Summary V ictorin, the host‐selective toxin produced by the fungus C ochliobolus victoriae , induces programmed cell death ( PCD ) in victorin‐sensitive oat lines with characteristic features of animal apoptosis, such as mitochondrial permeability transition, chromatin condensation, nuclear DNA laddering and rRNA / mRNA degradation. In this study, we characterized a calcium‐binding protein, namely AsALG ‐2, which might have a role in the victorin‐induced PCD . AsALG ‐2 is homologous to the A poptosis‐ L inked G ene ALG ‐2 identified in mammalian cells. Northern blot analysis revealed that the accumulation of AsALG ‐2 transcripts increased during victorin‐induced PCD , but not during necrotic cell death. Salicylic acid, chitosan and chitin strongly activated the expression of general defence response genes, such as PR ‐10 ; however, neither induced cell death nor the accumulation of AsALG ‐2 mRNA . Pharmacological studies indicated that victorin‐induced DNA laddering and AsALG ‐2 expression were regulated through similar pathways. The calcium channel blocker, nifedipine, moderately inhibited the accumulation of AsALG ‐2 mRNA during cell death. Trifluoperazine (calmodulin antagonist) and K252a (serine‐threonine kinase inhibitor) reduced the victorin‐induced phytoalexin accumulation, but did not prevent the victorin‐induced DNA laddering or accumulation of AsALG ‐2 mRNA . Taken together, our investigations suggest that there is a calcium‐mediated signalling pathway in animal and plant PCD in common.