Early leaf senescence observed in the pen1pen3 double mutant is not dependent on HIR2, a protein that physically interacts with PEN1.

The pen1pen3 double mutant displays early leaf senescence that depends on salicylic acid biosynthesis, a phytohormone associated with defense and leaf senescence. PEN1, a Qa SNARE, physically interacts with HIR2, a protein that tethers immune receptors to plasma membrane nanodomains. We hypothesized that PEN1 binding to HIR2 may prevent immune receptor localization. Consistent with this hypothesis is the expectation that pen1pen3hir2 mutants would show reduced early leaf senescence when compared to pen1pen3 . We constructed the triple mutant, quantified leaf senescence, and observed early leaf senescence that was not significantly different than pen1pen3 . This result does not support our hypothesis.