Secreted in Xylem 6 (SIX6) Mediates Fusarium oxysporum f. sp. fragariae Race 1 Avirulence on FW1-Resistant Strawberry Cultivars.

Fusarium oxysporum f. sp. fragariae (Fof) race 1 is avirulent on cultivars with the dominant resistance gene FW1, while Fof race 2 is virulent on FW1-resistant cultivars. We hypothesized there was a gene-for-gene interaction between a gene at the FW1 locus and an avirulence gene (AvrFW1) in Fof race 1. To identify a candidate AvrFW1, we compared genomes of 24 Fof race 1 and three Fof race 2 isolates. We found one candidate gene that was present in race 1, was absent in race 2, was highly expressed in planta, and was homologous to a known effector, secreted in xylem 6 (SIX6). We knocked out SIX6 in two Fof race 1 isolates by homologous recombination. All SIX6 knockout transformants (ΔSIX6) gained virulence on FW1/fw1 cultivars, whereas ectopic transformants and the wildtype isolates remained avirulent. ΔSIX6 isolates were quantitatively less virulent on FW1/fw1 cultivars Fronteras and San Andreas than fw1/fw1 cultivars. Seedlings from an FW1/fw1 × fw1/fw1 population were genotyped for FW1 and tested for susceptibility to a SIX6 knockout isolate. Results suggested that additional minor-effect quantitative resistance genes could be present at the FW1 locus. This work demonstrates that SIX6 acts as an avirulence factor interacting with a resistance gene at the FW1 locus. The identification of AvrFW1 enables surveillance for Fof race 2 and provides insight into the mechanisms of FW1-mediated resistance. [Formula: see text] Copyright © 2024 The Author(s). This is an open access article distributed under the CC BY-NC-ND 4.0 International license.

Accelerating genetic gains for quantitative resistance to verticillium wilt through predictive breeding in strawberry.

Verticillium wilt (VW), a devastating vascular wilt disease of strawberry (Fragaria × $\times$ ananassa), has caused economic losses for nearly a century. This disease is caused by the soil-borne pathogen Verticillium dahliae, which occurs nearly worldwide and causes disease in numerous agriculturally important plants. The development of VW-resistant cultivars is critically important for the sustainability of strawberry production. We previously showed that a preponderance of the genetic resources (asexually propagated hybrid individuals) preserved in public germplasm collections were moderately to highly susceptible and that genetic gains for increased resistance to VW have been negligible over the last 60 years. To more fully understand the challenges associated with breeding for increased quantitative resistance to this pathogen, we developed and phenotyped a training population of hybrids ( n = 564 $n = 564$ ) among elite parents with a wide range of resistance phenotypes. When these data were combined with training data from a population of elite and exotic hybrids ( n = 386 $n = 386$ ), genomic prediction accuracies of 0.47-0.48 were achieved and were predicted to explain 70%-75% of the additive genetic variance for resistance. We concluded that breeding values for resistance to VW can be predicted with sufficient accuracy for effective genomic selection with routine updating of training populations.

Novel Fusarium wilt resistance genes uncovered in natural and cultivated strawberry populations are found on three non-homoeologous chromosomes.

KEY MESSAGE: Several Fusarium wilt resistance genes were discovered, genetically and physically mapped, and rapidly deployed via marker-assisted selection to develop cultivars resistant to Fusarium oxysporum f. sp. fragariae, a devastating soil-borne pathogen of strawberry. Fusarium wilt, a soilborne disease caused by Fusarium oxysporum f. sp. fragariae, poses a significant threat to strawberry (Fragaria [Formula: see text] ananassa) production in many parts of the world. This pathogen causes wilting, collapse, and death in susceptible genotypes. We previously identified a dominant gene (FW1) on chromosome 2B that confers resistance to race 1 of the pathogen, and hypothesized that gene-for-gene resistance to Fusarium wilt was widespread in strawberry. To explore this, a genetically diverse collection of heirloom and modern cultivars and octoploid ecotypes were screened for resistance to Fusarium wilt races 1 and 2. Here, we show that resistance to both races is widespread in natural and domesticated populations and that resistance to race 1 is conferred by partially to completely dominant alleles among loci (FW1, FW2, FW3, FW4, and FW5) found on three non-homoeologous chromosomes (1A, 2B, and 6B). The underlying genes have not yet been cloned and functionally characterized; however, plausible candidates were identified that encode pattern recognition receptors or other proteins known to confer gene-for-gene resistance in plants. High-throughput genotyping assays for SNPs in linkage disequilibrium with FW1-FW5 were developed to facilitate marker-assisted selection and accelerate the development of race 1 resistant cultivars. This study laid the foundation for identifying the genes encoded by FW1-FW5, in addition to exploring the genetics of resistance to race 2 and other races of the pathogen, as a precaution to averting a Fusarium wilt pandemic.

Simultaneous dissection of grain carotenoid levels and kernel color in biparental maize populations with yellow-to-orange grain.

Maize enriched in provitamin A carotenoids could be key in combatting vitamin A deficiency in human populations relying on maize as a food staple. Consumer studies indicate that orange maize may be regarded as novel and preferred. This study identifies genes of relevance for grain carotenoid concentrations and kernel color, through simultaneous dissection of these traits in 10 families of the US maize nested association mapping panel that have yellow to orange grain. Quantitative trait loci were identified via joint-linkage analysis, with phenotypic variation explained for individual kernel color quantitative trait loci ranging from 2.4% to 17.5%. These quantitative trait loci were cross-analyzed with significant marker-trait associations in a genome-wide association study that utilized ∼27 million variants. Nine genes were identified: four encoding activities upstream of the core carotenoid pathway, one at the pathway branchpoint, three within the α- or ß-pathway branches, and one encoding a carotenoid cleavage dioxygenase. Of these, three exhibited significant pleiotropy between kernel color and one or more carotenoid traits. Kernel color exhibited moderate positive correlations with ß-branch and total carotenoids and negligible correlations with α-branch carotenoids. These findings can be leveraged to simultaneously achieve desirable kernel color phenotypes and increase concentrations of provitamin A and other priority carotenoids.

The Ptr1 Locus of Solanum lycopersicoides Confers Resistance to Race 1 Strains of Pseudomonas syringae pv. tomato and to Ralstonia pseudosolanacearum by Recognizing the Type III Effectors AvrRpt2 and RipBN.

Race 1 strains of Pseudomonas syringae pv. tomato, which cause bacterial speck disease of tomato, are becoming increasingly common and no simply inherited genetic resistance to such strains is known. We discovered that a locus in Solanum lycopersicoides, termed Pseudomonas tomato race 1 (Ptr1), confers resistance to race 1 P. syringae pv. tomato strains by detecting the activity of type III effector AvrRpt2. In Arabidopsis, AvrRpt2 degrades the RIN4 protein, thereby activating RPS2-mediated immunity. Using site-directed mutagenesis of AvrRpt2, we found that, like RPS2, activation of Ptr1 requires AvrRpt2 proteolytic activity. Ptr1 also detected the activity of AvrRpt2 homologs from diverse bacteria, including one in Ralstonia pseudosolanacearum. The genome sequence of S. lycopersicoides revealed no RPS2 homolog in the Ptr1 region. Ptr1 could play an important role in controlling bacterial speck disease and its future cloning may shed light on an example of convergent evolution for recognition of a widespread type III effector.