bkk1-1/bak1-5 plants show hyper suppression ofFv/Fm during P. syringaeDC3000 infection.
As primary PRRs mediate chloroplast immune signals, the cell surface
co-receptor mutants bak1-5 , bkk1-1 and double mutantbkk1-1/bak1-5 were used to assess their contribution to alteredFv/Fm dynamics during DC3000
infection. bkk1-1 plants pre-treated with flg22, elf18 and chitin
16 h prior to infection with DC3000 showedFv/Fm infection signatures
equivalent to those measured following DC3000hrpA infection in
Col-0 plants (Figure 4A-C, Sup Figure 1a, b). DC3000 challengedbak1-5 plants showed a small but significantly greater
suppression of Fv/Fm compared to
Col-0 (Figure 4D), as expected given its partial loss of MTI function
(Roux et al. , 2011). These data highlight both the power of
quantitative chlorophyll fluorescence measurements and the ability to
dynamically monitor effector impact on chloroplast physiology.
Interestingly, Fv/Fm dynamics in
DC3000hrpA challenged bak1-5 leaves pre-treated with flg22
or elf18 prior to infection were WT in response, whereas chitin
pre-treatment only partial protected againstFv/Fm suppression in thebak1-5 background (Figure 4D-F, Sup Figure 1c, d). Strikingly,
MAMP pre-treatment with flg22, elf18 or chitin had no protective effect
on Fv/Fm dynamics in thebkk1-1/bak1-5 double mutant withFv/Fm suppression being identical
and often greater than the respective Col-0 control treatment (Figure
4E-G, Sup Figure 1d, e).
Pre-treatment of leaves with DAMPs results in protection of