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Rapamycin mimics the incompatibility reaction in the fungus Podospora anserina
Karine Dementhon1, Mathieu Paoletti, Bérangère Pinan-Lucarré
1Laboratoire de Génétique Moléculaire des Champignons, Institut de Biochimie et de Génétique Cellulaires, UMR 5095 CNRS-Université de Bordeaux 2, Bordeaux, France.
Abstract:
In filamentous fungi, a programmed cell death (PCD) reaction occurs when cells of unlike genotype fuse. This reaction is caused by genetic differences at specific loci termed het loci (for heterokaryon incompatibility). Although several het genes have been characterized, the mechanism of this cell death reaction and its relation to PCD in higher eukaryotes remains largely unknown. In Podospora anserina, genes induced during the cell death reaction triggered by the het-R het-V interaction have been identified and termed idi genes. Herein, we describe the functional characterization of one idi gene (idi-1) and explore the connection between incompatibility and the response to nutrient starvation. We show that IDI-1 is a cell wall protein which localizes at the septum during normal growth. We found that induction of idi-1 and of the other known idi genes is not specific of the incompatibility reaction. The idi genes are induced upon nitrogen and carbon starvation and by rapamycin, a specific inhibitor of the TOR kinase pathway. The cytological hallmarks of het-R het-V incompatibility (increased septation, vacuolization, coalescence of lipid droplets, induction of autophagy, and cell death) are also observed during rapamycin treatment. Globally the cytological alterations and modifications in gene expression occurring during the incompatibility reaction are similar to those observed during starvation or rapamycin treatment.
Insights
Fungal heterokaryon incompatibility triggers programmed cell death (PCD) via specific genes. These genes are also activated by nutrient starvation and TOR pathway inhibition, suggesting a conserved stress response mechanism.
Area of Science:
- Mycology
- Cell Biology
- Genetics
Background:
- Filamentous fungi exhibit programmed cell death (PCD) when genetically dissimilar cells fuse, a phenomenon known as heterokaryon incompatibility.
- This incompatibility is mediated by specific genetic loci (het loci), but the underlying mechanisms and links to higher eukaryotic PCD remain unclear.
Purpose of the Study:
- To functionally characterize the idi-1 gene involved in the PCD reaction of Podospora anserina.
- To investigate the relationship between heterokaryon incompatibility and cellular responses to nutrient starvation.
Main Methods:
- Functional characterization of the idi-1 gene, a cell wall protein.
- Analysis of idi gene induction under nutrient starvation (nitrogen, carbon) and rapamycin treatment (TOR pathway inhibition).
- Comparative cytological and gene expression analysis between incompatibility, starvation, and rapamycin treatment.
Main Results:
- IDI-1 localizes to the septum during normal fungal growth.
- Induction of idi genes is not exclusive to heterokaryon incompatibility but also occurs during nitrogen/carbon starvation and rapamycin treatment.
- Cytological features of incompatibility, including increased septation, vacuolization, lipid droplet coalescence, autophagy, and cell death, are recapitulated by rapamycin treatment.
Conclusions:
- The idi genes are part of a conserved cellular stress response pathway, not solely linked to heterokaryon incompatibility.
- Fungal heterokaryon incompatibility shares significant mechanistic and molecular parallels with nutrient starvation and TOR pathway inhibition responses.
