Delta Fphog1 mutants of Fusarium proliferatum obtained by targeted gene disruption of Fphog1, an orthologue of the Saccharomyces cerevisiae hog1 MAPK gene showed increased sensitivity towards different abiotic stressors including UV-irradiation, heat, salt, osmotic and hydrogen peroxide treatments. Incubation of the Delta Fphog1 mutants under hyperosmotic conditions was accompanied with prolonged growth arrest, inhibition of conidial germination, morphological abnormalities and time-dependent increase of the cell death rate. The wild type Fphog1 gene, under the control of its own promoter, was able to rescue the multistress sensitivity of the mutant strain. Real time qPCR data demonstrated that under salt and sorbitol stress conditions the Fphog1 gene is not subject of transcriptional regulation. Levels of reactive oxygen species (ROS), mitochondrial membrane permeability transition, nuclear disintegration and DNA fragmentation, indicators of programmed cell death (PCD) all showed significant increases under osmotic stress conditions in the Delta Fphog1 mutant in comparison to the wild type strain. These results suggest that an important function of Fphog1 is attenuating apoptotic phenotypes under salt and sorbitol stressors.