The study integrates genome, transcriptome, and chromatin accessibility data from 380 soybean accessions to dissect the genetic and regulatory basis of symbiotic nitrogen fixation (SNF). Using GWAS, TWAS, eQTL mapping, and ATAC-seq, the authors identify key loci, co‑expression modules, and regulatory elements, and validate the circadian clock gene GmLHY1b as a negative regulator of nodulation via CRISPR and CUT&Tag. These resources illuminate SNF networks and provide a foundation for soybean improvement.
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 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.