Gain and loss of gene function shaped the nickel hyperaccumulation trait in Noccaea caerulescens
Authors: Belloeil, C., Garcia de la Torre, V. S., Contreras Aguilera, R., Kupper, H., Lopez-Roques, C., Iampetro, C., Vandecasteele, C., Klopp, C., Launay-Avon, A., Leemhuis, W., Yamjabok, J., van den Heuvel, J., Aarts, M. G. M., Quintela Sabaris, C., Thomine, S., MERLOT, S.
The study presents a high-quality genome assembly for the nickel hyperaccumulator Noccaea caerulescens and uses it as a reference for comparative transcriptomic analyses across different N. caerulescens accessions and the non‑accumulating relative Microthlaspi perfoliatum. It identifies a limited set of metal transporters (NcHMA3, NcHMA4, NcIREG2, and NcIRT1) whose elevated expression correlates with hyperaccumulation, and demonstrates that frameshift mutations in NcIRT1 can abolish the trait, indicating an ancient, transporter‑driven origin of nickel hyperaccumulation.
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 shows that the SnRK1 catalytic subunit KIN10 directs tissue-specific growth‑defense programs in Arabidopsis thaliana by reshaping transcriptomes. kin10 knockout mutants exhibit altered root transcription, reduced root growth, and weakened defense against Pseudomonas syringae, whereas KIN10 overexpression activates shoot defense pathways, increasing ROS and salicylic acid signaling at the cost of growth.