Abstract
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. the S-locus). However, other potential causes have rarely been tested. Here, we show that self-compatibility of S(1)S(1)-homozygotes in selfing populations of the otherwise self-incompatible Arabidopsis lyrata is not due to S-locus mutation. Between-breeding-system cross-progeny are self-compatible if they combine S(1) from the self-compatible cross-partner with recessive S(1) from the self-incompatible cross-partner, but self-incompatible with dominant S-alleles. Because S(1)S(1) homozygotes in outcrossing populations are self-incompatible, mutation of S(1) cannot explain self-compatibility in S(1)S(1) cross-progeny. This supports the hypothesis that an S(1)-specific modifier unlinked to the S-locus causes self-compatibility by functionally disrupting S(1). Self-compatibility in S(19)S(19) homozygotes may also be caused by an S(19)-specific modifier, but we cannot rule out a loss-of-function mutation of S(19). Taken together, our findings indicate that breakdown of self-incompatibility is possible without disruptive mutations at the S-locus.