We isolated 13 tobacco calmodulin (CaM) genes, NtCaM1-13, and analyzed their expression profile in response to pathogen infection and wounding using specific DNA probes for individual CaM genes and specific antibodies for CaM proteins in groups I (NtCaM1/2), II (NtCaM3/4/5/6/7/8/11/12 and 9/10) and III (NtCaM13), respectively. Synchronous cell death in tobacco mosaic virus (TMV)-infected N-gene-containing tobacco leaves accompanied a predominant accumulation of NtCaM1, 2 and 13 transcripts and NtCaM13-type protein, which is a possible ortholog of soybean defense-involved CaM (SCaM-4), preceding induction of PR-1 and PR-3 defense genes. Accumulation of NtCaM1, 2, 3 and 4 transcripts was induced within 30 min after wounding and NtCaM1-type protein accumulated transiently after wounding. NtCaM13-type protein, which was found at a low level in healthy leaves, decreased instantly after wounding. The treatment with a proteasome inhibitor, lactacystin, enhanced wound-induced accumulation of NtCaM1-type protein and inhibited wound-induced decrease of NtCaM13-type protein, suggesting that proteasome activity is involved in the degradation of these CaMs. Thus, our results indicate that levels of individual CaM proteins are differentially regulated both transcriptionally and post-transcriptionally in tobacco plants that are exposed to stresses such as pathogen-induced hypersensitive cell death and wounding.