Fungal incompatibility: evolutionary origin in pathogen defense?
In fungi, cell fusion between genetically unlike individuals triggers a cell death reaction known as the incompatibility reaction. In Podospora anserina, the genes controlling this process belong to a gene family encoding STAND proteins with an N-terminal cell death effector domain, a central NACHT domain and a C-terminal WD-repeat domain. These incompatibility genes are extremely polymorphic, subject to positive Darwinian selection and display a remarkable genetic plasticity allowing for constant diversification of the WD-repeat domain responsible for recognition of non-self. Remarkably, the architecture of these proteins is related to pathogen-recognition receptors ensuring innate immunity in plants and animals. Here, we hypothesize that these P. anserina incompatibility genes could be components of a yet-unidentified innate immune system of fungi. As already proposed in the case of plant hybrid necrosis or graft rejection in mammals, incompatibility could be a by-product of pathogen-driven divergence in host defense genes.
Laboratoire de Génétique Moléculaire des Champignons, Institut de Biochimie et de Génétique Cellulaires, UMR 5095 CNRS-Université de Bordeaux 2, 1 rue Camille St Saëns, 33077 Bordeaux Cedex, France.
Mathieu
M
Paoletti
Sven J
SJ
Saupe
D000818:Animals; D015551:Autoimmunity; D001343:Autophagy; D016923:Cell Death; D019143:Evolution, Molecular; D005656:Fungal Proteins / Q000378:metabolism; D014644:Genetic Variation; D006801:Humans; D007113:Immunity, Innate; D008024:Ligands; D008954:Models, Biological; D008957:Models, Genetic; D008962:Models, Theoretical; D009336:Necrosis; D048468:Podospora / Q000235:genetics / Q000276:immunology*; D017434:Protein Structure, Tertiary
D005656:Fungal Proteins; D008024:Ligands