scholarly journals Plant–necrotroph co-transcriptome networks illuminate a metabolic battlefield

eLife ◽  
2019 ◽  
Vol 8 ◽  
Author(s):  
Wei Zhang ◽  
Jason A Corwin ◽  
Daniel Harrison Copeland ◽  
Julie Feusier ◽  
Robert Eshbaugh ◽  
...  
Keyword(s):  
Fungal Pathogen ◽  
Interaction Network ◽  
Transcriptome Data ◽  
Wild Type ◽  
Systematic Map ◽  
Plant Host ◽  
Host Pathogen Interaction ◽  
Host Pathogen ◽  
Transcriptomic Level ◽  
The Impact

A central goal of studying host-pathogen interaction is to understand how 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 interact at the transcriptomic level. We assessed the impact of genetic diversity in pathogen and host by utilization of a collection of 96 isolates infection on Arabidopsis wild-type and two mutants with jasmonate or salicylic acid compromised immunities. We identified ten B. cinereagene co-expression networks (GCNs) that encode known or novel virulence mechanisms. Construction of a dual interaction network by combining four host- and ten pathogen-GCNs revealed potential connections between the fungal and plant GCNs. These co-transcriptome data shed lights on the potential mechanisms underlying host-pathogen interaction.

scholarly journals Plant-Necrotroph Co-transcriptome Networks Illuminate a Metabolic Battlefield

2018 ◽  
Author(s):  
Wei Zhang ◽  
Jason A. Corwin ◽  
Daniel Copeland ◽  
Julie Feusier ◽  
Robert Eshbaugh ◽  
...  
Keyword(s):  
Interaction Network ◽  
In Planta ◽  
Systematic Map ◽  
Plant Host ◽  
Host Pathogen Interaction ◽  
Host Pathogen ◽  
Species Dynamics ◽  
Transcriptomic Level ◽  
The Impact ◽  
Interaction Research

AbstractA 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.

scholarly journals Centromere deletion in Cryptococcus deuterogattii leads to neocentromere formation and chromosome fusions

eLife ◽  
2020 ◽  
Vol 9 ◽  
Author(s):  
Klaas Schotanus ◽  
Joseph Heitman
Keyword(s):  
Fungal Pathogen ◽  
Species Complex ◽  
Wild Type ◽  
Genomic Changes ◽  
Growth Defects ◽  
Human Fungal Pathogen ◽  
Mutant Strains ◽  
Chromosome Fusions ◽  
The Impact ◽  
Active Centromere

The human fungal pathogen Cryptococcus deuterogattii is RNAi-deficient and lacks active transposons in its genome. C. deuterogattii has regional centromeres that contain only transposon relics. To investigate the impact of centromere loss on the C. deuterogattii genome, either centromere 9 or 10 was deleted. Deletion of either centromere resulted in neocentromere formation and interestingly, the genes covered by these neocentromeres maintained wild-type expression levels. In contrast to cen9∆ mutants, cen10∆ mutant strains exhibited growth defects and were aneuploid for chromosome 10. At an elevated growth temperature (37°C), the cen10∆ chromosome was found to have undergone fusion with another native chromosome in some isolates and this fusion restored wild-type growth. Following chromosomal fusion, the neocentromere was inactivated, and the native centromere of the fused chromosome served as the active centromere. The neocentromere formation and chromosomal fusion events observed in this study in C. deuterogattii may be similar to events that triggered genomic changes within the Cryptococcus/Kwoniella species complex and may contribute to speciation throughout the eukaryotic domain.

scholarly journals Visualizing and Quantifying Fusarium oxysporum in the Plant Host

2012 ◽  
Vol 25 (12) ◽  
pp. 1531-1541 ◽  
Author(s):  
Andrew Diener
Keyword(s):  
Arabidopsis Thaliana ◽  
Fusarium Oxysporum ◽  
Disease Severity ◽  
Fungal Pathogen ◽  
Vascular Cylinder ◽  
Wild Type ◽  
Fusarium Spp ◽  
Plant Host ◽  
Below Ground ◽  
Root Apices

Host-specific forms of Fusarium oxysporum infect the roots of numerous plant species. I present a novel application of familiar methodology to visualize and quantify F. oxysporum in roots. Infection in the roots of Arabidopsis thaliana, tomato, and cotton was detected with colorimetric reagents that are substrates for Fusarium spp.-derived arabinofuranosidase and N-acetyl-glucosaminidase activities and without the need for genetic modification of either plant host or fungal pathogen. Similar patterns of blue precipitation were produced by treatment with 5-bromo-4-chloro-3-indoxyl-α-l-arabinofuranoside and 5-bromo-4-chloro-3-indoxyl-2-acetamido-2-deoxy-β-d-glucopyranoside, and these patterns were consistent with prior histological descriptions of F. oxysporum in roots. Infection was quantified in roots of wild-type and mutant Arabidopsis using 4-nitrophenyl-α-l-arabinofuranoside. In keeping with an expectation that disease severity above ground is correlated with F. oxysporum infection below ground, elevated levels of arabinofuranosidase activity were measured in the roots of susceptible agb1 and rfo1 while a reduced level was detected in the resistant eir1. In contrast, disease severity and F. oxysporum infection were uncoupled in tir3. The distribution of staining patterns in roots suggests that AGB1 and RFO1 restrict colonization of the vascular cylinder by F. oxysporum whereas EIR1 promotes colonization of root apices.

scholarly journals The Impact of Hypoxia on the Host-Pathogen Interaction between Neutrophils and Staphylococcus aureus

2019 ◽  
Vol 20 (22) ◽  
pp. 5561 ◽  
Author(s):  
Natalia H Hajdamowicz ◽  
Rebecca C Hull ◽  
Simon J Foster ◽  
Alison M Condliffe
Keyword(s):  
Staphylococcus Aureus ◽  
Immune Cells ◽  
Molecular Mechanisms ◽  
Neutrophil Function ◽  
Tissue Destruction ◽  
Host Pathogen Interaction ◽  
Host Pathogen ◽  
Life Threatening ◽  
The Impact ◽  
Bactericidal Function

Neutrophils are key to host defence, and impaired neutrophil function predisposes to infection with an array of pathogens, with Staphylococcus aureus a common and sometimes life-threatening problem in this setting. Both infiltrating immune cells and replicating bacteria consume oxygen, contributing to the profound tissue hypoxia that characterises sites of infection. Hypoxia in turn has a dramatic effect on both neutrophil bactericidal function and the properties of S. aureus, including the production of virulence factors. Hypoxia thereby shapes the host–pathogen interaction and the progression of infection, for example promoting intracellular bacterial persistence, enabling local tissue destruction with the formation of an encaging abscess capsule, and facilitating the establishment and propagation of bacterial biofilms which block the access of host immune cells. Elucidating the molecular mechanisms underlying host–pathogen interactions in the setting of hypoxia will enable better understanding of persistent and recalcitrant infections due to S. aureus and may uncover novel therapeutic targets and strategies.

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