MdBRC1 and MdFT2 Interaction Fine-Tunes Bud Break Regulation in Apple
Authors: Gioppato, H. A., Estevan, J., Al Bolbol, M., Soriano, A., Garighan, J., Jeong, K., Georget, C., Soto, D. G., El Khoury, S., Falavigna, V. d. S., George, S., Perales, M., Andres, F.
The study identifies the transcription factor MdBRC1 as a key inhibitor of bud growth during the ecodormancy phase in apple (Malus domestica), directly regulating dormancy‑associated genes and interacting with the flowering promoter MdFT2 to modulate bud break. Comparative transcriptomic analysis and gain‑of‑function experiments in poplar demonstrate that MdFT2 physically binds MdBRC1, attenuating its repressive activity and acting as a molecular switch for the transition to active growth.
The study introduced full-length SOC1 genes from maize and soybean, and a partial SOC1 gene from blueberry, into tomato plants under constitutive promoters. While VcSOC1K and ZmSOC1 accelerated flowering, all three transgenes increased fruit number per plant mainly by promoting branching, and transcriptomic profiling revealed alterations in flowering, growth, and stress‑response pathways.
The study examines how the SnRK1 catalytic subunit KIN10 integrates carbon availability with root growth regulation in Arabidopsis thaliana. Loss of KIN10 reduces glucose‑induced inhibition of root elongation and triggers widespread transcriptional reprogramming of metabolic and hormonal pathways, notably affecting auxin and jasmonate signaling under sucrose supplementation. These findings highlight KIN10 as a central hub linking energy status to developmental and environmental cues in roots.
SnRK2.4 and SnRK2.10 redundantly control developmental leaf senescence by sustaining ABA production and signaling
Authors: Anielska-Mazur, A., Rachowka, J., Polkowska-Kowalczyk, L., Krzyszton, M., Cieslak, D., Mazur, R., Bucholc, M., Rakowska, J., Trzmiel, D., Stachula, P., Olechowski, M., Swiezewski, S., Dobrowolska, G., Kulik, A.
The study reveals that the Arabidopsis SnRK2.4 and SnRK2.10 kinases, previously known for stress responses, are activated during normal developmental leaf senescence and act redundantly to promote this process. They stimulate ABA accumulation by up‑regulating NCED2 and modulate expression of ABA‑responsive and senescence genes, while also enhancing MAPKKK18 expression and activity, linking SnRK2 signaling to MAPK pathways.
The study generated a temporal physiological and metabolomic map of leaf senescence in diverse maize inbred lines differing in stay‑green phenotype, identifying 84 metabolites associated with senescence and distinct metabolic signatures between stay‑green and non‑stay‑green lines. Integration of metabolite data with genomic information uncovered 56 candidate genes, and reverse‑genetic validation in maize and Arabidopsis demonstrated conserved roles for phenylpropanoids such as naringenin chalcone and eriodictyol in regulating senescence.