SGT1 contributes to maintaining protein levels of MEK2DD to facilitate hypersensitive response-like cell death in Nicotiana benthamiana

• SGT1 is required for HR-like cell death induced by MEK2DD.
• Silencing SGT1 reduces protein levels of MEK2DD, but not MEK2WT.
• SKP1 is not required for HR-like cell death induced by MEK2DD.
• SGT1 may have novel functions for maintaining protein levels of MEK2 active form other than those already described.

Gene silencing revealed that the mitogen-activated protein kinase (MAPK) cascade in Solanaceae consisted with MEK2-WIPK/SIPK, is required for R protein-induced hypersensitive response (HR) cell death and/or resistance. Overexpression of MEK2DD results in HR-like cell death. MEK2DD is a phospho-mimic and constitutive active form harboring mutations at putative phosphorylation sites of upstream MAPKKK. The molecular mechanism that induces HR-like cell death is unknown. Here we report SGT1 is required for the accumulation of MEK2DD protein, not MEK2WT. Virus-induced gene silencing of SGT1 resulted in low protein accumulation of MEK2DD. This result suggests that SGT1 has a positive role in the accumulation of the MEK2 active form protein to facilitate signal transduction.