Breakdown of self-incompatibility has frequently been attributed to loss-of-function mutations of alleles at the locus responsible for recognition of self-pollen (i.e. theS-locus). However, other potential causes have rarely been tested. Here, we show that self-compatibility ofS1S1-homozygotes in selfing populations of the otherwise self-incompatibleArabidopsis lyratais not due toS-locus mutation. Between-breeding-system cross-progeny are self-compatible if they combineS1from the self-compatible cross-partner with recessiveS1from the self-incompatible cross-partner, but self-incompatible with dominantS-alleles. BecauseS1S1homozygotes in outcrossing populations are self-incompatible, mutation ofS1cannot explain self-compatibility inS1S1cross-progeny. This supports the hypothesis that anS1-specific modifier unlinked to theS-locus causes self-compatibility by functionally disruptingS1. Self-compatibility inS19S19homozygotes may also be caused by anS19-specific modifier, but we cannot rule out a loss-of-function mutation ofS19. Taken together, our findings indicate that breakdown of self-incompatibility is possible without disruptive mutations at theS-locus.