Skip to main content
. 2016 Mar 4;12(3):e1005835. doi: 10.1371/journal.pgen.1005835

Fig 4. TOPP1 and AtI-2 suppress SnRK2.6 signaling.

Fig 4

(A) TOPP1 and AtI-2 suppressed the activity of SnRK2.6, which can be released by PYL11 in the presence of ABA. ABA signaling pathway was reconstituted by co-expression of TOPP1, AtI-2, PYL11, SnRK2.6 and ABF2 in wild type (Col-0) protoplasts. The induction of RD29B::LUC was used as the ABA-responsive reporter, while ZmUBQ::GUS was used as the control for transformation efficiency. After co-transformation, protoplasts were incubated for 4 h under light without (close bars) or with 5 μM ABA (open bars). Relative luciferase activities were statistically summarized from at least three biological replicates. Error bars indicate SD. (n = 3). (B) Increased SnRK2.2/3/6 activities in topp1 and ati-2 mutants in in-gel kinase assay. The total proteins were extracted from 4-day-old seedlings without or with ABA treatment. Histone was used as a substrate for SnRK2.2/3/6. Coomassie blue staining indicates the equal loading. The experiment was repeated at least three times with similar results.