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We have shown that AHK5 functions in guard cells to mediate stomatal responses to various stimuli that generate H2O2.
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Stomatal responses to drought stress are often mediated by signaling pathways including Abscisic Acid (ABA) [ 2, 15, 16].
In summary so far, the data presented show that darkness-induced H2O2 synthesis, which is generated by ATRBOHD/F, signals through AHK5 to mediate stomatal closure, and that AHK5 is positioned downstream of H2O2 and NO in the signal response pathway.
Finally, in the context of the evolution of stomatal signaling pathways [ 58 60], our evidence that [CO2]-induced stomatal responses require ABA suggests that stomatal ABA responses are in evolutionary terms ancestral to elevated [CO2] responses.
This lack of a stomatal response to changes in VPD strongly implicates ABA biosynthesis in the stomatal responses to changes in VPD in angiosperms.
We observed the three phases of stomatal responses to D [ 6, 12, 25, 37].
These two proteins cooperate with CBL9 to activate K+-channels and regulate stomatal responses [ 89].
Abscisic acid has already been linked to NO in germination and stomatal responses.
These results also correlate with in planta stomatal responses and whole plant phenotypes of higher order pp2c mutants that show constitutive stomatal closing.
We describe a model for stomatal responses to increasing D based upon cellular water relations.
describe the requirement for ABA and ABA signaling in both elevated CO2-induced stomatal closure and elevated CO2-induced reductions in stomatal density, suggesting that ABA itself is downstream of stomatal CO2 perception and that ABA signaling is likely to predate the origin of CO2-induced stomatal responses.
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