Abstract
Innate immunity signaling pathways in plants are regulated by mitogen-activated protein kinase (MAPK) cascades. Arabidopsis MEKK1, a MAPK kinase kinase (MAPKKK) is an important factor of innate immunity signaling in the upstream of MPK4, but not essential for MPK3 and MPK6 (MAPKs). We already showed that loss of MEKK1 results in temperature-sensitive and tissue-specific cell death and H2O2 accumulation that are partly dependent on both RAR1 and SID2. Here, we show that overexpression of MEKK1 N-terminal domain (MEKK1N) which possibly has a regulatory role for MEKK1 kinase activity resulted in similar phenotype of mekk1. Constitutive overexpression of MEKK1N showed severe growth retardation. Interestingly, the MEKK1N-OX phenotype was suppressed by either high temperature, rar1 or sgt1b mutation. The MEKK1N construct fused to a steroid-inducible promoter also exhibited vasculature-preferred cell death with steroid dependent manner. These data strongly suggest that MEKK1N negatively regulates MEKK1 function.
