Fig. 1

Invalidation of Mtr reduces methionine synthase expression in the retina and disrupts one-carbon metabolism and remethylation pathway resulting in decreased SAM/SAH ratio and enhanced transsulfuration pathway activity. A Genetic model of Mtr-cKO. Mice expressing the Cre recombinase under the control of the Thy1 promoter are bred with mice carrying floxed exons 4 and 5 of the Mtr gene (indicated by red triangles). Offspring from this cross exhibit conditional deletion of the Mtr gene (Created with BioRender.com). B Representative PCR analysis of the Cre gene in tail extracts obtained on postnatal day 15 (CI: internal control; TC: Cre gene; T + : positive control; T-: negative control). C Quantification of mRNA levels of Thy1 and Cre using RT-qPCR in several tissues. D Quantification of mRNA and protein levels of the Mtr gene and methionine synthase (MS) protein in retinal and liver tissue using RT-qPCR and WES Simple Protein. α-tubulin serves as an internal control for protein expression, and densitometric analysis of the WES assay provides quantification of protein expression. E Analysis of one-carbon metabolites in retinal tissue using LC/MSMS. F SAM/SAH ratio in the retina. G Schematic representation of altered one-carbon metabolism. Increased protein/metabolite expression/concentration is indicated in orange, decreased in green, and unchanged in gray (Created with BioRender.com). Data are presented as means ± SEM. Statistical analysis was performed using the Student t test (*P < 0.05, **P < 0.01, ***P < 0.001). N = 4 to 6 per group