Arabidopsis MAP Kinase 4 Negatively Regulates Systemic Acquired Resistance

Arabidopsis MAP Kinase 4 Negatively Regulates Systemic Acquired Resistance

December 22, 2000 | Morten Petersen, Peter Brodersen, Henrik Naested, Erik Andreasson, Ursula Lindhart, Bo Johansen, Henrik B. Nielsen, Michelle Lacy, Mark J. Austin, Jane E. Parker, Sashi B. Sharma, Daniel F. Klessig, Rob Martienssen, Ole Mattsson, Anders B. Jensen, and John Mundy
The study investigates the role of Arabidopsis MAP kinase 4 (MPK4) in systemic acquired resistance (SAR) and plant defense responses. The mpk4 mutant, generated by transposon inactivation, exhibits constitutive SAR, elevated salicylic acid (SA) levels, and enhanced resistance to virulent pathogens. RNA blot and microarray analyses show that mpk4 constitutively expresses pathogenesis-related (PR) genes and fails to induce PDF1.2 and THI2.1 mRNA expression in response to jasmonic acid (JA). MPK4 kinase activity is required for repressing SAR, as an inactive MPK4 form fails to complement the mpk4 phenotype. Genetic analysis indicates that MPK4 functions upstream of SA in SAR signaling and is independent of NPR1. Additionally, MPK4 is required for JA-mediated gene expression, suggesting its role in integrating SA- and JA-dependent responses. The expression pattern of MPK4 suggests that it may be involved in cross-talk between pathogen and osmotic stress signaling. Overall, the findings highlight the importance of MPK4 in regulating plant defenses against pathogens.The study investigates the role of Arabidopsis MAP kinase 4 (MPK4) in systemic acquired resistance (SAR) and plant defense responses. The mpk4 mutant, generated by transposon inactivation, exhibits constitutive SAR, elevated salicylic acid (SA) levels, and enhanced resistance to virulent pathogens. RNA blot and microarray analyses show that mpk4 constitutively expresses pathogenesis-related (PR) genes and fails to induce PDF1.2 and THI2.1 mRNA expression in response to jasmonic acid (JA). MPK4 kinase activity is required for repressing SAR, as an inactive MPK4 form fails to complement the mpk4 phenotype. Genetic analysis indicates that MPK4 functions upstream of SA in SAR signaling and is independent of NPR1. Additionally, MPK4 is required for JA-mediated gene expression, suggesting its role in integrating SA- and JA-dependent responses. The expression pattern of MPK4 suggests that it may be involved in cross-talk between pathogen and osmotic stress signaling. Overall, the findings highlight the importance of MPK4 in regulating plant defenses against pathogens.
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