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 used Arabidopsis thaliana mutants with low (vtc2, vtc4) and high (vtc2/OE-VTC2) ascorbate levels to examine how ascorbate concentration affects gene expression and cellular homeostasis. Transcriptomic analysis revealed that altered ascorbate levels modulate defense and stress pathways, and that TAA1/TAR2‑mediated auxin biosynthesis is required for coping with elevated ascorbate in a light‑dependent manner.

A biparental Vicia faba mapping population was screened under glasshouse conditions for resistance to a mixture of Fusarium avenaceum and Fusarium oxysporum, revealing several families with moderate to high resistance. Using the Vfaba_v2 Axiom SNP array, a high-density linkage map of 6,755 SNPs was constructed, enabling the identification of a major QTL on linkage group 4 associated with partial resistance to foot and root rot.

The study shows that silencing of NOR2 rRNA genes in Arabidopsis thaliana depends primarily on CHH-context cytosine methylation, particularly mediated by CMT2 and the chromatin remodeler DDM1, rather than CG or CHG methylation. Comparative promoter analysis revealed a prevalence of CHH sites in plant rDNA promoters, explaining why CHH methylation mutants disrupt NOR2 silencing more strongly, while NOR2 loci are hyper‑methylated and more condensed than NOR4.