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PubMed2026

Prevalence and risk factors for persistent faecal carriage of extended spectrum beta-lactamase producing Escherichia coli in a paediatric community population.

OBJECTIVE: To investigate clinical and microbiological factors associated with persistent faecal carriage of extended spectrum beta-lactamase (ESBL) producing Escherichia coli in infants. METHODS: Between 2010 and 2022, children aged 3 months to 2 years old were sampled in a community setting in France, at two visits, V1 and V2, 3-24 months apart, to screen for prolonged faecal carriage of ESBL-producing E. coli. Patient clinical information and whole genome sequence of each isolate were used for association studies. RESULTS: A total of 4641 children were sampled. 375 (8%) carried an ESBL-producing Enterobacterales, among which 142 of ESBL-producing E. coli carriers were once again sampled at V2 and included in this study. 21.8% (n = 31/142) and 18.4% (n = 16/99) carried the same ESBL-producing E. coli clone for at least 3 and 6 months, respectively. B2 phylogroup, and among which ST131 clones were associated with an increased risk of persistent carriage. Multivariate analysis identified virulence associated genes involved in adhesion (papC/papGII allele and a tia-like gene) and encoding toxin (senB) as major risk factors for persistence. A genome wide association study highlighted the potential role of the frz metabolic operon, known to be involved in enterocytes adhesion/internalisation. CONCLUSION: Main extraintestinal pathogenic E. coli genomic features (phylogenetic background, adhesion properties) are associated with ESBL-producing E. coli gut colonisation persistence in infants, which could potentially lead to an increased risk of febrile urinary tract infection in these patients.

Child↗
PubMed2026

The phosphate exporter XPR1 promotes gasdermin D-independent mature IL-1β secretion.

Interleukin (IL)-1β is a leaderless inflammatory cytokine that is not secreted via the classical endoplasmic reticulum-Golgi pathway. Instead, m(ature) IL-1β secretion is classically associated with pyroptosis, a caspase-dependent inflammatory cell death mediated by gasdermin D (GSDMD) pore formation at the plasma membrane. However, human monocytes can secrete mIL-1β in the absence of cell death, and the contribution of GSDMD in this secretory pathway remains poorly defined. Here, we distinguished two pathways for mIL-1β secretion in living human monocytic cells : a rapid, GSDMD-dependent pathway and a slower, GSDMD-independent pathway. Using a genome-wide CRISPR-Cas9 screen, we identified XPR1 (Xenotropic and Polytropic retrovirus Receptor 1) as a regulator of the GSDMD-independent pathway. XPR1, the only phosphate exporter identified in metazoans, has not previously been implicated in cytokine secretion. Genetic invalidation of XPR1 in GSDMD-deficient monocytic cells markedly reduced IL-1β secretion. We further showed that this regulatory function requires XPR1 surface expression and phosphate export activity. These findings reveal an unexpected link between phosphate homeostasis and non-lytic mIL-1β secretion, opening new opportunities to modulate IL-1β-driven inflammatory diseases.

IL-1β secretion↗
PubMed2026

5-Iodotubercidin inhibits Epithelial to Mesenchymal Transition by inhibiting IKK/NFκB-dependent gene expression.

Epithelial to mesenchymal transition (EMT) is a process of trans-differentiation important for development, inflammation and cancer. Transforming Growth Factor-β (TGFβ) is a physiologically relevant inducer of EMT. We had recently characterized the adenosine analogue, adenosine kinase inhibitor 5-Iodotubercidin (5-ITu), as a compound which preferentially sensitizes MK2-deficient cells to TNFα-induced, RIPK1-dependent cell death. Here we investigated the effect of 5-ITu on TGFβ-induced EMT. 5-ITu suppressed TGFβ-induced morphological changes and migration in A549 (lung cancer) and PANC1 (pancreatic cancer) cell lines. Consistent with these effects, there was significant suppression of EMT markers as indicated by qPCR, immunoblotting and immunofluorescence and confocal microscopy. Mechanistic investigations revealed that 5-ITu-mediated EMT suppression was independent of adenosine kinase inhibition and RIPK1 activation. 5-ITu suppressed NFκB activity in cells undergoing EMT and IKK inhibition phenocopied the effect of 5-ITu on EMT. The effect of 5-ITu on EMT was lost upon IκBα knockdown. Kinase assays revealed IKKβ as a potential direct target of 5-ITu. We identified a TGFβ-associated, NFκB-dependent gene signature consisting of 4 genes, that are differentially regulated upon 5-ITu treatment. Interestingly, this 4 gene signature could predict survival in lung and pancreatic cancer. The identification of this role for the multitarget kinase inhibitor 5-ITu in NFκB activity-dependent EMT, in addition to RIPK1-dependent necroptosis has potential implications in anticancer strategies.

5-iodo-tubercidin↗
PubMed2026

Mammalian DNA methyltransferases in DNA methylation and imprinted gene expression in extraembryonic ectoderm of post-implantation embryos.

DNA methylation in mammals is mainly catalyzed by three DNA methyltransferases (DNMTs). Conventionally, DNMT1 is considered the primary DNMT protein for maintenance DNA methylation, whereas DNMT3A and DNMT3B function in de novo DNA methylation. In two previous studies, we demonstrated that DNMT3A and DNMT3B maintain genome-wide DNA methylation in embryonic stem (ES) cells and in the epiblast of post-implantation embryos. Interestingly, DNMT3A and DNMT3B also sustain genome-wide DNA methylation in the extraembryonic ectoderm (EXE) of post-implantation embryos, including repeats, genic and intergenic regions. Although DNMT1 plays a major role in maintaining DNA methylation at the imprinting control regions (ICRs) in the imprinted regions, DNMT3A and DNMT3B are required for preserving DNA methylation at the ICRs of a subset of imprinted regions in EXE, similar to the observations in ES cells and epiblast. Surprisingly, de novo DNA methylation mediated by DNMT3A and DNMT3B leads to increased DNA methylation at a large subset of imprinted regions. These results are consistent with what we previously elucidated in the epiblast of post-implantation embryos. Importantly, loss of DNA methylation at the ICR of an imprinted region, resulting from the absence of DNMT1 or two DNMT3 proteins, causes allelic expression switch of the corresponding imprinted genes in that imprinted region. This study provides further evidence that DNMT3A and DNMT3B exert both maintenance and de novo DNA methylation functions across the genome in post-implantation embryos. It also validates some previous findings for DNA methylation-dependent allelic expression switch of imprinted genes.

DNA methylation↗
PubMed2026

Long-term clinical and genomic surveillance of rare respiratory enterovirus C types in France, 2013-2025.

INTRODUCTION: Rare enterovirus types assigned to species C (EV-C) display respiratory tropism and may be associated with neurological involvement, which display similarities to EV-D68 disease. PATIENTS AND METHODS: We conducted continuous enterovirus/rhinovirus (EV/RV) surveillance between 2013 and 2025, including systematic EV/RV screening of all respiratory samples and reflex VP4/VP2 sequencing (a total of 5855 samples). When an EV-C strain was detected, the VP1-coding and complete genome sequence was sequenced to investigate phylogenetic relationships and to identify any recombinant forms. RESULTS: Over the 13-year period, 30 EV-C infections were identified from respiratory samples, with 23 cases (77%) detected between 2013 and 2018. EV-C105 was the most frequent type (n = 11), followed by EV-C104 (n = 8), EV-C109 (n = 6), and EV-C117 (n = 5). We also document the first detection of EV-C117 in France and only the second case reported in Europe since its initial description in 2011 in Lithuania. Clinical data were available for 25 patients, of whom 19 (76%) were children. Respiratory symptoms predominated (17/25, 68%), and 7 patients presented with lower respiratory tract infections. Hospitalization was required in 18 cases (72%), including three with ICU admissions (12%). Nearly half of the patients (12/25, 48%) had at least one risk factor for severe respiratory disease. Across all respiratory EV-C types, recovered sequences clustered with contemporary global strains. CONCLUSIONS: This long-term surveillance highlights the sustained circulation of multiple respiratory EV-C types in France and underscores the need for continued clinical and genomic monitoring to assess the evolution and pathogenic potential of these enteroviruses.

Complete genome characterization↗
PubMed2026

Contact hypersensitivity promotes hair regeneration through SPP1-secreting macrophages.

Allergic contact dermatitis, or contact hypersensitivity (CHS), is a pathological adaptive immune response that paradoxically induces hair regeneration, yet its underlying mechanisms remain unclear. We integrated high-resolution spatial transcriptomics and single-cell RNA sequencing to map the intricate interactions between immune cells, stroma, and hair follicles during CHS-induced hair growth in mice. Among all immunocytes, macrophages underwent the most prominent compositional and functional remodeling. We resolved five transcriptionally distinct macrophage subsets, with contact hypersensitivity driving a shift from homeostatic antigen-presenting cells toward a pro-inflammatory CD14+SPP1+ population. Trajectory analysis revealed divergent differentiation paths under homeostatic versus allergic conditions, highlighting the plasticity of skin macrophages. Mechanistically, CD14+SPP1+ macrophages secreted SPP1 (osteopontin), which engaged CD44 on hair follicle stem cells to activate PI3K-AKT signaling and trigger their proliferation. Notably, canonical pro-inflammatory cytokine signaling through TNF-α and IL-1 was dispensable for this process, underscoring the specificity of the SPP1-CD44 axis in immune-mediated hair regeneration. These findings reveal a macrophage-dependent mechanism of immune-mediated hair regeneration, offering therapeutic insights into immune-stem cell crosstalk.

Journal Article↗
PubMed2026

Towards a Robust cell-free DNA Isolation Protocol for NGS Applications in a Clinical Molecular Diagnostics Setting.

Cell-free DNA (cfDNA), released from apoptotic and necrotic cells into body fluids, is a non-invasive source of genetic information for disease prediction, diagnosis, and monitoring. However, its low abundance makes cfDNA highly susceptible to various pre-analytical influences, potentially increasing high molecular weight (HMW) or genomic DNA (gDNA) compromising downstream cfDNA analyses. This study evaluated the impact of different cfDNA-stabilizing blood collection tubes (BCT; Cell-Free DNA BCT, Streck; S-Monovette cfDNA Exact, Sarstedt) stored at room temperature for 1, 5, or 10 days, prior to plasma isolation using different isolation methods (magnetic bead-based or silica column-based) on cfDNA stability and yield. DNA quantity and quality were assessed by fluorometric quantification, automated fragment analysis, and gene-specific quantitative PCR. Streck-based workflows maintained stable cfDNA yields and characteristic mononucleosomal fragmentation profiles across all storage times. In contrast, Sarstedt tubes showed reduced cfDNA concentrations after 5 days and a pronounced increase at 10 Days, accompanied by high-molecular weight DNA patterns consistent with white-blood cells (WBC) lysis. These trends were largely independent of the extraction method. Overall, the results demonstrate that blood collection tube chemistry critically influences cfDNA integrity during delayed processing. Streck tubes, particularly when combined with silica column-based isolation method, provided the most robust and reproducible workflow for routine molecular diagnostics, whereas Sarstedt tubes produced physiologically implausible results after extended storage.

blood collection tubes↗
PubMed2026

Long-read sequencing resolves complex CYP21A2 variants and identifies 2+0 carriers in 21-hydroxylase deficiency.

The complex CYP21A2 variants arising from high homology with its pseudogene CYP21A1P challenge the diagnosis of 21-hydroxylase deficiency (21-OHD). This study systematically evaluated long-read sequencing (LRS) for identifying complex structural variants of the CYP21A2 gene in 21-OHD in comparison with conventional molecular diagnostic methods, including multiplex ligation-dependent probe amplification (MLPA), CNVplex, and SNaPshot. Twenty patients with suspected 21-OHD and defined CYP21A2 structural variants identified via initial MLPA screening were enrolled. Variants were further analyzed using CNVplex and SNaPshot, then all samples underwent LRS for comprehensive variant detection, breakpoint mapping, and haplotype resolution. LRS overcame key limitations of conventional methods. It reliably identified a novel large-fragment deletion and defined its boundaries. Notably, LRS identified "2+0" carriers, where deletions masked by duplications cause false-negatives with standard techniques. Moreover, LRS accurately distinguished CYP21A1P/CYP21A2_CH-4 and CH-9 chimera subtypes which were indistinguishable by the combined conventional assays. Furthermore, LRS enabled the precise identification and characterization of TNXA/TNXB chimeric deletions. These are frequently misclassified as CYP21A1P/CYP21A2 chimeras by conventional methods but are critical for diagnosing associated conditions such as CAH-X syndrome. LRS provides a superior, integrated solution for the molecular diagnosis of 21-OHD, offering precise structural variant characterization, accurate carrier detection, and reliable breakpoint mapping. Its application enhances diagnostic accuracy, supports advanced genetic counseling, and paves the way for genotype-informed clinical management.

Journal Article↗
PubMed2026

Mutational Landscape and Clonal Dynamics in AML Undergoing PTCy Hematopoietic Cell Transplantation.

To improve risk stratification, we performed targeted NGS at diagnosis in 191 patients with AML undergoing myeloablative allogeneic HCT with PTCy-based prophylaxis. We also investigated clonal evolution using paired diagnostic and relapse samples from 39 individuals. A total of 610 mutations were detected in 184 patients (96%), most commonly in FLT3 (26%), DNMT3A (25%), RUNX1 (24%), and NPM1 (19%). Sixteen unique fusion genes were identified in 35 patients, with KMT2A (43%) and core binding factor rearrangements (23%) being the most frequent. TP53 and WT1 mutations were strongly associated with adverse outcomes, whereas NPM1 retained favorable significance. RUNX1 co-mutations with SF3B1 or NRAS were associated with inferior survival. In an exploratory allelic analysis, multi-hit TP53 alterations, but not single-hit mutations, were associated with distinctly poorer OS, EFS, and relapse risk. Relapse involved mutational shifts in ∼70% of cases, with significant enrichment of WT1 and more modest increases in TP53, KRAS, ASXL1, NF1, and MECOM, while DNMT3A, TET2, and ASXL1 persisted stably. Neither acute nor chronic graft-versus-host disease was associated with molecular remodeling at relapse. Incorporating TP53 and WT1 into risk models, recognizing context-dependent effects of DNMT3A and RUNX1, and applying longitudinal genomic monitoring may help guide personalized strategies to prevent relapse. Extended abstract BACKGROUND Relapse remains the leading cause of treatment failure after allogeneic hematopoietic cell transplantation (HCT) for acute myeloid leukemia (AML), yet the genetic mechanisms underlying post-transplant relapse remain poorly understood, particularly in the era of post-transplant cyclophosphamide (PTCy). Characterizing the mutational landscape at diagnosis and the clonal evolution leading to relapse may improve post-transplant risk stratification and identify opportunities for personalized surveillance and intervention. OBJECTIVES To characterize the diagnostic mutational landscape, evaluate its prognostic significance, and investigate clonal evolution from diagnosis to relapse in AML patients undergoing myeloablative HCT with PTCy-based graft-versus-host disease prophylaxis. STUDY DESIGN We performed targeted next-generation sequencing (NGS) at diagnosis in 191 consecutive AML patients undergoing myeloablative allogeneic HCT with PTCy-based prophylaxis. Paired diagnostic and relapse samples were available for 39 patients to evaluate clonal evolution. RESULTS A total of 610 mutations were detected in 184 patients (96%), most commonly in FLT3 (26%), DNMT3A (25%), RUNX1 (24%), and NPM1 (19%). Sixteen unique fusion genes were identified in 35 patients, with KMT2A (43%) and core binding factor rearrangements (23%) being the most frequent. TP53 and WT1 mutations were strongly associated with adverse outcomes, whereas NPM1 retained favorable significance. RUNX1 co-mutations with SF3B1 or NRAS were associated with inferior survival. In an exploratory allelic analysis, multi-hit TP53 alterations, but not single-hit mutations, were associated with distinctly poorer OS, EFS, and relapse risk. Relapse involved mutational shifts in ∼70% of cases, with significant enrichment of WT1 and more modest increases in TP53, KRAS, ASXL1, NF1, and MECOM, while DNMT3A, TET2, and ASXL1 persisted stably. Neither acute nor chronic graft-versus-host disease was associated with molecular remodeling at relapse. CONCLUSIONS This study provides a comprehensive characterization of the mutational landscape and clonal evolution of AML undergoing contemporary PTCy-based allogeneic HCT. TP53 and WT1 identify patients at particularly high risk of post-transplant relapse, whereas NPM1 retains favorable prognostic significance. The frequent acquisition of new genetic lesions at relapse underscores the dynamic nature of post-transplant clonal evolution and supports longitudinal molecular monitoring together with genomically informed post-transplant surveillance and relapse-prevention strategies.

Clonal Dynamics↗
PubMed2026

Phenotypic and genomic characterization of a blaOXA-181-producing ST656 Klebsiella pneumoniae isolate from China.

Carbapenem-resistant Klebsiella pneumoniae (CRKP) has emerged as a major global health threat due to its rapid dissemination and severely limited treatment options. Here, we report the phenotypic and genomic characterization of an ST656 K. pneumoniae clinical isolate carrying blaOXA-181 in China. Antimicrobial susceptibility testing confirmed carbapenem resistance, whereas the isolate remained susceptible to aztreonam, amikacin and trimethoprim/sulfamethoxazole, with a colistin MIC of ≤0.5 μg/mL. Whole-genome sequencing identified the blaOXA-181 gene on a 51,391-bp ColKP3/IncX3 plasmid co-harboring multiple resistance determinants. Conjugation assays yielded blaOXA-181 -positive transconjugants at a recovery frequency of 2 × 10-4. Following serial passage, blaOXA-181 was stably maintained for 100 generations. Comparative genomic analysis showed that the blaOXA-181-carrying plasmid shared a highly conserved backbone with plasmids from geographically diverse isolates, while KP413706 represents a distinct ST656 lineage. These findings expand the genomic evidence for blaOXA-181-carrying ST656 K. pneumoniae in China and underscore the urgent need for enhanced genomic surveillance and stringent infection control strategies.

Carbapenem-resistant Klebsiella pneumoniae↗
PubMed2026

Directed evolution of Lactiplantibacillus plantarum for utilizing ethanol to produce postbiotics.

Alcohol is a recognized carcinogen worldwide. In this study, we aimed to utilize probiotics to metabolize ethanol and produce postbiotics. Initially, we identified a lactic acid bacteria community in kimchi with excellent probiotic activity. By employing our previously developed directed evolution techniques, a Lactiplantibacillus plantarum mutant with safe characteristics and an ethanol utilization capacity of 40 g/L and 0.15 g/L/OD was obtained. Genome sequencing and RT-qPCR analysis revealed the up-regulated expression of alcohol dehydrogenase and aldehyde dehydrogenase genes greatly contributed to ethanol utilization. Furthermore, the mutant strain demonstrated marked superiority in producing postbiotics, including antimicrobial peptides and beneficial organic acids such as lactic acid, phenyllactic acid, succinic acid, and indole-3-lactic acid. In the ethanol-fed fermentation process, the mutant strain achieved a lactic acid yield of 8.47 g/L and a carbon conversion rate of 21.8%. In vivo testing further validated its safety and ability to assist alcohol metabolism.

Adaptive laboratory evolution↗
PubMed2026

Membrane-associated compartmentalization of zearalenone biosynthetic enzymes and Syn2-associated zearalenone homeostasis in Fusarium graminearum.

Subcellular compartmentalization has attracted increasing attention in fungal secondary metabolism, particularly in the biosynthesis and trafficking of mycotoxins. However, the subcellular site of zearalenone (ZEA) biosynthesis and the mechanisms underlying its export in Fusarium graminearum remain poorly understood. ZEA is a polyketide mycotoxin that poses a serious threat to food safety through contamination of cereal grains and induces severe estrogenic effects in mammals. Its biosynthesis is governed by a dedicated biosynthetic gene cluster consisting of PKS4, PKS13, ZEB1, and ZEB2. In this study, we investigated the subcellular organization of the ZEA biosynthetic machinery and found that key biosynthetic enzymes accumulated in punctate structures that overlapped with small CMAC-positive vacuolar structures and were closely associated with FM4-64-labeled membranes. Furthermore, our results suggest that the syntaxin-like t-SNARE protein Syn2 contributes to extracellular ZEA accumulation and intracellular toxin homeostasis. Disruption of SYN2 abolished visible ZEA crystal formation on the hyphal surface and was associated with increased intracellular ZEA retention. This intracellular accumulation was accompanied by strong induction of the ZEA biosynthetic gene cluster and reduced cellular viability. Moreover, deletion of ZEB2 in the Δsyn2 background abolished ZEA production and restored cell viability, supporting an association between Zeb2-dependent ZEA biosynthesis and the cytotoxic phenotype of the Δsyn2 mutant. Together, our findings suggest a potential link between membrane-associated organization of ZEA biosynthetic enzymes, Syn2-associated ZEA distribution, intracellular toxin homeostasis, and fungal viability. Further studies will be required to define the precise mechanisms underlying ZEA transport and compartment function.

Fusarium graminearum↗
PubMed2026

Motor coordination and behavioural deficits in a mouse model of KMT2B-related dystonia.

INTRODUCTION: Pathogenic variants in KMT2B cause early-onset dystonia, but a mouse model that has undergone comprehensive, dystonia-oriented phenotyping is lacking. METHODS: We conducted detailed phenotyping on heterozygous Kmt2b constitutive knockout mice and wild-type littermates, assessing growth, neurobehavioural traits, motor coordination, sensorimotor gating, social behaviour and metabolic parameters, combined with striatal RNA sequencing. RESULTS: Kmt2b knockout mice of both sexes were viable but significantly smaller and lighter than littermate controls. Knockouts were hyperlocomotive in the open field and showed approximately two-fold larger acoustic startle responses; unexpectedly, prepulse inhibition was enhanced rather than reduced at all prepulse intensities. On the balance beam, knockouts crossed more slowly and paused more frequently; female knockouts also paused more on the ladder rung task. Frame-by-frame video analysis revealed a claw-like hindpaw posture characterized by abnormal inward flexion of the digits. Knockout mice spent less time investigating a novel conspecific, while social recognition memory remained intact. Striatal RNA sequencing confirmed reduction of Kmt2b transcript to approximately half of control levels and identified 177 differentially expressed genes, including Maob, encoding monoamine oxidase B; gene set enrichment analysis implicated neurodevelopmental, glial and mitochondrial processes. Nociception, vision, body-weight-adjusted grip strength, and clinical chemistry and haematological measures were largely unaffected. CONCLUSION: Heterozygous Kmt2b knockout mice show hyperlocomotion, altered sensorimotor gating, impaired motor coordination with dystonic-like paw posturing and reduced sociability, alongside a striatal transcriptomic signature implicating neurodevelopmental processes. The model mirrors aspects of human KMT2B-related dystonia and provides a platform for mechanistic study; environmental or pharmacological challenge may be needed to unmask overt dystonic features.

Dystonia↗
PubMed2026

Genome-wide association study of patterns of perinatal exposure to polyunsaturated fatty acids from the EDEN mother-child cohort.

The genetic determinants of polyunsaturated fatty acid (PUFA) status during the perinatal window require deeper understanding. We conducted a genome-wide association study of perinatal PUFA patterns in 1352 mother-child pairs from the French EDEN cohort using maternal genotype data. Five perinatal PUFA patterns had been previously derived using PUFA levels measured in maternal blood, cord blood, and colostrum simultaneously. We used linear regression models assuming additive genetic effects to assess the associations between common SNPs and each pattern, adjusting for maternal age, study center, and genetic ancestry. Pattern 1 "High omega-3 Long-chain (LC)-PUFAs, low omega-6 LC-PUFAs" was not associated with any genetic variants. Patterns 2 to 5-"Omega-6 LC-PUFAs," "Colostrum LC-PUFAs," "Omega-6 precursor (LA) and DGLA," and "LA and colostrum ALA"-were strongly associated with variants in the FADS gene cluster. The strongest association was observed between Pattern 4 "Omega-6 precursor (LA) and DGLA," and rs174546 located on FADS1 gene region (&#x3b2; (SE) = 0.80 (0.034), p < 10&#x207b;102). No other robust association was found with other genes. These findings underscore the main contribution of FADS variants to the variability of four specific perinatal PUFA patterns in our cohort. This study should be replicated in larger, ancestrally diverse populations beyond individuals of European descent.

EDEN cohort↗
PubMed2026

Generation of TWO iPSC lines (CRICKi025-A and CRICKi026-A) from healthy donor bone marrow mesenchymal stromal cells.

Mesenchymal stromal cells (MSCs) are key components of the bone marrow (BM), providing structural support and paracrine signals that regulate haematopoietic stem cell maintenance, self-renewal and differentiation. However, primary BM MSCs are rare, heterogeneous, and subject to donor variability and have limited ex-vivo expansion capacity, restricting their utility. Here, we describe two human induced pluripotent stem cells lines, CRICKi0025-A and CRICKi0026-A, reprogrammed from adult BM-derived MSCs using non-integrating Sendai virus vectors. Both lines showcase grade-A morphology, are genomically stable, upregulate essential pluripotent markers and can differentiate into the three germ layers. These lines are a well-characterised resource for generating MSCs.

Journal Article↗
PubMed2026

Endogenous tagging of the TBXT (Brachyury) gene with 2A-EGFP in BJNhem19 human embryonic stem cells using CRISPR-Cas9 genome editing.

Brachyury (TBXT) is a T-box transcription factor essential for directing human embryonic stem cells (hESCs) toward mesodermal lineage specification. Here, we report the generation of a Brachyury/TBXT-2A-EGFP knock-in reporter line in the BJNhem19 hESC line using CRISPR/Cas9-mediated homology-directed repair. Accurate integration of the reporter cassette was confirmed by DNA sequencing and validated by the comparison of EGFP expression to endogenous TBXT gene expression following directed mesodermal differentiation. This reporter line provides a tractable fluorescence-based platform for real-time monitoring of mesodermal commitment, which will help in high-content screening of differentiation protocols.

Journal Article↗