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 engineers Type‑B response regulators to alter their transcriptional activity and cytokinin sensitivity, enabling precise modulation of cytokinin‑dependent traits. Using tissue‑specific promoters, the synthetic transcription factors were deployed in Arabidopsis thaliana to reliably increase or decrease lateral root numbers, demonstrating a modular platform for controlling developmental phenotypes.

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 characterizes the tomato class B heat shock factor SlHSFB3a, revealing its age‑dependent expression in roots and its role in enhancing lateral root density by modulating auxin homeostasis. Overexpression of SlHSFB3a increases lateral root emergence, while CRISPR‑mediated knockouts produce the opposite phenotype, indicating that SlHSFB3a regulates auxin signaling through repression of auxin repressors and activation of the ARF7/LOB20 pathway.

The study investigated unexpected leaf spot symptoms in Psa3‑resistant kiwifruit (Actinidia) germplasm, finding that Psa3 was detectable by qPCR and metabarcoding despite poor culturing. Metabarcoding revealed distinct bacterial community shifts in lesions versus healthy tissue, and whole‑genome sequencing identified diverse Pseudomonas spp. that, while not individually more pathogenic, could enhance Psa3 growth, suggesting pathogenic consortia on resistant hosts.