Transcriptionally and post-transcriptionally regulated response of 13 calmodulin genes to tobacco mosaic virus-induced cell death and wounding in tobacco plant.

Publisher: Blackwell Science Ltd. on behalf of the Federation of European Biochemical Societies Country of Publication: England NLM ID: 0107600 Publication Model: Print Cited Medium: Print ISSN: 0014-2956 (Print) Linking ISSN: 00142956 NLM ISO Abbreviation: Eur J Biochem Subsets: MEDLINE

Publication: -2004: Oxford, UK : Blackwell Science Ltd. on behalf of the Federation of European Biochemical Societies
Original Publication: Berlin, New York, Springer.

Genes, Plant* ; Plants, Toxic*; Acetylcysteine/*analogs & derivatives ; Calmodulin/*genetics ; Nicotiana/*genetics ; Nicotiana/*virology ; Tobacco Mosaic Virus/*growth & development; Acetates/pharmacology ; Acetylcysteine/pharmacology ; Calmodulin/metabolism ; Cloning, Molecular ; Cyclopentanes/pharmacology ; Cysteine Endopeptidases/metabolism ; Cysteine Proteinase Inhibitors/pharmacology ; Gene Expression Regulation, Plant ; Multienzyme Complexes/antagonists & inhibitors ; Multienzyme Complexes/metabolism ; Oxylipins ; Plant Diseases/genetics ; Plant Growth Regulators/pharmacology ; Plant Leaves/virology ; Proteasome Endopeptidase Complex ; Protein Isoforms/genetics ; Protein Isoforms/metabolism ; RNA Processing, Post-Transcriptional ; Salicylic Acid/pharmacology ; Signal Transduction ; Tissue Distribution

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.

0 (Acetates)
0 (Calmodulin)
0 (Cyclopentanes)
0 (Cysteine Proteinase Inhibitors)
0 (Multienzyme Complexes)
0 (Oxylipins)
0 (Plant Growth Regulators)
0 (Protein Isoforms)
133343-34-7 (lactacystin)
900N171A0F (methyl jasmonate)
EC 3.4.22.- (Cysteine Endopeptidases)
EC 3.4.25.1 (Proteasome Endopeptidase Complex)
O414PZ4LPZ (Salicylic Acid)
WYQ7N0BPYC (Acetylcysteine)

Date Created: 20010717 Date Completed: 20010816 Latest Revision: 20231213

20240513

10.1046/j.1432-1327.2001.02301.x

11453984