Thanks bro. 😎

(4) Overall, we proved phosphorylation by ERECTA-YODA pathway positively regulates SCRM in embryos, which differs with the phosphor-dependent degradation model found in stomata. That's a novel example of how MAPK signaling differentially regulates a single target in distinct developmental contexts.

(3) Reported stomatal gain-of-function scrm-D (R236H) mutant brings overproliferation of stomata by disrupting the interaction with MPK3/6. However, scrm-D leads to a severe loss of zygotic polarity & impaired embryo. Phosphor-inactive SCRM 6A can rescue stomatal phenotypes, but not in the embryo.

(2) SCRM functions in parallel with the well-known target WRKY2 of the ERECTA-YODA signaling pathway during embryo development. Double mutation of SCRM and WRKY2 results in phenotypes strikingly similar to those of yoda, along with a nearly complete loss of the WOX8-YFP signal in vivo.

(1) SCRM is a key factor in promoting zygotic polarity by activating the embryo-specific gene WOX8 in Arabidopsis zygotes and early embryos.