A common bean truncated CRINKLY4 kinase controls gene-for-gene resistance to the fungus Colletotrichum lindemuthianum

Identifying the molecular basis of resistance to pathogens is critical to promote a chemical-free cropping system.
In plants, nucleotide-binding leucine-rich repeat constitute the largest family of disease resistance (R) genes, but this resistance can be rapidly overcome by the pathogen, prompting research into alternative sources of resist- ance. Anthracnose, caused by the fungus Colletotrichum lindemuthianum, is one of the most important diseases of common bean. This study aimed to identify the molecular basis of Co-x, an anthracnose R gene conferring total resistance to the extremely virulent C. lindemuthianum strain 100. To that end, we sequenced the Co-x 58 kb target region in the resistant JaloEEP558 (Co-x) common bean and identified KTR2/3, an additional gene encoding a truncated and chimeric CRINKLY4 kinase, located within a CRINKLY4 kinase cluster. The presence of KTR2/3 is strictly correlated with resistance to strain 100 in a diversity panel of common beans. Furthermore, KTR2/3 expression is up-regulated 24 hours post-inoculation and its transient expression in a susceptible geno- type increases resistance to strain 100. Our results provide evidence that Co-x encodes a truncated and chimeric CRINKLY4 kinase probably resulting from an unequal recombination event that occurred recently in the Andean domesticated gene pool. This atypical R gene may act as a decoy involved in indirect recognition of a fungal effector.