Photosynthetic linear electron transfer (LET) comprises a solar energy driven pathway tha directs electrons to the production of NADPH, via ferredoxin-NADP+ reductase (FNR), while generating a proton motive force (pmf) to drive ATP synthesis. Both NADPH and ATP are consumed for carbon fixation. However, this pathway can be altered to block NADPH formation while maintaining pmf to produce ATP to enable acclimation of the organism to stress conditions at the expense of carbon fixation. LET and the alternative pathway, cyclic electron transfer (CET) both rely on protein-protein interactions with FNR but creating a knock-out mutant to explore its contribution to LET/CET regulation would be problematic given that FNR is essential. Instead, this project employs two mutants expressing a chimeric FNR-PSAF protein created by CRISPR-Cas9 gene editing: (1) NT12 = fnr-psaf/fnr/Δpsaf and (2) T7 = fnr-psaf/Δfnr/Δpsaf. The effects of these mutants, compared to wild-type cells, on the abundance of selected photosynthesis-related proteins are determined by MS-based quantitative proteomic analysis.