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Biology subjects

Corwin, J. A.

Publications and source records attributed to Corwin, J. A..

4 recordsLinked to original sources

Heritable associations with microbial communities are essential for necrotrophic pathogen resistance

Host-microbe interactions are increasingly recognized as important drivers of organismal health, growth, longevity, and community-scale ecological processes. However, less is known about how genetic variation affects hosts associated microbiomes and downstream phenotypes. We demonstrate that sunflower (Helianthus annuus) harbors substantial, heritable variation in microbial communities under field conditions. We show that microbial communities explain up to 77.5% of the heritable variation in resistance to root infection caused by the necrotrophic pathogen Sclerotinia sclerotiorum, and that plants grown in sterilized soil showed almost complete elimination of pathogen resistance. Association mapping revealed 69 genetic locations related to microbial abundance and Sclerotinia resistance. Although the genetic architecture is complex and quantitative, we have, in large part, elucidated previously unexplained genetic variation for resistance to this pathogen. This suggests new targets for plant breeding and demonstrates the potential for heritable microbial associations to play important roles in defense in natural and human-altered environments.

ecology↗

Pathogen genetic control of transcriptome variation in the Arabidopsis thaliana - Botrytis cinerea pathosystem

Disease symptoms arise from the interaction of the host and pathogen genomes. However, little is known about how genetic variation in the interaction modulates both organisms transcriptomes, especially in complex interactions like those between generalist pathogens and their plant hosts. To begin mapping how polygenic pathogen variation influences both organisms transcriptomes, we used the Botrytis cinerea - Arabidopsis thaliana pathosystem. We measured the co-transcriptome across a genetically diverse collection of 96 B. cinerea isolates infected on the Arabidopsis wildtype, Col-0. Using the B. cinerea genomic variation, we performed genome-wide association (GWA) for each of 23,947 measurable transcripts in the host, and 9,267 measurable transcripts in the pathogen. Unlike other eGWA studies, there was a relative absence of cis-eQTL that is likely explained by structural variants and allelic heterogeneity within the pathogens genome. This analysis identified mostly trans-eQTL in the pathogen with eQTL hotspots dispersed across the pathogen genome that altered the pathogens transcripts, the hosts transcripts, or both the pathogen and the host. Gene membership in the trans-eQTL hotspots suggests links to several known and many novel virulence mechanisms in the plant-pathogen interaction. Genes annotated to these hotspots provide potential targets for blocking manipulation of the host response by this ubiquitous generalist pathogen. This shows that genetic control over the co-transcriptome is polygenic, similar to the virulence outcome in the interaction of Botrytis cinerea on Arabidopsis thaliana.

plant biology↗

Plant-Necrotroph Co-transcriptome Networks Illuminate a Metabolic Battlefield

A central goal of studying host-pathogen interaction research is to understand how the host and pathogen manipulate each other to promote their own fitness in a pathosystem. Co-transcriptomic approaches can simultaneously analyze dual transcriptomes during infection and provide a systematic map of the cross-kingdom communication between two species. Here we used the Arabidopsis-B. cinerea pathosystem to test how plant host and fungal pathogen interaction at the transcriptomic level during infection. We assessed the impact of natural genetic diversity in the pathogen and plant host by utilization of a collection of 96 isolates of B. cinerea infection on Arabidopsis wild-type and two mutants with jasmonate or salicylic acid compromised immunities. We identified ten B. cinerea gene co-expression networks (GCNs) that encode known or novel virulence mechanisms. We constructed a dual interaction network by combining four host-and ten pathogen-GCNs into a single network, which revealed potential connections between the fungal and plant GCNs involving both novel and conserved mechanisms. These co-transcriptome data shed lights on the potential mechanisms underlying host-pathogen interaction and illustrate the continued need for advancements of in planta analysis of dual-species dynamics.

systems biology↗

Combining Digital Imaging and Genome Wide Association Mapping to Dissect Uncharacterized Traits in Plant/Pathogen Interactions

Plant resistance to generalist pathogens with broad host ranges, such as Botrytis cinerea, is typically quantitative and highly polygenic. Recent studies have begun to elucidate the molecular genetic basis underpinning plant-pathogen interactions using commonly measured traits including lesion size and/or pathogen biomass. Yet with the advent of digital imaging and phenomics, there are a large number of additional resistance traits available to study quantitative resistance. In this study, we used high-throughput digital imaging analysis to investigate previously uncharacterized visual traits of plant-pathogen interactions related disease resistance using the Arabidopsis thaliana/Botrytis cinerea pathosystem. Using a large collection of 75 visual traits collected from every lesion, we focused on lesion color, lesion shape, and lesion size, to test how these aspects of the interaction are genetically related. Using genome wide association (GWA) mapping in A. thaliana, we show that lesion color and shape are genetically separable traits associated with plant-disease resistance. Using defined mutants in 23 candidate genes from the GWA mapping, we could identify and show that novel loci associated with each different plant-pathogen interaction trait, which expands our understanding of the functional mechanisms driving plant disease resistance.\n\nSummaryDigital imaging allows the identification of genes controlling novel lesion traits.

plant biology↗