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Soltis, N.

Publications and source records attributed to Soltis, N..

4 recordsLinked to original sources

Polygenic pathogen networks control of host and pathogen transcriptional plasticity in the Arabidopsis-Botrytis pathosystem

Bidirectional flow of information shapes the outcome of the host-pathogen interactions and depends on the genetics of each organism. Recent work has begun to use co-transcriptomic studies to shed light on this bidirectional flow, but it is unclear how plastic the co-transcriptome is in response to genetic variation in both the host and pathogen. To study co-transcriptome plasticity, we conducted transcriptomics using natural genetic variation in the pathogen, Botrytis cinerea, and large effect genetic variation abolishing defense signaling pathways within the host, Arabidopsis thaliana. We show that genetic variation in the pathogen has a greater influence on the co-transcriptome than mutations that abolish defense signaling pathways in the host. Genome wide association mapping using the pathogens genetic variation and both organisms transcriptomes allowed an assessment of how the pathogen modulates plasticity in response to the host. This showed that the differences in both organisms responses were linked to trans-eQTL hotspots within the pathogens genome. These hotspots control gene sets in either the host or pathogen and show differential allele sensitivity to the hosts genetic variation rather than qualitative host specificity. Interestingly, nearly all the trans-eQTL hotspots were unique to the host or pathogen transcriptomes. In this system of differential plasticity, the pathogen mediates the shift in the co-transcriptome more than the host.

plant biology↗

A generalist pathogen view of plant evolution

Botrytis cinerea is a polyphagous fungal pathogen that causes necrotic disease on more than a thousand known hosts widely spread across the plant kingdom. While it is known that quantitative resistance in the host and quantitative virulence in the pathogen largely mediate this pathosystem, how this pathogen interacts with the extensive host diversity is unknown. Does this pathogen have quantitative virulence efficiency on all hosts or individual solutions for each host? To address this question, we generated an infectivity matrix of 98 strains of Botrytis cinerea on 90 genotypes representing eight host plants. This experimental infectivity matrix showed that the predominant sources of quantitative variation are between host species and among pathogen strains. Furthermore, the eight eudicot hosts interacted individually with Botrytis cinerea strains independently of the evolutionary relatedness between hosts. An additive quantitative model can explain the complexity of these interactions in which Botrytis host specificity and general virulence have distinct polygenic architectures.

plant biology↗

Resequencing and association mapping of the generalist pathogen Botrytis cinerea

We performed whole genome resequencing of 84 field isolates of Botrytis cinerea, largely collected from a local set of plant species. Combined with 13 previously resequenced isolates sampled from diverse locations, this gave a collection of 97 isolates for studies of natural variation. Alignment to the reference sequence T4 and SNP detection provided further data for population genetics analysis including a mapping population for association studies. Although much of the genomic diversity was captured in the original 13 isolates, the additional genomes increased total diversity in the population by a third. Surprisingly, the same additional genomes increase mitochondrial diversity 2-fold. Across the population, LD was limited and decayed rapidly, reflecting frequent outcrossings. Effectively, this sampling strategy increased the level of genetic diversity available, whilst limiting the problem of population stratification and enabling GWAS of several phenotypes on common Arabidopsis plants affected in disease pathways. Overlap of results using all GWAS methods revealed numerous candidate genes / pathways that potentially contribute to its broad host range and offer conceivable pathogen decrease targets.

genomics↗

GONST2 transports GDP-Mannose for sphingolipid glycosylation in the Golgi apparatus of Arabidopsis

The Golgi lumen is the site of many different glycosylation events, including cell wall polysaccharide biosynthesis and lipid glycosylation. Transporters are necessary for the import of the substrates required for glycosylation (nucleotide sugars) from the cytosol where they are synthesized. Plants use four GDP-linked sugars to glycosylate macromolecules: GDP-L-Fucose, GDP-D-Mannose, GDP-L-Galactose and GDP-D-Glucose. Of the predicted fifty-one members of the nucleotide sugar transporter/triose phosphate transporter family in Arabidopsis, only four appear to contain the conserved motif needed for the transport of GDP-linked sugars, GOLGI LOCALIZED NUCLEOTIDE SUGAR TRANSPORTER (GONST) 1-4. Previously, we have demonstrated that GONST1 provides GDP-D-Mannose for glycosylation of a class of sphingolipids, the glycosylinositolphosphorylceramides (GIPCs). Here, we characterize its closest homologue, GONST2, and conclude that it also specifically provides substrate for GIPC glycosylation. Expression of GONST2 driven by the GONST1 promoter is able to rescue the severe growth phenotype of gonst1. Loss of GONST2 exacerbates the gonst1 constitutive hypersensitive response, as well as the reduced cell wall cellulose content. The gonst2 mutant grows normally under standard conditions, but has enhanced resistance to the powdery mildew-causing fungus Golovinomyces orontii.

plant biology↗