Breakdown of self-incompatibility due to genetic interaction between a specific S-allele and an unlinked modifier.

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 S₁S₁-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 S₁ from the self-compatible cross-partner with recessive S₁ from the self-incompatible cross-partner, but self-incompatible with dominant S-alleles. Because S₁S₁ homozygotes in outcrossing populations are self-incompatible, mutation of S₁ cannot explain self-compatibility in S₁S₁ cross-progeny. This supports the hypothesis that an S₁-specific modifier unlinked to the S-locus causes self-compatibility by functionally disrupting S₁. Self-compatibility in S₁₉S₁₉ homozygotes may also be caused by an S₁₉-specific modifier, but we cannot rule out a loss-of-function mutation of S₁₉. Taken together, our findings indicate that breakdown of self-incompatibility is possible without disruptive mutations at the S-locus.