The study identifies two maize genes, Discordia3a and Discordia3b, that encode the microtubule‑severing protein KATANIN. Loss‑of‑function allele combinations reduce microtubule severing, impair cell elongation, delay mitotic entry, and disrupt preprophase band and nuclear positioning, leading to dwarfed, misshapen plants.

The study identified lineage-specific long non‑coding RNAs (lncRNAs) from the aphid‑specific Ya gene family in Rhopalosiphum maidis and R. padi, demonstrating that these Ya lncRNAs are secreted into maize, remain stable, and move systemically. RNA interference of Ya genes reduced aphid fecundity, while ectopic expression of Ya lncRNAs in maize enhanced aphid colonization, indicating that Ya lncRNAs act as cross‑kingdom effectors that influence aphid virulence.

The study used a computer‑vision phenotyping pipeline (EarVision.v2) based on Faster R-CNN to map Ds‑GFP mutant kernels on maize ears and a statistical framework (EarScape) to assess spatial patterns of allele transmission from the apex to the base. They found that alleles causing pollen‑specific transmission defects often show significant spatial biases, whereas Mendelian alleles do not, indicating that reduced pollen fitness can shape the spatial distribution of progeny genotypes in Zea mays.

The study characterizes insertion mutants of the Arabidopsis thaliana CKL12 kinase, revealing its role in hypocotyl and primary root growth and indicating that the 3' end of its transcript is crucial for function. Evidence suggests CKL12 is transcriptionally regulated by brassinosteroid signaling, as its promoter binds BR-related transcription factors and their RNAi-mediated knock‑down reduces CKL12 expression, placing CKL12 downstream of BR signaling in seedling development.

The study investigates how the pleiotropic maize genes GRASSY TILLERS1 (GT1) and RAMOSA3 (RA3) are differentially regulated to suppress axillary meristems and floral organs, using a newly developed high-throughput quantitative phenotyping method for grass flowers. Distinct environmental mechanisms were found to control each suppression process, and upstream regulatory pathways of GT1 and RA3 have diverged, illustrating how ancient developmental genes can be redeployed to increase genetic pleiotropy during evolution.

The study identifies the brown planthopper salivary protein NlAnnexin-like5 (NlANX5) as a key virulence effector that disrupts rice annexin (OsANN) function, leading to altered calcium signaling and reduced plant resistance. RNAi silencing of NlANX5 impairs BPH feeding, while transgenic rice overexpressing OsANN2/OsANN8 or NlANX5 restores resistance, demonstrating an anti‑virulence breeding strategy for rice.

The study reveals that the maize catalytic trehalose-6-phosphate phosphatase RA3 interacts with the non‑catalytic TPS ZmTPS1, and together with the catalytic TPS ZmTPS14 they form a protein complex that enhances enzymatic activity. Genetic analyses show that mutations in ZmTPS1 and its paralog ZmTPS12 exacerbate ra3 branching phenotypes, while loss of the catalytic TPSs ZmTPS11 and ZmTPS14 causes embryonic lethality, indicating essential and regulatory roles for both catalytic and non‑catalytic TPS/TPP proteins in plant development.

Using CRISPR‑Cas9‑generated Zmcry mutants, the study shows that maize cryptochromes redundantly mediate blue‑light signaling, suppress mesocotyl elongation, and enhance UV‑B stress tolerance by upregulating genes for phenylpropanoid, flavonoid, and fatty‑acid pathways. Blue light also promotes epidermal wax accumulation, and ZmCRY1 directly interacts with GLOSSY2 in a light‑dependent manner to drive C32 aldehyde synthesis, linking cryptochrome activity to wax biosynthesis and UV‑B resistance.

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.

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.