AbstractSelf-incompatibility (SI) is a genetic mechanism utilized by many flowering plants to promote outcrossing by recognizing and rejecting self-pollen. While the molecular mechanisms controlling SI can differ in various families, plants in the Brassicaceae family have been found to regulate SI through a S-haplotype-specific receptor-ligand interaction. The recognition of self-pollen leads to the activation of ARMADILLO-REPEAT-CONTAINING1 (ARC1), an E3 ligase which is thought to degrade the

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... ompatibility factors required for pollen germination, thus resulting in SI. However, the role of ARC1 in SI in the Brassicaceae family has been disputed within the scientific community. While various studies demonstrate that the manipulation of ARC1 and its downstream targets can break-down the SI response, others show that the SI phenotype can be imparted to self-compatible cultivars without the ARC1 gene. This study investigated the involvement of ARC1 in SI through the generation of loss-of-function ARC1 mutants using CRISPR-Cas9 in B. napus. Loss of ARC1 resulted in complete breakdown of SI in two different S-haplotypes providing strong evidence for the essential nature of ARC1 for mounting a successful SI response.