Wounding increases salt tolerance in tomato plants: evidence on the participation of calmodulin-like activities in cross-tolerance signalling.
Cross-tolerance is the phenomenon by which a plant resistance to a stress results in resistance to another form of stress. It has previously been shown that salt stress causes the accumulation of proteinase inhibitors and the activation of other wound-related genes in tomato plants (Solanum lycopersicum). However, very little is known about how different stresses interact with one another, and which are the signalling components that interrelate the responses triggered by different stress types. In the present work, it is shown that mechanical wounding increases salt-stress tolerance in tomato plants through a mechanism that involves the signalling peptide systemin and the synthesis of JA. Data are also provided indicating that calmodulin-like activities are necessary for the downstream signalling events that lead to cross-tolerance between wounding and salt stress. Finally, evidence was gathered supporting the hypothesis that LeCDPK1, a Ca2+ -dependent protein kinase from tomato previously described in our laboratory, could participate in this cross-tolerance mechanism interrelating the signalling responses to wounding and salt stress.
Capiati
Daniela Andrea
DA
Instituto de Investigaciones en Ingeniería Genética y Biología Molecular, Consejo Nacional de Investigaciones Científicas y Técnicas, Facultad de Ciencias Exactas y Naturales, Universidad de Buenos Aires, 1428 Buenos Aires, Argentina.
País
Silvia Marina
SM
Téllez-Iñón
María Teresa
MT
D000040:Abscisic Acid / Q000502:physiology; D000222:Adaptation, Physiological / Q000502:physiology*; D002147:Calmodulin / Q000502:physiology; D003517:Cyclopentanes / Q000378:metabolism*; D018506:Gene Expression Regulation, Plant; D017343:Genes, Plant; D018551:Solanum lycopersicum / Q000235:genetics / Q000502:physiology*; D054883:Oxylipins; D010455:Peptides / Q000502:physiology*; D011494:Protein Kinases / Q000378:metabolism; D015398:Signal Transduction / Q000502:physiology; D012965:Sodium Chloride / Q000378:metabolism*; D017871:Calcium-Calmodulin-Dependent Protein Kinases
D000040:Abscisic Acid; D002147:Calmodulin; D003517:Cyclopentanes; D054883:Oxylipins; D010455:Peptides; D011494:Protein Kinases; D012965:Sodium Chloride; D017871:Calcium-Calmodulin-Dependent Protein Kinases; C073704:systemin; C011006:jasmonic acid