The study demonstrates that ABI5‑Binding Proteins (AFPs) interact with multiple components of the core ABA signaling pathway and serve as substrates for SnRK2 kinases and PP2C phosphatases, linking them to MAP kinases and 14‑3‑3 proteins. Phosphorylation of AFP2, promoted by ABA, stabilizes the protein and influences its subcellular localization, thereby modulating its ability to inhibit ABA responses during seed germination.

The study identifies the RNA‑binding protein AtG3BP1 as a phosphorylation target of MAPKs MPK3, MPK4, and MPK6 at Ser257 in Arabidopsis thaliana and shows that this modification promotes susceptibility to bacterial pathogens, suppresses ROS accumulation and salicylic acid biosynthesis, and maintains stomatal opening. Phospho‑mimic and phospho‑dead mutants reveal that phosphorylation stabilizes AtG3BP1 by preventing proteasomal degradation, highlighting a novel post‑translational control layer in plant immunity.

The study identifies a moss‑specific fusion protein, Rosetta NATD‑MAPK 1 (RAK1), that combines a MAPK domain with an N‑acetyltransferase and demonstrates that its acetyltransferase activity is enhanced upon MAPK activation. Knockout of RAK1 impairs the 2D‑to‑3D developmental transition in Physcomitrium patens, and mass‑spectrometry reveals associated changes in acetylation and phosphorylation linked to metabolic reprogramming.

The study reveals that a conserved serine adjacent to the catalytic glutamate in TIR domains is essential for NAD+‑cleaving activity, and that phosphorylation of this serine by plant calcium‑dependent protein kinases (CPKs) or mammalian kinases (CAMK2D, TBK1) inhibits the activity, thereby preventing growth repression and cell death. This phosphorylation-based mechanism provides a universal means to balance growth and immune defense across species.

The study identifies RAF24, a B4 Raf-like MAPKKK, as a novel regulator of flowering time in Arabidopsis, demonstrating that RAF24 controls the phosphorylation of the ubiquitin ligase HUB2 via SnRK2 kinases, thereby modulating H2Bub1 levels. Phospho‑mimetic and phospho‑ablative HUB2 mutants confirm that phosphorylation at S314 is critical for proper flowering timing.

The study uncovers a feedback mechanism wherein phosphomimic mutation (PetD T4E) or deletion of the N‑terminal five amino acids of the b6f subunit PetD suppresses STT7 kinase activity, leading to a State 1‑locked phenotype and impaired electron transfer, highlighting the essential regulatory role of the PetD N‑terminus in photosynthetic state transitions.