals. However, qPCR analysis of gene expression in the SCN isolated from CT16 light pulsed Mafg+/+ and Mafg-/- mice shows very little difference in a subset of the light regulated genes assessed between the genotypes. In summary, a novel role for MAFG in regulating circadian photoentrainment was shown, however discrepancies in the mechanism of action remain to be addressed.