Fusarium wilt is the most destructive fungal disease in flax, limiting flax cultivation in all the main flax and linseed growing countries. The causative agent is seedborne and soilborne fungus F. oxysporum f. sp. lini. Here, we report, for the first time, genome assemblies of five highly pathogenic isolates of Fusarium oxysporum f. sp. lini, namely monoisolate 39 and strains F329, F324, F282, F287. In addition, syntenic analysis provided a powerful approach to distinguish between core and lineage-specific parts of the genome. These results lay a solid foundation for comparative genomics studies of plant fungal pathogens, evolution of pathogenicity, and virulence factors underlying the dynamics of host-pathogen interactions, thus eventually offering solutions to Fusarium disease control.

Fusarium wilt of flax is an aggressive disease caused by the soil-borne fungal pathogen Fusarium oxysporum f. sp. lini. It is a challenging pathogen presenting a constant threat to flax production industry worldwide. Previously, we reported chromosome-level assemblies of 5 highly pathogenic F. oxysporum f. sp. lini strains. We sought to characterize the genomic architecture of the fungus and outline evolutionary mechanisms shaping the pathogen genome. Here, we reveal the complex multi-compartmentalized genome organization and uncover its diverse evolutionary dynamics, which boosts genetic diversity and facilitates host adaptation. In addition, our results suggest that host of functions implicated in the life cycle of mobile genetic elements are main contributors to dissimilarity between proteomes of different Fusaria. Finally, our experiments demonstrate that mobile genetics elements are expressed in planta upon infection, alluding to their role in pathogenicity. On the whole, these results pave the way for further in-depth studies of evolutionary forces shaping the host–pathogen interaction.

Chickpea (Cicer arietinum L.) is a major grain legume and a good source of plant-based protein. However, comprehensive knowledge of flowering time control in Cicer is lacking. In this study, we acquire high-throughput transcriptome sequencing data and analyze changes in gene expression during floral transition in the early flowering cultivar ICCV 96029, later flowering C. arietinum accessions, and two wild species, C. reticulatum and C. echinospermum. We identify Cicer orthologs of A. thaliana flowering time genes and analyze differential expression of 278 genes between four species/accessions, three tissue types, and two conditions. Our results show that the differences in gene expression between ICCV 96029 and other cultivated chickpea accessions are vernalization-dependent. In addition, we highlight the role of FTa3, an ortholog of FLOWERING LOCUS T in Arabidopsis, in the vernalization response of cultivated chickpea. A common set of differentially expressed genes was found for all comparisons between wild species and cultivars. The direction of expression change for different copies of the FT-INTERACTING PROTEIN 1 gene was variable in different comparisons, which suggests complex mechanisms of FT protein transport. Our study makes a contribution to the understanding of flowering time control in Cicer, and can provide genetic strategies to further improve this important agronomic trait.

The authors used the split-marker recombination approach to obtain SIX13 gene knockouts from the genome of highly virulent F. oxysporum f. sp. lini strain MI39. Deleterious constructs were created to replace the SIX13 gene with hygromycin B phosphotransferase gene HPH under control of strong constitutive TrpC promoter by homologous integration into the MI39 genome. After selection and verification, the frequency of obtaining Δsix13 knockouts was 63.2% of the total number of obtained isolates. The remaining 36.8% of isolates were transformed; however, in addition to the HPH marker gene, they retained the intact target SIX13 gene. Transformation with constructs lacking the TrpC promoter did not result in getting mutants, and all the resulting transformants also carried both HPH and SIX13 genes.