Figure 9.

Model for the Function of Sulfate in ABA Biosynthesis and Stomatal Closure.

Enzymes catalyzing reactions (black arrows) in the biosynthesis pathways of Cys and ABA as well as the sensing of ABA for stomatal closure are shown in yellow boxes. Red box indicates the nonactive apoenzyme, which requires the cofactor for activation. Asterisks indicate enzymes that have been shown by this study to be essential for sulfate/Cys-induced stomatal closure. The stimulating effects of metabolites or enzymes on downstream reactions are depicted as blue arrows or green open arrows, respectively. Numbers in gray circles indicate references for known regulations/processes not experimentally addressed:

1: Synthesis of Cys is limited by provision of O-actylserine and sulfide (Takahashi et al., 2011).

2: Cys is the substrate of the MoCo-sulfurylase ABA3 required for activation of AAO3 (Bittner et al., 2001).

3: Cys level affects AAO activity in vivo (Cao et al., 2014).

4: PYR/PYL acts as an ABA receptor and controls PP2C activity (e.g. ABI1; Park et al., 2009).

5: PP2C activity regulates activation of OST1 in response to ABA (Vlad et al., 2009).

6: OST1 activates SLAC1 by phosphorylation at multiple residues (Geiger et al., 2009; Lee et al., 2009).

7: OST1 phosphorylates RBOHF (NADPH oxidase; Sirichandra et al., 2009).

8: ROS induce stomatal closure in an ABA2-dependent manner (Sierla et al., 2016).

9: SLAC1 is essential for ABA-induced stomatal closure (Vahisalu et al., 2008).