Figure 13.

Alteration of phenotypes for a LEAP and one of its client proteins, depending on the physiology of the cell being examined. (a) The AtPP2-B11 F-BOX protein targets the SUCROSE NON-FERMENTING KINASEs (SnRK2.2, 2.3), positive regulators of ABA signal transduction, reducing the titer of these kinases in the cell. Both atpp2-b11 RNAi lines and LEA1-overexpressing lines have enhanced ABA sensitivity. Reducing the F-BOX titer through RNAi stabilizes the SnRK2s titer and results in increased ABA sensitivity. When the LEA1 binds AtPP2-B11, it may sequester the F-BOX protein away from SnRK2.2 and 2.3, preventing their polyubiquitination, and also increasing ABA sensitivity. (b) ATPP2-B11 F-BOX overexpression results in greater salt tolerance as does LEA1 overexpression. Reasons for the similar phenotypes under salt stress are, at this time, a matter of speculation, but a model presented in the reference supplied in the figure suggests that a transcriptional repressor is targeted by the F-BOX, and the F-BOX is stabilized during salt stress by LEA1. Green: protein stimulatory for ABA sensitivity or salt tolerance; Red: protein inhibitory for ABA sensitivity or salt tolerance; “P” = phosphorylated; tfs: transcription factors; PP2C: PROTEIN PHOSPHATASE 2C; SnRK: SUCROSE NON-FERMENTING RECEPTOR KINASES; PYR: PYRABACTIN RESISTANT PROTEIN; Rep: transcriptional repressor; UBI: UBIQUITIN.