Rocky D. Payet

Virus yellows disease (VY) is a global issue caused by a complex of virus species and affects sugar beet crops worldwide. Previous studies undertaken prior to the widespread use of neonicotinoid seed treatments had identified beet mild yellowing virus (BMYV) as the predominant cause of the disease in the United Kingdom. Up-to-date knowledge of the causal agent(s) of this disease is important for the successful deployment of integrated pest management strategies, including the use of resistant sugar beet varieties. However, only a limited number of studies have been conducted into the epidemiology of VY in recent decades. The findings of this 3-year monitoring survey, utilizing a novel small RNA sequencing approach, suggest beet chlorosis virus (BChV) as the most prevalent virus associated with VY in the United Kingdom during this period. In comparison with conventional detection tools, the methodology described here permitted the detection of nontarget viruses including beet mosaic virus and beet cryptic virus, but no new causative agents of VY were identified. Copyright © 2026 The Author(s). This is an open access article distributed under the CC BY-NC-ND 4.0 International license .

The allododecaploid cordgrass Spartina anglica thrives in saltmarshes, where it grows vigorously despite facing extreme environmental stresses. The species was formed through a genome duplication of an infertile hybrid in ∼1870, and is today listed amongst 100 of the World’s Worst Invasive Alien Species. Here, we use long-read sequencing to provide a genomic sequence of S. anglica and undertake a detailed transcriptomic analysis of different tissues. We demonstrate that S. anglica has undergone at least two whole-genome duplication events and exhibits segmental allopolyploidy. We also show that S. anglica has evolved novel mechanisms to tolerate abiotic stress, including expansion and neofunctionalization of genes involved in sucrose synthesis, detoxification of reactive oxygen species and heavy metals, and calcium signalling associated with salt, ionic, and nutrient stress. Furthermore, we demonstrate that S. anglica produces a diverse array of osmolytes, including dimethylsulfoniopropionate (DMSP), and reveal that a retrotransposon with a unique 55 bp insertion causes high-level expression of the DMSP-amine oxidase (DOX) gene and contributes to the exceptionally high levels of DMSP production. Taken together, our results highlight the specialised genomic, transcriptomic, and biochemical adaptations that S. anglica has evolved to tolerate severe abiotic stresses in saltmarshes.

Recent developments in single-cell -omic and metabolite imaging technologies and the increasing availability of high-quality genome assemblies are having a transformative impact on the way research is carried out into plant specialised metabolism. Integrating these technologies into pathway discovery projects is therefore highly advantageous. Here, we present a general introduction into methods and workflows in specialised metabolism research. We review a range of recent methodologies, highlighting what they might be used for and common pitfalls which may be encountered. Finally, we provide a practical guide on how these technologies may be incorporated into a specialised metabolic pathway discovery pipeline for researchers who are new to the field.

The organosulfur compound dimethylsulfoniopropionate (DMSP) has key roles in stress protection, global carbon and sulfur cycling, chemotaxis, and is a major source of climate-active gases. Saltmarshes are global hotspots for DMSP cycling due to Spartina cordgrasses that produce exceptionally high concentrations of DMSP. Here, in Spartina anglica, we identify the plant genes that underpin high-level DMSP synthesis: methionine S-methyltransferase (MMT), S-methylmethionine decarboxylase (SDC) and DMSP-amine oxidase (DOX). Homologs of these enzymes are common in plants, but differences in expression and catalytic efficiency explain why S. anglica accumulates such high DMSP concentrations and other plants only accumulate low concentrations. Furthermore, DMSP accumulation in S. anglica is consistent with DMSP having a role in oxidative and osmotic stress protection. Importantly, administration of DMSP by root uptake or over-expression of Spartina DMSP synthesis genes confers plant tolerance to salinity and drought offering a route for future bioengineering for sustainable crop production.

Summary: Calcium signalling is central to many plant processes, with families of calcium decoder proteins having expanded across the green lineage and redundancy existing between decoders. The liverwort Marchantia polymorpha has fast become a new model plant, but the calcium decoders that exist in this species remain unclear. We performed phylogenetic analyses to identify the calcineurin B‐like (CBL) and CBL‐interacting protein kinase (CIPK) network of M. polymorpha. We analysed CBL‐CIPK expression during salt stress, and determined protein–protein interactions using yeast two‐hybrid and bimolecular fluorescence complementation. We also created genetic knockouts using CRISPR/Cas9. We confirm that M. polymorpha has two CIPKs and three CBLs. Both CIPKs and one CBL show pronounced salt‐responsive transcriptional changes. All M. polymorpha CBL‐CIPKs interact with each other in planta. Knocking out CIPK‐B causes increased sensitivity to salt, suggesting that this CIPK is involved in salt signalling. We have identified CBL‐CIPKs that form part of a salt tolerance pathway in M. polymorpha. Phylogeny and interaction studies imply that these CBL‐CIPKs form an evolutionarily conserved salt overly sensitive pathway. Hence, salt responses may be some of the early functions of CBL‐CIPK networks and increased abiotic stress tolerance required for land plant emergence.

Hypomorphic CYP24A1 protein coding mutations causing inappropriate 1,25(OH)₂D concentrations are associated with idiopathic infantile hypercalcemia and adult-onset hypercalciuria and nephrolithiasis. It is unclear why some cases present with CYP24A1-mediated abnormal calcium handling lack protein-coding CYP24A1 mutations. Non-coding region mutations, e.g. the 3’ UTR, impacting messenger RNA (mRNA) structure have rarely been studied in patients. RNAs fold into complex structures critical for their function and regulation including post-transcriptional modifications, localisation, translation and degradation. Non-coding variants altering CYP24A1 mRNA structure may be the fundamental mechanism behind cases with absent protein coding pathogenic mutations. Biochemical profiling, next generation sequencing, bioinformatics, proteomic and molecular cytogenetic approaches were used to examine CYP24A1 in a patient cohort of four adults with hypercalciuria and nephrolithiasis and two infants with nephrocalcinosis. We identified inappropriate 1,25(OH)₂D concentrations (mean±SD=247.3±189.3pmol/l [range=55-139 pmol/l]) in our cohort, associated with elevated 25OHD:24,25(OH)₂D (32 [range 7-23]) in one adult and both 25OHD:24,25(OH)₂D (35) and 1,25(OH)₂D:24,25(OH)₂D (176 [range=11-62]) in one infant. CYP24A1 direct sequencing revealed single nucleotide variants located in the 3’ UTR of each patient (c.1993C>T, c.2083T>C, c.2512T>A, c.2658C>G and c.2691G>A) causing mRNA misfolding in silico. These mRNA structural abnormalities are associated with significant increase in CYP24A1 retention (PCYP24A1 3’ UTR mRNA structural alterations for in vitro investigations into non-canonical CYP24A1 pathogenesis. Single molecule fluorescence in situ hybridisation (smFISH) in this model revealed no significant effect on CYP24A1 mRNA cellular localisation and abundance. We present insights into novel non-coding 3’UTR CYP24A1 hypomorphic variants that alter mRNA folding, associated with CYP24A1 biological function. These results will improve knowledge of structure-function relationships affecting RNA translation and protein expression, expanding our understanding of the molecular basis of disease pathogenesis in patients lacking protein coding abnormalities.