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Rivera-Varas, V.

Publications and source records attributed to Rivera-Varas, V..

2 recordsLinked to original sources

Dispensable genome and segmental duplications drive the genome plasticity in Fusarium solani

Fusarium solani is a species complex encompassing a large phylogenetic clade with diverse members occupying varied habitats. We recently reported a unique opportunistic F. solani associated with unusual dark galls in sugarbeet. We assembled the chromosome-level genome of the F. solani sugarbeet isolate strain SB1 using Oxford Nanopore and Hi-C sequencing. SB1 has a large genome (59.38 Mb) organized into 15 chromosomes. The genome expansion is due to the high repeats and massive segmental duplications within its three potentially accessory chromosomes. These chromosomes are absent in the closest reference genome with chromosome-level assembly, F. vanettenii 77-13-4. The extensive segmental duplications between the two SB1 chromosomes suggest that this isolate may have doubled its accessory genes. Further comparison of the F. solani strain SB1 genome demonstrates inversions and syntenic regions to an accessory chromosome of F. vanettenii 77-13-4. The pan-genome of 12 publicly available F. solani isolates nearly reached gene saturation, with few new genes discovered after the addition of the last genome. Based on orthogroups and average nucleotide identity, F. solani is not grouped by lifestyle or origin. The pan-genome analysis further revealed the enrichment of several enzymes-coding genes within the dispensable (accessory + unique genes) genome, such as hydrolases, transferases, oxidoreductases, lyases, ligases, isomerase, and dehydrogenase. The evidence presented here suggests that genome plasticity, genetic diversity, and adaptive traits in Fusarium solani are driven by the dispensable genome with significant contributions from segmental duplications.

genomics↗

Genome-wide association studies reveal the complex genetic architecture of DMI fungicide resistance in Cercospora beticola

Cercospora leaf spot is the most important disease of sugar beet worldwide. The disease is caused by the fungus Cercospora beticola and is managed principally by timely application of fungicides including those of the sterol demethylation inhibitor (DMI) class. However, reliance on DMIs has caused an increase in resistance to this class of fungicides in multiple C. beticola populations. To better understand the genetic and evolutionary basis for resistance in C. beticola, a genome-wide association study (GWAS) and selective sweep analysis were conducted for the first time in this fungal plant pathogen. We performed whole genome resequencing of 190 C. beticola isolates predominantly from North Dakota and Minnesota that were phenotyped for sensitivity to tetraconazole, the most widely used DMI fungicide in this region. GWAS identified mutations in genes associated with DMI fungicide resistance including a Regulator of G-protein Signaling (RGS) protein, an ATP-binding cassette (ABC) pleiotropic drug resistance transporter, a dual-specificity tyrosine phosphorylation-regulated kinase (DYRK), and a gene annotated as a hypothetical protein. A SNP upstream of CbCYP51, the gene encoding the target of DMI fungicides, was also identified via GWAS. Haplotype analysis of CbCYP51 identified a synonymous mutation (E170) in high linkage disequilibrium with the upstream SNP, and multiple non-synonymous mutations (L144F, I387M and Y464S) associated with DMI resistance. Additionally, a putative codon bias effect for the L144F substitution was identified that generated different resistance potentials. We also identified a CbCYP51 paralog in C. beticola, CbCYP51-like, with high protein homology to CYP51C found uniquely in Fusarium species but CbCYP51-like does not appear to influence DMI sensitivity. Genome-wide scans of selection showed that several of the GWAS mutations for fungicide resistance resided in regions that have recently undergone a selective sweep. Using radial plate growth on selected media as a fitness proxy, we did not find a trade-off associated with DMI fungicide resistance suggesting that resistance mutations can persist in C. beticola populations. Taken together, we show that population genomic data from a crop pathogen can allow the identification of mutations conferring fungicide resistance and inform about their origins in the pathogen population.

evolutionary biology↗