Arabidopsis basal immunity depends on cooperation between EDS1-PAD4 dimers and ADR1-family helper NLRs to limit pathogen infection. We investigated the genetic and functional relationships of rice (Oryza sativa) EDS1, PAD4 and ADR1 orthologs in disease resistance. Single and combinatorial eds1, pad4 and adr1 CRISPR/Cas9 mutants were generated in O. sativa ssp. japonica varieties Kitaake and Zhonghua 11. Growth, physiological fitness and disease resistance phenotypes were assessed together with RNA expression and phytohormone profiles. Contributions of EDS1, PAD4 and ADR1 to resistance against fungal and bacterial pathogens suggest these components also cooperate in promoting rice basal immunity. However, combined loss of EDS1 with PAD4 leads to ADR1-dependent reduced growth and fitness of rice plants accompanied by constitutively high salicylic acid accumulation and enhanced resistance. The eds1 pad4 double mutant displays features of imbalanced defense - nutrient homeostasis. Data reveal both cooperative and antagonistic EDS1, PAD4 and ADR1 activities in rice. In pathogen-challenged rice plants, EDS1-PAD4-ADR1 likely function together as a module conferring basal immunity. In pathogen-unchallenged plants, EDS1 and PAD4 individually constrain ADR1 activity, thereby suppressing immune responses and maintaining fitness. ADR1-dependent autoimmunity in rice eds1 pad4 plants indicates a different mode of ADR1 recruitment and action than via EDS1-PAD4.