The concerted regulation of chloroplast biosynthetic pathways and NADPH extrusion via malate valve depends onfandmthioredoxins (Trxs). The finding that decreased levels of the thiol-peroxidase 2-Cys peroxiredoxin (Prx) suppress the severe phenotype of Arabidopsis mutants lacking NADPH-dependent Trx reductase C (NTRC) and Trxsfuncovered the central function of the NTRC-2-Cys-Prx redox system in chloroplast performance. These results suggest that Trxsmare also regulated by this system; however, the functional relationship between NTRC, 2-Cys Prxs, andm-type Trxs is unknown. To address this issue, we generatedArabidopsis thalianamutants combining deficiencies in NTRC, 2-Cys Prx B, Trxsm1, andm4. The singletrxm1andtrxm4mutants showed a wild-type phenotype, growth retardation being noticed only in thetrxm1m4double mutant. Moreover, thentrc-trxm1m4mutant displayed a more severe phenotype than thentrcmutant, as shown by the impaired photosynthetic performance, altered chloroplast structure, and defective light-dependent reduction in the Calvin–Benson cycle and malate-valve enzymes. These effects were suppressed by the decreased contents of 2-Cys Prx, since the quadruplentrc-trxm1m4-2cpbmutant displayed a wild-type-like phenotype. These results show that the activity ofm-type Trxs in the light-dependent regulation of biosynthetic enzymes and malate valve is controlled by the NTRC-2-Cys-Prx system.