“…To date, genetic screens for ABA-hypersensitive mutants have indicated that processes including farnesylation (era1; Cutler et al, 1996;Pei et al, 1998), inositol 1,4,5-triphosphate (IP 3 ) dephosphorylation (fry1; Xiong et al, 2001b), and RNA metabolism (hyl1; Lu and Fedoroff, 2000;abh1, Hugouvieux et al, 2001;sad1, Xiong et al, 2001a) are required to attenuate the ABA signal. However, surprisingly few non-transcription factor-encoding genes have been identified as recessive ABA-insensitive disruption mutants, namely, the G-protein a-subunit GPA1 , the RCN1 protein phosphatase type 2A subunit , the OST1/ SnRK2E protein kinase (Mustilli et al, 2002;Yoshida et al, 2002), the AtRBOHD/F NADPH oxidases (Kwak et al, 2003), ABI8 (Brocard-Gifford et al, 2004), RPK1 (Osakabe et al, 2005), and GCA2 (Himmelbach et al, 1998).…”