Table I.
Ler
|
jar1-1
|
ost1-2
|
gork1
|
|||||
---|---|---|---|---|---|---|---|---|
H2O2 | SA | H2O2 | SA | H2O2 | SA | H2O2 | SA | |
% | μm | % | μm | % | μm | % | μm | |
Control | 100.0 ± 3.1 | 4.47 ± 0.27 | 94.4 ± 3.8 | 3.69 ± 0.17 | 98.6 ± 2.7 | 3.65 ± 0.12 | 101.1 ± 3.5 | 4.51 ± 0.21 |
MJ | 128.4 ± 2.5 | 1.33 ± 0.16 | 97.5 ± 3.0 | 3.50 ± 0.26 | 112.8 ± 3.5 | 2.41 ± 0.17 | 127.4 ± 3.5 | 4.22 ± 0.15 |
ABA | 121.5 ± 3.1 | 1.62 ± 0.29 | 116.0 ± 2.8 | 2.54 ± 0.20 | 99.3 ± 3.7 | 3.59 ± 0.13 | 120.5 ± 3.7 | 2.67 ± 0.18 |
Influence of jar1-1, ost1-2, and gork1 mutations on H2O2 production and stomatal closure in response to 20 μm MJ or ABA. Changes in ROS levels were analyzed by measuring H2DCF-DA fluorescence levels in guard cells in response to a 30-min treatment with ABA, MJ, or solvent control addition. To determine the consequence of mutations on stomatal closure, leaf epidermis were allowed to open in light for 2 h, then ABA or MJ was applied for 2 h. Results are the averages ± se (n = 60) of 3 to 4 independent experiments. The extents of H2O2 production in the guard cells of wild-type plants, without MJ or ABA, are taken as 100%. SA, stomatal apertures.