8.A.211.1.1
Sal1, a PP2C.D phosphatase of 399 aas and at least one TMS.  SAL1 (SENSITIVE TO ALUMINUM 1) is a major negative regulator of abscisic acid (ABA) responses during seed germination and cold acclimation. This phosphatase confers insensitivity to ABA and modulates negatively the AKT2/3 activity, which mediates K⁺ transport and membrane polarization during stress situations, probably by protein dephosphorylation. It prevents stomata closure by inactivating the S-type anion efflux channel SLAC1 and its activator SRK2E. It also represses KIN10 activity by the specific dephosphorylation of its T-loop Thr-198, leading to a poststress inactivation of SnRK1 signaling (Rodrigues et al. 2013). SAL1 encodes a plasma membrane (PM)-localized PP2C.D phosphatase which is a crucial regulator of Al resistance. SAL1 interact s with and inhibits the activity of PM H⁺-ATPases, and mutation of SAL1 increased PM H⁺-ATPase activity and Al uptake, causing hypersensitivity to internal Al toxicity. Furthermore, knockout of NRAT1 (NRAMP ALUMINUM TRANSPORTER 1), encoding an Al uptake transporter in a sal1 background, rescued the Al-sensitive phenotype of sal1, revealing that coordination of Al accumulation in the cell wall and symplasm is critical for Al resistance in rice. By contrast, Rodrigues et al. 2013 found that mutations of PP2C.D phosphatase-encoding genes in Arabidopsis thaliana enhanced Al resistance, which was attributed to increased malate secretion. This protein shows 29% identity and 50% similarity with the P-type ATPase with TC# 3.A.3.5.4, residues 253 - 331 aligning with 635 - 714 in the latter protein.