The root is in direct contact with soil. Modulation of root growth in response to alterations in soil conditions is pivotal for plant adaptation. Extensive research has been conducted concerning the adjustment of root elongation and architecture in response to environmental factors. However, little is known about the modulation of the root growth trajectory, as well as its hormonal mechanism. Here we report that abscisic acid (ABA) participated in controlling root growth trajectory. The roots upon ABA treatment or from ABA-accumulation double mutantcyp707a1,3exhibit agravitropism-like growth pattern (wavy growth trajectory). The agravitropism-like phenotype is mainly ascribed to the compromised shootward transportation of auxin since we detected a reduced fluorescence intensity of auxin reporter DR5:VENUS in the root epidermis upon exogenous ABA application or in the endogenous ABA-accumulation double mutantcyp707a1,3. We then tried to decipher the mechanism by which ABA suppressed shootward auxin transport. The membrane abundance of PIN2, a facilitator of shootward auxin transport, was significantly reduced following ABA treatment and incyp707a1,3. Finally, we revealed that ABA reduced the membrane PIN2 intensity through suppressing thePIN2expression rather than accelerating PIN2 degradation. Ultimately, our results suggest a pivotal role for ABA in the root growth trajectory and the hormonal interactions orchestrating this process.

The molecular mechanisms underlying wound-induced tissue and organ regeneration in plants are unclear. Here, we identified a signaling pathway that governs the wound-induced regeneration of Arabidopsis (Arabidopsis thaliana) roots, highlighting a key role for the peptide RAPID ALKALINIZATION FACTOR33 (RALF33) and its receptor FERONIA (FER). Wounding triggers RALF33 accumulation, which promotes root regeneration, and fer mutants exhibit an enhanced regeneration capacity. The accumulated RALF33 hinders FER-mediated phosphorylation of the transcriptional co-repressor TOPLESS-RELATED4 (TPR4), impairing TPR4 nuclear localization and inhibiting its interaction with the transcription factor ETHYLENE RESPONSE FACTOR115 (ERF115). ERF115 has greater transcriptional activity when it is not associated with TPR4. Disrupting the FER-targeted phosphorylation sites in TPR4 via alanine substitutions (TPR4A) resulted in TPR4 mislocalization and impaired binding of TPR4A to ERF115. Our findings reveal that RALF33–FER–TPR4–ERF115 compose a key signaling cascade that orchestrates wound-induced regeneration, providing valuable insights into the regulation of plant regenerative responses.

The silkworm (Bombyx mori) is an economically important insect that plays a crucial role in agricultural development. Antimony tin oxide, a high-tech multifunctional nanomaterial, is extensively utilized in contemporary industries due to its properties of transparency, conductivity, and stability. Nevertheless, the toxicity and potential adverse effects of antimony tin oxide on living organisms remain poorly understood. In this study, we evaluated the effects of antimony tin oxide at varying concentrations (0–3.2 μg/μL) on the growth, oxidative stress response, gene expression, and midgut integrity of fifth-instar silkworm larvae. Exposure to high concentrations of antimony tin oxide resulted in a significant reduction in larval weight and severely disrupted the antioxidant defense system. RNA sequencing (RNA-Seq) analysis identified 239 differentially expressed genes (DEGs), which were confirmed by qPCR, revealing up-regulated lipid synthesis gene AGPAT5, down-regulated chitin degradation gene Chi, and suppressed glycerolipid hydrolysis gene H9J6N7_BOMMO. Histopathological and ultrastructural examinations revealed severe damage to the structure of midgut epithelial cells. Structural and functional analysis of conserved domains in key DEG-encoded proteins revealed that gene dysregulation disrupted energy metabolism and compromised the physical barrier, ultimately linking molecular abnormalities to observed tissue damage. These findings elucidate the mechanisms by which antimony tin oxide induces midgut toxicity through interference with critical metabolic pathways and functional perturbations at the molecular level.

Brassica napus L. is a vital oil crop and exhibits notable salt tolerance, making the enhancement of this trait crucial for cultivation in saline soils. Uncovering its underlying mechanism may further heighten the salt tolerance of B. napus. In this study, we conducted a genome-wide analysis of the Root Meristem Growth Factor (RGF) gene family in Brassica species and identified BnaRGF8 as a key regulator of salt tolerance. Under 200 mM NaCl treatment, all RGF genes were induced, with BnaRGF8 showing the greatest upregulation. This response was consistently observed across 10 genotypes, indicating a universal trend in B. napus. Functional characterization revealed that chemically synthesized BnaRGF8 alleviated salt-induced growth inhibition by restoring primary root elongation and lateral root formation. Additionally, BnaRGF8 preserved membrane integrity and maintained cell division under salt stress, establishing itself as a novel anti-salt peptide in B. napus.

Electrochemical biosensors have emerged as a promising tool for the early detection of diseases in oilseed crops such as rapeseed, soybean, and peanut. These biosensors offer high sensitivity, portability, and cost-effectiveness. Timely diagnosis is critical, as many pathogens exhibit latent infection phases or produce invisible metabolic toxins, leading to substantial yield losses before visible symptoms occur. This review summarises recent advances in the field of nanomaterial-assisted electrochemical sensing for oilseed crop diseases, with a particular focus on sensor mechanisms, interface engineering, and biomolecular recognition strategies. The following innovations are highlighted: nanostructured electrodes, aptamer- and antibody-based probes, and signal amplification techniques. These innovations have enabled the detection of pathogen DNA, enzymes, and toxins at ultra-low concentrations. Notwithstanding these achievements, challenges persist, including signal interference from plant matrices, limitations in device miniaturization, and the absence of standardized detection protocols. Future research should explore the potential of AI-assisted data interpretation, the use of biodegradable sensor materials, and the integration of these technologies with agricultural IoT networks. The aim of this integration is to enable real-time, field-deployable disease surveillance. The integration of laboratory innovations with field applications has been demonstrated to have significant potential in supporting sustainable agriculture and strengthening food security through intelligent crop health monitoring.

Spermatogenesis in Drosophila melanogaster is a classical model for studying cell polarity establishment, organelle remodeling, and extreme cellular morphogenesis. Spermatid elongation involves a series of highly coordinated dynamic events, including nuclear polarization, axonemal extension, mitochondrial remodeling, and individualization-mediated cytoplasmic clearance. Current studies have largely focused on individual structures, molecules, or pathways, resulting in a fragmented understanding of this process and a lack of an integrated framework that links mitochondrial function, cytoskeletal dynamics, and temporal translational regulation. Based on existing evidence, this review organizes current findings into three regulatory layers involving mitochondrial remodeling, cytoskeletal dynamics, and post-transcriptional translational control. Mitochondrial remodeling provides structural and metabolic support for sperm-tail formation, cytoskeletal processes execute axoneme organization and individualization, and post-transcriptional regulation controls the timing of protein production. Experimental evidence is strongest for mechanisms operating within each layer, whereas direct molecular coupling among the three layers remains incompletely established. We therefore present this model as a working framework rather than an established causal pathway. This framework helps organize current knowledge of extreme cellular differentiation and provides a basis for comparative studies of spermatogenesis and selected mechanisms associated with human male infertility.