Fungal incompatibility: evolutionary origin in pathogen defense?

Area of Science:

• Mycology
• Evolutionary Biology
• Immunology

Background:

• Fungal cell fusion between unlike individuals triggers an incompatibility reaction, a form of programmed cell death.
• In *Podospora anserina*, this process is controlled by genes encoding STAND proteins, characterized by N-terminal death effector, central NACHT, and C-terminal WD-repeat domains.

Purpose of the Study:

• To investigate the potential role of fungal incompatibility genes as components of an innate immune system.
• To explore the hypothesis that fungal incompatibility is a byproduct of pathogen-driven divergence in host defense genes.

Main Methods:

• Analysis of the genetic architecture and evolutionary patterns of fungal incompatibility genes.
• Comparative analysis of fungal STAND proteins with pathogen-recognition receptors in plants and animals.

Main Results:

• Fungal incompatibility genes exhibit high polymorphism and are under positive Darwinian selection.
• These genes show remarkable plasticity, particularly in the WD-repeat domain responsible for non-self recognition.
• The protein architecture of these fungal genes is analogous to pathogen-recognition receptors in other eukaryotes.

Conclusions:

• Fungal incompatibility genes, particularly STAND proteins, are strong candidates for components of a fungal innate immune system.
• Incompatibility may represent an evolutionary byproduct of host-pathogen interactions, similar to phenomena observed in plant and animal immunity.