14-3-3 proteins and the response to abiotic and biotic stress

• Published in: Plant molecular biology Vol. 50; no. 6; pp. 1031 - 1039
• Main Authors: Roberts, Michael R., Salinas, Julio, Collinge, David B.
• Format: Journal Article
• Language: English
• Published: Netherlands Springer Nature B.V 01.12.2002
• Subjects: 14-3-3 Proteins; Ascomycota; Ascomycota - growth & development; binding proteins; Binding sites; Blotting, Northern; cold stress; defense mechanisms; disease resistance; Environmental control; Gene expression; Gene Expression Regulation, Plant; Gene Expression Regulation, Plant - radiation effects; genetics; growth & development; heat stress; Light; mechanical damage; metabolism; microbiology; osmotic pressure; plant diseases and disorders; plant pathogens; plant physiology; plant proteins; Plants; Plants - genetics; Plants - metabolism; Plants - microbiology; Proteins; radiation effects; RNA, Messenger; RNA, Messenger - genetics; RNA, Messenger - metabolism; RNA, Messenger - radiation effects; salinity; Signal transduction; Stress, Mechanical; Temperature; Tyrosine 3-Monooxygenase; Tyrosine 3-Monooxygenase - genetics; Tyrosine 3-Monooxygenase - metabolism
• ISSN: 0167-4412; 1573-5028
• DOI: 10.1023/A:1021261614491

14-3-3 proteins function as regulators of a wide range of target proteins in all eukaryotes by effecting direct protein-protein interactions. Primarily, interactions between 14-3-3 proteins and their targets are mediated by phosphorylation at specific sites on the target protein. Hence, interactions with 14-3-3s are subject to environmental control through signalling pathways which impact on 14-3-3 binding sites. Because 14-3-3 proteins regulate the activities of many proteins involved in signal transduction, there are multiple levels at which 14-3-3 proteins may play roles in stress responses in higher plants. In this article, we review evidence which implicates 14-3-3 proteins in responses to environmental, metabolic and nutritional stresses, as well as in defence responses to wounding and pathogen attack. This evidence includes stress-inducible changes in 14-3-3 gene expression, interactions between 14-3-3 proteins and signalling proteins and interactions between 14-3-3 proteins and proteins with defensive functions.