Nature Communications (Jun 2023)

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

  • Yan Li,
  • Ekaterina Mamonova,
  • Nadja Köhler,
  • Mark van Kleunen,
  • Marc Stift

DOI
https://doi.org/10.1038/s41467-023-38802-0
Journal volume & issue
Vol. 14, no. 1
pp. 1 – 10

Abstract

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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.