Agricultural systems face unprecedented threats from climate change-induced environmental stresses (e.g., drought, salinity, and heatwaves). These environmental stresses limit crop productivity, degrade soil health, and threaten global food security, highlighting the urgent need for innovative and sustainable solutions. Harnessing soil and plant-associated microbiomes offers transformative potential to enhance plant resilience and sustainability. However, translating lab-based plant-microbiome research into scalable agricultural applications remains a significant challenge. This review explores the dynamic interplay between plants and their associated microbiomes under abiotic stresses, focusing on the mechanisms by which plants recruit and modulate microbial communities in the rhizosphere, phyllosphere, and endosphere. We conceptualize how environmental abiotic stresses alter plant–microbe interactions and highlight microbiome-mediated strategies for stress mitigation. Finally, we evaluated practical interventions (e.g., synthetic microbial communities (SynComs), host-mediated microbiome engineering (HMS), and metabolites) for their potential to enhance agricultural resilience. Bridging lab-based discoveries with the success of field applications will require overcoming key scientific and translational challenges related to improving plant–microbe communication, microbial community stability, product performance, ecological risks, and interdisciplinary collaboration. We advocate for systems-based approaches that integrate plant and microbiome engineering, metabolic and genetic innovations, agronomic practices, and policy frameworks to accelerate the adoption of new and sustainable tools. We identified key research gaps, including long-term ecological impacts and optimization of microbiome-host compatibility. By integrating cutting-edge science with scalable, real-world solutions, plant-microbiome interactions can significantly contribute towards climate-smart agriculture, supporting ecosystem resilience in an era of global change.
Plant productivity is severely constrained by diverse pathogens, among which oomycetes represent some of the most destructive threats to global agriculture. These filamentous microorganisms cause devastating diseases, including potato late blight and downy mildew, leading to significant yield losses in major crops. Successful infection relies on the formation of haustoria through which oomycetes deliver numerous effector proteins that manipulate host cellular processes and suppress both pattern-triggered and effector-triggered immunity. To date, three major classes of oomycete effectors, including RXLR, Crinkler, and CHXC, along with a putative class YxSL [RK], have been identified in oomycetes. These effector molecules, along with the recently identified apoplastic effectors, play key roles in governing compatible and incompatible interactions and establishing disease in the host plant. Plants perceive these effectors by deploying multilayered immune strategies including plasma-membrane localized pattern-recognition receptors (PRRs) and intracellular NLR receptors that induce redox- and hormone-regulated defense pathways, and dynamic remodeling of transcriptional and metabolic networks. Understanding these effectors and how they manipulate host defense is a prerequisite for the generation of disease-resistant plants. In this review, we discuss the recent progress in the oomycete effectors, their secretion system, and their targets in the plant cells. By integrating pathogen strategies with host immune responses, we highlight how effector-mediated manipulation of plant signaling provides new opportunities for breeding and engineering broad-spectrum and durable resistance against oomycete pathogens.
Carbon nanotubes (CNTs) are promising nanomaterials with applications in biomedicine, including drug delivery and biosensing, due to their stability, biocompatibility, and ease of surface modification. However, toxicity concerns from their manufacturing limit their use. Functionalizing CNTs can reduce toxicity and enhance transport in physiological systems, while their optimal dosing is influenced by biodistribution and pharmacokinetics. In this study, multiwalled carbon nanotubes (MWCNTs) were synthesized via Chemical Vapor Deposition (CVD) and functionalized with Bovine Serum Albumin (BSA) and Fe3O4. MWCNTs were characterized using various techniques, and their 96 h lethal concentration was assessed through the Zebrafish Embryo Toxicity Test (ZFET). The LC50 and LC20 values for Fe3O4-MWCNTs were 685.51 mg/L and 198.3 mg/L, while for BSA-MWCNTs, they were 401.25 mg/L and 150.45 mg/L, respectively. Genotoxicity analysis showed no DNA damage, and histological examinations of liver, gills, intestine, and brain revealed no major alterations. The pharmacokinetics and biodistribution of BSA-MWCNTs (T1) and Fe3O4-MWCNTs (T2) were examined following oral administration in D. rerio. Results indicated longer T1/2 in blood and gut tissues from the T1 group, and faster clearance in blood compared to gut. By day 28, MWCNTs showed higher accumulation in the liver, followed by the gut and brain. This study delineates the pharmacokinetics and biodistribution, and confirms the optimal dose of MWCNTs, and promotes its application in the field of biomedical research.
Anthropogenic stressors often co-occur in ecosystems, but their combined impacts are rarely assessed using field experiments. Press disturbances particularly can reshape community dynamics, altering their capacity to withstand or recover from acute pulse disturbances by modifying response diversity. We assessed macroinvertebrate responses to co-occurring anthropogenic disturbances by manipulating streamflow in eight Tasmanian streams along a gradient of upstream catchment conversion to agriculture (0-45%). Temporary half-weirs created high- and low-flow reaches, simulating pulse disturbances. Chao's species richness declined, and community composition was altered in sites with 0% agricultural conversion, but these recovered once normal base flows were restored. In comparison, under reduced flows, there was no change in Chao's species richness in sites with 33-45% agricultural conversion, but community composition was altered, with recovery indicated once base flows were restored. Under low flows in forested streams, response-trait diversity declined but under higher proportions of agricultural conversion, response-trait diversity declined minimally. Some single traits declined within high-flow reaches only to recover after baseflow restoration. Catchment conversion to agriculture altered stream community response diversity, leading to differential responses to flow changes. Although agricultural land-use altered the ability of communities to respond to pulse disturbances, the presence and direction of change for some treatments would have been difficult to predict a priori. Combined press- and pulse-disturbances altered communities more than independently acting disturbances but the press disturbance (max 45% catchment area) was too weak to prevent recovery.
We investigated the pathogenicity of a homozygous intronic variant in CDK5RAP3, a key UFMylation adapter, in three individuals from two unrelated families with a lethal neurodevelopmental disorder. CDK5RAP3 variants have not been linked to human disorders to date; however, murine Cdk5rap3 knockout is embryonic lethal and variants in five other UFMylation components cause severe neurodevelopmental conditions. A segregating homozygous variant, chr17(GRCh38):g.47974691G > A, CDK5RAP3 NM_176096.3:c.334 + 243G > A, was identified by trio whole-genome and proband RNA sequencing in Family A and by trio whole-exome sequencing data reanalysis in Family B. Variant pathogenicity investigations included RT-PCR, Western blot, co-immunoprecipitation and (phospho)proteomics to assess transcript, protein and UFMylation complex effects. Antisense oligonucleotide-mediated rescue of CDK5RAP3 expression combined with proteomics and phosphoproteomics defined the mechanistic impact of CDK5RAP3 deficiency and rescue in amniocytes from an affected individual. All three affected individuals showed foetal growth restriction, foetal akinesia, pontocerebellar hypoplasia, arthrogryposis and hepatic pathology. CDK5RAP3 c.334 + 243G > A activates a cryptic donor splice-site causing pseudoexon/intron inclusion triggering nonsense-mediated decay and deficiency of full-length CDK5RAP3 (NP_788276.1), while potentially allowing retained expression of C-terminal alternative isoforms. Co-immunoprecipitation revealed only full-length CDK5RAP3 binds UFL1, whereas C-terminal isoforms cannot. Primary amniocytes showed CDK5RAP3 deficiency was associated with impaired UFMylation of known substrates, RPL26 and UFBP1. Proteomic and phosphoproteomic analyses revealed dysregulation of extracellular matrix organisation, cell adhesion, mitotic/genome stability pathways, cytoskeletal networks and neuronal guidance, which were reversed by restoration of canonical CDK5RAP3 expression via splice-correcting antisense oligonucleotides. Phosphoproteomic data implicate CDK5RAP3 as an upstream regulator of UFL1 S462 phosphorylation, known to be regulated by Ataxia-telangiectasia mutated (ATM) signalling. Our findings provide strong evidence linking deficiency of full-length CDK5RAP3 to severe neurodevelopmental, liver and muscle dysfunction. This study further highlights the therapeutic potential of ASO-based deep-intronic splicing defect correction.
