Pseudogymnoascus destructans transcriptome changes during white-nose syndrome infections.
Sophia M Reeder1, Jonathan M Palmer2, Jenni M Prokkola1
1a Department of Biology , Bucknell University , Lewisburg , PA , USA.
Virulence
|June 15, 2017
Summary
White nose syndrome (WNS) in bats is caused by the fungus Pseudogymnoascus destructans. This study reveals fungal gene expression changes during infection, highlighting responses to host interactions and potential targets for mitigation.
Area of Science:
- Mycology
- Bat biology
- Pathogen genomics
Background:
- White nose syndrome (WNS) is a devastating fungal disease affecting hibernating bats in North America.
- The causative agent, Pseudogymnoascus destructans, exhibits both saprotrophic and parasitic growth modes.
- WNS leads to significant bat mortality, disrupting hibernation and impacting ecosystems.
Purpose of the Study:
- To investigate fungal gene expression patterns of Pseudogymnoascus destructans during bat infection.
- To identify specific fungal pathways involved in host-pathogen interactions and WNS pathology.
- To explore potential targets for therapeutic interventions against WNS.
Main Methods:
- Comparative RNA-Sequencing (RNA-Seq) of P. destructans.
- Gene expression analysis of the fungus cultured in vitro versus during in vivo infection of Myotis lucifugus.
- Analysis of differential gene expression under varying temperature conditions (in vitro: 10–14°C; in vivo: 4–37°C).
Main Results:
- Significant differential gene expression in P. destructans during WNS infection.
- Upregulated pathways include heat shock responses, cell wall remodeling, and micronutrient acquisition.
- Fungal adaptations suggest mechanisms for evading host immune responses.
Conclusions:
- Pseudogymnoascus destructans actively regulates gene expression in response to host-pathogen interactions during WNS.
- Fungal cell wall alterations may facilitate immune evasion.
- Identified upregulated pathways offer potential targets for WNS mitigation strategies and understanding host-pathogen co-evolution.


