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URMD-Seq: A high-throughput method for scalable detection of ultra-rare mutations in the human mitochondrial genome.

The study of mitochondrial genetics has long been limited to polymorphisms and high frequency mutations owing in part to technical and technological limitations in reliably detecting and quantifying rare somatic mutations. Over the past decade or so, the study of rare somatic mitochondrial DNA (mtDNA) variants has expanded and continues to garner increasing interest in a wide range of research fields. Here, we describe Ultra-Rare Mutation Detection-Sequencing (URMD-Seq), a high-throughput method that combines unique molecular identifier (UMI)-based library preparation and Next Generation Sequencing (NGS) for the accurate and scalable detection of ultra-rare mutations in the mtDNA control region. Our method exploits degenerate primers to label individual mtDNA molecules. This is followed by several purification, quantification and amplification steps, to obtain high quality amplicons for sequencing on the Illumina MiSeq platform. Our approach enables the use of total genomic DNA extract as starting point for the assay, overcoming the need for organelle isolation and/or mtDNA enrichment, hence broadening the type of specimen that can be studied, while offering cost and time benefits. The assay described herein has been demonstrated to reliably measure variants present at on average 0.09%, but as low as 0.03%, variant allele frequency in a variety of tissues, including fresh and frozen biobanked specimens. Using this protocol, library preparation of 300 specimens can be completed by a single individual with general nucleic acid handling experience in approximately 20 days. Given its flexibility and scalability, URMD-Seq is particularly well suited for epidemiological studies using a large number of specimens.

Humans

Joint, multifaceted genomic analysis enables diagnosis of diverse, ultra-rare monogenic presentations.

Genomics for rare disease diagnosis has advanced at a rapid pace due to our ability to perform in-depth analyses on individual patients with ultra-rare diseases. The increasing sizes of ultra-rare disease cohorts internationally newly enables cohort-wide analyses for new discoveries, but well-calibrated statistical genetics approaches for jointly analyzing these patients are still under development. The Undiagnosed Diseases Network (UDN) brings multiple clinical, research and experimental centers under the same umbrella across the United States to facilitate and scale case-based diagnostic analyses. Here, we present the first joint analysis of whole genome sequencing data of UDN patients across the network. We introduce new, well-calibrated statistical methods for prioritizing disease genes with de novo recurrence and compound heterozygosity. We also detect pathways enriched with candidate and known diagnostic genes. Our computational analysis, coupled with a systematic clinical review, recapitulated known diagnoses and revealed new disease associations. We further release a software package, RaMeDiES, enabling automated cross-analysis of deidentified sequenced cohorts for new diagnostic and research discoveries. Gene-level findings and variant-level information across the cohort are available in a public-facing browser ( https://dbmi-bgm.github.io/udn-browser/ ). These results show that case-level diagnostic efforts should be supplemented by a joint genomic analysis across cohorts.

Humans

Pleomorphic rhabdomyosarcoma, outcomes of patients with advanced disease treated with systemic agents: Retrospective study from the global pushing ultra-rare sarcomas towards hope (PUSH) consortium.

OBJECTIVES: To report the outcomes in adult patients with advanced pleomorphic rhabdomyosarcoma (P-RMS) treated with systemic therapy. METHODS: This global, multicenter, retrospective study conducted within the Pushing Ultra-Rare Sarcomas Towards Hope consortium (PUSH) included patients > 40 years with histologically confirmed advanced P-RMS, treated with at least one line of systemic therapy between 2013 and 2023. The primary endpoint was progression-free survival from first diagnosis of advanced disease, and from systemic treatment start (PFS-1 and PFS-2). Secondary endpoints included overall response rate (ORR), overall survival from first diagnosis of advanced disease and from treatment start (OS-1 and OS-2), and treatment-specific outcomes. RESULTS: Seventy-seven patients were included from 21 sarcoma reference centers. At a median follow-up of 44 months (IQR: 17.0-74.8), 49 (64%) patients had died and 48 (62%) had progressed. The median OS-1 and PFS-1 were 13.6 (95% confidence interval (CI): 9.4-22.5) and 5.4 (95% CI: 4.2-7.3) months, respectively. Two- and three-year OS-1 were 32.5% and 30.3%. Anthracycline-based regimens (n = 42) achieved a 50% ORR, with mPFS-2 and mOS-2 of 5.2 and 19.2 months; gemcitabine-based regimens (n = 15) a 42% ORR, with mPFS-2 and mOS-2 of 3.7 and 7.8 months; pazopanib (n = 6) a 33% ORR, with mPFS-2 and mOS-2 of 2.4 and 4.2 months; PD-1 inhibitors (n = 2) induced one response lasting 53 months. CONCLUSIONS: This series of advanced P-RMS treated with systemic agents, the largest available to date, showed meaningful activity of anthracycline- and gemcitabine-based regimens, and anecdotal responses to pazopanib and PD-1 inhibitors. Further prospective validation is planned.

Humans

Genetic Determinants of Early Heart Failure in Hypoplastic Left Heart Syndrome: A Prospective NC-DEFINE Study.

BACKGROUND: Survivors of hypoplastic left heart syndrome (HLHS), the most severe form of congenital heart disease, are at high risk for heart failure (HF). HF in early life is a major contributor to mortality in this vulnerable population. However, reliable approaches to identify infants at highest risk for early HF are currently lacking. OBJECTIVES: The purpose of this study was to evaluate whether ultra-rare variants in cardiomyopathy-associated genes are associated with HF risk in HLHS. METHODS: Neonates with HLHS were prospectively enrolled within the first 21 days of life at Duke University Health System. Children and adults with HLHS who were older than 21 days were enrolled from Duke University Health System and the University of North Carolina into an ambispective cohort. External HLHS cohorts from Nationwide Children's Hospital and Vanderbilt University Medical Center were evaluated to assess for reproducibility across institutions. Participants underwent genome sequencing, and ultra-rare variants in dilated cardiomyopathy-associated genes (minor allele frequency &#x2264;0.01%) were evaluated. The primary outcome was HF, categorized as severe (ventricular assist device implantation, heart transplantation, or death) or medically managed (reduced systemic ventricular ejection fraction and/or HF diagnosis requiring initiation or escalation of HF therapy). Associations between variant status and HF risk were assessed using Cox regression. RESULTS: Among 35 neonates in the prospective cohort, 7 (20.0%) developed severe HF, 10 (28.6%) developed medically managed HF, and 18 (51.4%) remained HF free. The presence of a likely pathogenic/pathogenic variant was associated with a marked 9-fold increased risk of severe HF compared with genotype-negative individuals (P = 0.02). Most severe HF events occurred within the first month of life (67%). Similar associations between likely pathogenic/pathogenic variants and severe HF were observed in the Nationwide Children's Hospital and Vanderbilt University Medical Center cohorts (11- and 3-fold increased risk, respectively; all P < 0.05). Associations were attenuated in the ambispective cohort (all P > 0.05), which consisted of individuals significantly older than the prospective cohort (P < 0.0001). CONCLUSIONS: This study provides the first prospective evidence linking dilated cardiomyopathy-associated variants to early-onset HF in HLHS. These findings suggest that genetic variation may contribute to myocardial vulnerability in HLHS, highlighting the potential for genetic screening to enable early risk stratification and guide precision medicine approaches in this high-risk population.

Humans

Rare variant contribution to the heritability of coronary artery disease.

Whole genome sequences (WGS) enable discovery of rare variants which may contribute to missing heritability of coronary artery disease (CAD). To measure their contribution, we apply the GREML-LDMS-I approach to WGS of 4949 cases and 17,494 controls of European ancestry from the NHLBI TOPMed program. We estimate CAD heritability at 34.3% assuming a prevalence of 8.2%. Ultra-rare (minor allele frequency &#x2264;&#x2009;0.1%) variants with low linkage disequilibrium (LD) score contribute ~50% of the heritability. We also investigate CAD heritability enrichment using a diverse set of functional annotations: i) constraint; ii) predicted protein-altering impact; iii) cis-regulatory elements from a cell-specific chromatin atlas of the human coronary; and iv) annotation principal components representing a wide range of functional processes. We observe marked enrichment of CAD heritability for most functional annotations. These results reveal the predominant role of ultra-rare variants in low LD on the heritability of CAD. Moreover, they highlight several functional processes including cell type-specific regulatory mechanisms as key drivers of CAD genetic risk.

Humans

Calcium release channel deficiency syndrome in patients diagnosed with idiopathic ventricular fibrillation and decedents classified as sudden unexplained death in the young.

AIMS: Calcium release channel deficiency syndrome (CRCDS) results from loss-of-function (LOF) variants in the RYR2-encoded type 2 ryanodine receptor (RyR2), predisposing patients to sudden cardiac arrest/death (SCA/SCD) without abnormalities on a stress electrocardiogram (ECG). Undetected CRCDS may underlie idiopathic ventricular fibrillation (IVF) and sudden unexplained death in the young (SUDY). We aimed to determine the prevalence of potential CRCDS-causative RYR2 variants in IVF and SUDY. METHODS AND RESULTS: We reviewed clinical evaluation and RYR2 genetic analysis of 169 IVF patients and 279 SUDY victims. Only ultra-rare (<0.005% in gnomAD) nonsynonymous RYR2 variants were considered potentially pathogenic. Among IVF patients, 6/169 (3%) overall-and 6/67 (9%) with exertion-related SCA-harboured an RYR2 variant and represent potential CRCDS cases. All exhibited normal resting and stress ECGs. Genetic analysis revealed six distinct RYR2 variants, two previously characterized as LOF. In SUDY, 31/279 victims (11%) had a RYR2 variant (30 unique variants), predominantly observed in exertion-related SCD 20/83 (24%) vs. rest-related 11/196 (6%). Of the 14 SUDY victims with functionally characterized RYR2 variants, five (2% of total cohort) had a LOF variant; among the 56 exertion-related SUDY cases, four (7%) had a LOF variant. CONCLUSION: CRCDS may account for 3% of IVF overall and 9% of exertion-related SCA in IVF. Ultra-rare RYR2 variants may underlie up to 11% of SUDY, with 65% of RYR2-positive cases occurring during exertion. LOF-RYR2 variants may contribute to &#x2265;7% of exercise-associated SUDY. Accurate identification of the underlying ryanodinopathy is essential for clinical management of affected patients.

Humans

Diagnosis and management of very rare primary arrhythmia syndromes in children and adults: a Clinical Consensus Statement of the European Heart Rhythm Association of the ESC and the Association of Cardiovascular Nursing & Allied Professions of the ESC, endorsed by the Association for European Paediatric and Congenital Cardiology.

Very rare and ultra-rare primary inherited arrhythmia syndromes (IAS) represent a heterogeneous group of disorders associated with a significant risk of sudden cardiac death, often manifesting from foetal life to early adulthood. Current guidelines primarily address more common IAS and provide limited, non-specific recommendations for these rare entities, particularly in paediatric populations. This European Heart Rhythm Association Clinical Consensus Statement, developed in collaboration with the Association of Cardiovascular Nursing and Allied Professions and endorsed by the Association for European Paediatric and Congenital Cardiology, integrates available evidence with expert opinion. Recommendations were formulated through structured discussion and voting, following ESC consensus methodology, with a focus on clinically actionable gene-disease associations. The document provides a comprehensive framework for the diagnosis and management of very rare IAS, including calmodulinopathies, Andersen-Tawil syndrome, Timothy syndrome, TRDN-related disease, calcium release deficiency syndrome, and other atypical channelopathies. It highlights age-specific clinical presentations, the importance of genetic testing, and tailored therapeutic strategies, including pharmacological treatments, left cardiac sympathetic denervation, and selective use of implantable cardioverter-defibrillators. Special attention is given to paediatric considerations, foetal diagnosis, and the role of multidisciplinary care. The document also addresses arrhythmic risk in metabolic and cardiomyopathic conditions, as well as the importance of molecular autopsy and family screening in sudden unexplained death. This consensus document fills a critical gap by providing expert-driven, pragmatic guidance for the management of very rare IAS across the lifespan. It underscores the need for specialized care, international collaboration, and prospective registries to improve evidence generation, risk stratification, and patient outcomes in this vulnerable population.

Humans

Structural variation detection and association analysis of whole-genome-sequence data from 16,543 Alzheimer's disease sequencing project subjects.

INTRODUCTION: The role of structural variations (SVs) in Alzheimer's disease (AD) remains understudied. METHODS: We analyzed whole-genome sequencing data from the Alzheimer's Disease Sequencing Project (N&#xa0;=&#xa0;16,543) and identified 400,234 (168,223 high-quality) SVs. Laboratory validation yielded a sensitivity of 82% (85% for high-quality). RESULTS: We found a burden of singletons (odds ratio [OR]&#xa0;=&#xa0;1.07, p&#xa0;=&#xa0;0.0017) and homozygous deletions (OR&#xa0;=&#xa0;1.14, p&#xa0;<&#xa0;0.0001) in cases. On AD genes, we observed the ultra-rare SVs associated with the disease, including protein-altering SVs in ABCA7, APP, PLCG2, and SORL1. Twenty-one SVs are in linkage disequilibrium (LD) with known AD-risk variants, exemplified by a 5k deletion in LD (R2&#xa0;=&#xa0;0.99) with rs143080277 in NCK2. We identified a rare deletion near RNA5SP293 associated with AD (OR&#xa0;=&#xa0;1.99, p&#xa0;=&#xa0;1.3&#xa0;&#xd7;&#xa0;10-5), which was replicated using an independent dataset. DISCUSSION: This study highlights the pivotal role of SVs in AD genetics. HIGHLIGHTS: Observed a significant burden of singletons and homozygous deletions in Alzheimer's disease (AD) patients. Identified rare protein-altering structural variations (SVs) in ABCA7, APP, PLCG2, and SORL1. Established linkages between SVs and AD risk-associated single nucleotide variants (SNVs). Discovered a novel deletion near RNA5SP293 linked to AD, replicated independently. Uncovered over-representation of SVs in neuronal function pathways.

Humans

Phenotypic and transcriptomic characterization of biallelic RNU2-2 developmental and epileptic encephalopathy.

OBJECTIVE: A significant proportion of individuals with suspected genetic developmental and epileptic encephalopathies (DEEs) remain unsolved following whole genome sequencing (WGS). Here we describe biallelic RNU2-2 variants causing a recently reported, severe, recessive DEE. METHODS: We screened individuals who have received WGS analyses at the Genomic Medicine Centre Karolinska for Rare Diseases for biallelic RNU2-2 variants. Deep phenotyping was performed through reviewing entire medical histories and phenotypic traits were transcribed to their corresponding Human Phenotype Ontology (HPO) term. HPO terms were used to generate pairwise phenotypic similarity scores and assess for significantly shared phenotype enrichment in the RNU2-2 sub-cohort. RNA sequencing analyses were performed in fibroblast and blood tissues to compare splicing events between RNU2-2 individuals and two independent control groups. RESULTS: We identified 14 individuals from nine families with 12 ultra-rare biallelic RNU2-2 variants clustering in the conserved 5' domains. Genotype data from 13 of 14 individuals has been reported previously as part of a larger cohort. All individuals presented with a highly concordant, severe DEE, characterized by severe to profound intellectual disability, inability to walk or communicate, hyperkinesia, and refractory seizures. Infantile spasms and tonic seizures were the predominant seizure types and a Lennox-Gastaut syndrome-like phenotype was common. These individuals had a significantly similar phenotypic signature when compared with 703 individuals with complex pediatric epilepsies (two-sided Monte Carlo permutation test, p&#x2009;=&#x2009;.005). RNA sequencing analyses showed aberrant splicing, with the most pronounced effects in fibroblast tissues in mutually exclusive exon and alternate 3' splice-site events, which were not detectable in blood. SIGNIFICANCE: We present deep phenotyping data and transcriptomic analyses that provide support for rare, 5' clustering biallelic RNU2-2 variants causing this novel, severe DEE. We propose an RNA sequencing methodology on fibroblast tissue for future validation of RNU2-2 variants.

autosomal recessive disease

A novel variant combination in COASY associates with severe prenatal onset PCH12: expanding the clinical and genetic spectrum.

Pontocerebellar hypoplasia type 12 (PCH12) is an ultra-rare, perinatal lethal, neurodegenerative disorder with microcephaly and arthrogryposis. Previous reports have associated PCH12 with complete loss-of-function variants in COASY identified in 14 fetuses and newborns from eight unrelated families. In contrast, COASY partial loss-of-function variants have been linked to COASY protein-associated neurodegeneration (CoPAN), a subtype of neurodegeneration with brain iron accumulation (NBIA). Emerging evidence suggests that COASY-related disorders may represent a phenotypic continuum between PCH12 and CoPAN. Using exome sequencing, we identified a previously reported missense variant (c.641C>T, p.Ala214Val) as well as a previously unreported rare nonsense variant (c.1015C>T, p.Arg339*) in a compound heterozygous state in the COASY gene in a patient presenting with clinical features consistent with PCH12. The p.Ala214Val variant has only been described in combination with another missense variant (p.Arg499Cys) in two siblings with CoPAN. The presence of p.Ala214Val in trans with the truncating p.Arg339* variant in this patient is associated with a severe perinatal lethal phenotype resembling PCH12. This case broadens the reported genetic and phenotypic spectrum of COASY-associated disorders and highlights the importance of continued genotype-phenotype correlation investigation.

Humans

Next-generation sequencing in head and neck sarcoma: a single-centre institutional experience and review of the literature.

Head and neck sarcomas (HNS) are rare, heterogeneous malignancies representing less than 1% of head and neck cancers. Their complex anatomy and overlapping morphologies pose significant challenges for traditional diagnosis. We aimed to evaluate the clinical utility of next-generation sequencing (NGS) within a tertiary referral centre and synthesise these findings with current global molecular standards. We conducted a retrospective review of an original, previously unpublished, cohort of 12 patients with histologically verified HNS treated at University College London Hospital (UCLH) between 2023 and 2024. Molecular profiling included targeted DNA (RMH200) and RNA-fusion panels. This was supplemented by a qualitative synthesis of 16 key studies (2010-2026) identified through a systematic search strategy. In the institutional cohort, NGS provided definitive diagnostic or therapeutic clarification in 66% of cases (8/12). Key findings included the identification of pathognomonic fusions (such as EWSR1::FLI1, PAX3::MAML3), a novel MAMLD1::VGLL3 fusion, and actionable variants such as BRAF V600E and MYOD1. Furthermore, the formal exclusion of Neurotrophic tropomyosin receptor kinase (NTRK) fusions in some cases allowed for therapeutic streamlining. Literature synthesis aligned these results and emphasised the need for NGS for more accurate diagnosis and adequate treatment. NGS is a clinical necessity in the management of ultra-rare HNS. By transitioning from traditional morphology to high-resolution molecular interrogation, clinicians can resolve diagnostic ambiguity and identify targeted therapeutic pathways. Integration with emerging 2026 standards, including epigenetic classification and liquid biopsy monitoring, represents the future of precision surgery in head and neck sarcoma.

Humans

A novel ASCC1 splice-site variant broadens the phenotypic spectrum of spinal muscular atrophy with congenital bone fractures type 2.

Spinal muscular atrophy with congenital bone fractures type 2 (SMABF2) is an ultra-rare neuromuscular disorder caused by pathogenic variants affecting the ASC-1 complex, most commonly ASCC1. The disorder is typically characterized by severe congenital hypotonia, prenatal or congenital fractures, and early respiratory failure. We report a girl with a novel homozygous intronic donor-site variant, c.95+5G>C, in ASCC1. In contrast to the classic SMABF2 phenotype, she had no congenital fractures and survived until 7 years of age. Her clinical presentation included generalized hypotonia, areflexia, minimal spontaneous movements, dysmorphic features related to fetal hypomobility, progressive respiratory insufficiency requiring tracheostomy and gastrostomy, and cardiac involvement. This case expands both the genetic and phenotypic spectrum of ASCC1-associated disease. The comparatively prolonged survival and absence of congenital fractures suggest that not all ASCC1 variants result in a fully loss-of-function phenotype. However, this interpretation remains hypothetical because functional RNA studies were not performed.

Humans

Clinical and biochemical footprints of inherited disorders of autophagy.

Autophagy is an evolutionarily conserved lysosomal recycling system that integrates nutrient sensing, organelle quality control, proteostasis, cellular stress responses and metabolic adaptation. Autophagy is particularly relevant for post-mitotic tissue such as neurons, skin, and immune cells. Monogenic disorders disrupting autophagy or closely coupled endolysosomal trafficking pathways have recently emerged as a recognizable group of inherited metabolic diseases. These conditions are individually rare inborn errors of metabolism and collectively important because they bridge neurodevelopmental, neuromuscular and neurodegenerative disorders, including hereditary forms of Parkinson's disease, spastic paraplegias and neurodegeneration with brain iron accumulation. Multisystem involvement is common but variable. The prototypic disorder is EPG5-related Vici syndrome, in which defective autophagosome-lysosome fusion causes severe neurodevelopmental and multisystem disease. Other disorders may affect any step of the pathway, from phosphatidylinositol 3-phosphate effector biology and ATG conjugation/lipidation to autophagosome maturation, ATG9 trafficking, HOPS/CORVET-related vesicle trafficking (including VPS16 and VPS33A), autophagosome-lysosome fusion, autolysosome reformation and lysosome-mTOR signaling. Clinically, affected individuals commonly present with global developmental delay and/or intellectual disability, epilepsy, movement disorders including dystonia, parkinsonism, ataxia and spasticity, and both neuropathic and myopathic neuromuscular manifestations. A biphasic course with progressive neurodegeneration and variable multisystem (including ocular, cardiac, immunological, cutaneous and growth) involvement are important clinical clues. Diagnosis relies on careful phenotyping, brain MRI, targeted metabolic exclusion of mimics, genomic sequencing and functional assays in patient-derived cells as required. Supportive multidisciplinary management is essential. No disease-modifying therapy is currently established in humans, but pathway-based cellular assays, model systems and small-molecule or gene-replacement strategies are creating a rational therapeutic pipeline. Importantly, IEMbase dyadic nomenclature with system-level clinical annotations provides a standardized framework for quantifying shared phenotypic signatures across these ultra-rare conditions. This review summarizes pathobiochemistry, genetics, clinical presentation, diagnosis and treatment prospects for inherited disorders of autophagy.

Autophagosome

Persistent tic disorders are associated with 17q12 duplications.

Tourette Syndrome (TS) and Persistent Tic Disorder (PTD) are childhood-onset neuropsychiatric conditions with high heritability. Due to current sample size limitations, identifying TS/PTD risk genes has been challenging. This study addressed this issue by conducting a meta-analysis of microarray copy number variant (CNV) studies from three TS/PTD genomics consortia, supplemented with new data from 3291 cases. This approach more than doubled the sample size of previous TS/PTD CNV studies, with CNV calls generated from 5725 TS/PTD cases and 10,982 matched controls. The results confirmed that TS/PTD cases 1) have a higher burden of ultra-rare deletions overlapping loss-of-function intolerant genes (OR&#x2009;=&#x2009;1.68, P&#x2009;=&#x2009;9.3&#xd7;10-5) and 2) are more likely to carry established neurodevelopmental CNVs (OR&#x2009;=&#x2009;1.42, P&#x2009;=&#x2009;3.9&#xd7;10-2) compared to controls. Additionally, a novel, genome-wide significant CNV locus for TS/PTD was discovered, involving duplications at 17q12 (hg19 chr17:34.8 - 36.2&#x2009;Mb). This locus is associated with a known duplication syndrome associated with variable neuropsychiatric traits, but has not been previously linked to tic disorders. Eight cases and one control carried the canonical ~1.4&#x2009;Mb duplication at chr17:34.8-36.2&#x2009;Mb, while one additional case had a smaller 110&#x2009;kb duplication within this known CNV that included only one gene, ACACA (acetyl-CoA carboxylase, OR&#x2009;=&#x2009;26.7, P&#x2009;=&#x2009;5.69&#xd7;10-7). Overall, this study provides further evidence that rare, genic CNVs play a substantial role in the genetic architecture of TS/PTD and identifies a new genome-wide significant association with this neurodevelopmental disorder.

Journal Article

AAV gene therapy for hereditary spastic paraplegia type 50: a phase 1 trial in a single patient.

There are more than 10,000 individual rare diseases and most are without therapy. Personalized genetic therapy represents one promising approach for their treatment. We present a road map for individualized treatment of an ultra-rare disease by establishing a gene replacement therapy developed for a single patient with hereditary spastic paraplegia type 50 (SPG50). Through a multicenter collaboration, an adeno-associated virus-based gene therapy product carrying the AP4M1 gene was created and successfully administered intrathecally to a 4-year-old patient within 3 years of diagnosis as part of a single-patient phase 1 trial. Primary endpoints were safety and tolerability, and secondary endpoints evaluated efficacy. At 12 months after dosing, the therapy was well tolerated. No serious adverse events were observed, with minor events, including transient neutropenia and Clostridioides difficile gastroenteritis, experienced but resolved. Preliminary efficacy measures suggest a stabilization of the disease course. Longer follow-up is needed to confirm the safety and provide additional insights on the efficacy of the therapy. Overall, this report supports the safety of gene therapy for SPG50 and provides insights into precision therapy development for rare diseases. Clinical trial registration: NCT06069687 .

Humans

De novo chromatin remodelling variants in sporadic Chiari 1 malformation.

Chiari 1 malformation (CM1) is the most common congenital malformation of the human hindbrain. Although prior studies have implicated chromatin-remodeling genes in CM1, the de novo genetic architecture and underlying neurodevelopmental mechanisms remain incompletely defined. To investigate the molecular genetics of a novel familial form of CM1 linked with syringomyelia and tethered cord and determine whether rare, damaging de novo variants (DNVs) contribute to sporadic CM1 risk with gene- and pathway-level resolution, we performed whole-exome sequencing in an ultra-rare multigenerational family with CM1 and associated spinal pathology, and in the largest assembled trio-based cohort to date, comprising 1,585 proband-parent trios with sporadic, idiopathic CM1 (2017-2025). The comparison cohort included 1,798 unaffected control siblings. Clinical phenotyping was by systematic medical record review. Structural domain mapping, in silico modeling, and integration with single-cell transcriptomic data from developing human cerebellum was conducted to assess biological plausibility. A heterozygous loss-of-function variant in CHD3 segregated with CM1 and syringomyelia in a multigenerational family. In the trio-based cohort, rare protein-altering DNVs were significantly enriched across multiple chromodomain helicase DNA-binding (CHD) genes, including CHD1, CHD3, CHD4, and CHD8, exceeding gene-specific mutation expectations (protein-damaging variants: P = 1.3 &#xd7; 10-9; predicted loss-of-function variants: P = 8.6 &#xd7; 10-5). CHD1 contained two pathogenic DNVs (p.A999D and p.E984K). CHD4 (p.D744N, p.T1813P, and p.I1102T) and CHD8 (p.R1402X, p.R1472X, and p.R2035X) each contained three new DNVs. Variants clustered within conserved ATPase, helicase, and chromodomain regions essential for chromatin remodeling, and these patients frequently had comorbid developmental delay and related neurodevelopmental features. Single-cell transcriptomic analyses demonstrated enrichment in Purkinje cells and inhibitory neurons of midgestational cerebellum, where CHD gene products form a coherent chromatin-regulatory network. Rare, large-effect DNVs that disrupt chromatin-remodeling programs contribute to sporadic CM1, implicating genetically encoded dysregulation of cerebellar development as a central disease mechanism. Exome sequencing may complement surgical evaluation of children with sporadic CM1, particularly when accompanied by neurodevelopmental concerns, informing prognosis and family counseling.

de novo variants

DENND3-p.R534S disrupts dyadic microdomain architecture to drive potentially pro-arrhythmic calcium and electrophysiologic instability.

AIMS: Inherited ventricular arrhythmias (VAs) frequently occur in the absence of pathogenic variants in canonical ion channel genes, suggesting alternative mechanisms of electrical instability. DENND3 is a guanine nucleotide exchange factor that regulates Rab GTPase-mediated trafficking, but its role in cardiac excitation-contraction coupling and membrane microdomain organization remains undefined. METHODS AND RESULTS: We studied induced pluripotent stem cell-derived cardiomyocytes generated from a CRISPR/CAS9-engineered ultra-rare DENND3-p.R534S variant-inserted line (previously identified in an idiopathic ventricular fibrillation pedigree) and matched isogenic controls. Multielectrode array recordings, live-cell calcium imaging, super-resolution imaging using expansion microscopy, and biochemical analyses were used to assess electrical activity, calcium handling, membrane architecture, and calcium release unit organization. Potentially therapeutic studies were performed using genetic and pharmacologic inhibition of Rab11b. DENND3-p.R534S induced pluripotent stem cell-derived cardiomyocytes exhibited multicellular electrical instability characterized by increased beat-to-beat variability, arrhythmic activity, conduction slowing, and prolonged excitation-contraction delay. These abnormalities were accompanied by heterogeneous and dyssynchronous calcium cycling despite preserved expression of major calcium-handling proteins. Super-resolution imaging revealed disruption of BIN1-dependent membrane architecture and nanoscale uncoupling of Cav1.2 and RyR2. Inhibition of Rab11b restored BIN1 organization, re-established dyadic coupling, normalized calcium cycling, and improved electrical stability. CONCLUSION: These findings support a model in which altered trafficking balance contributes to disruption of membrane microdomain organization, leading to dyadic uncoupling, calcium instability, and electrical dysfunction. Modulation of the Rab11b-mediated trafficking pathway restored structural and functional abnormalities, supporting the trafficking-associated pathway as a potential therapeutic target in DENND3-associated ventricular arrhythmia.

Myocytes, Cardiac

Rare variant analysis of whole genome sequenced juvenile idiopathic arthritis multiplex pedigrees identifies rare variants in NOD2 and ACVR1.

Juvenile idiopathic arthritis is a complex rheumatic disease that is influenced by environmental and genetic factors. Linkage and genome-wide association studies have identified genes that contribute to the risk of developing juvenile idiopathic arthritis but are limited in their ability to identify disease-risk variants of large effect. Penetrant, heritable risk variants can be detected in high-risk families, but such cases are uncommon due to the low prevalence of juvenile idiopathic arthritis. This study utilizes whole-genome sequencing of 23 multiplex families, the largest such cohort to date, to discover variants and genes relevant to JIA pathogenesis. Pathogenic variants in NOD2 associated with Blau syndrome, an ultra-rare Mendelian inflammatory disorder, are the most recurrent variants in the cohort, consistent with previous reports that milder presentations of Blau syndrome are oftentimes misdiagnosed as juvenile idiopathic arthritis. For the first time, however, rare variants in ACVR1 and SMAD6, integral components of the Bone Morphogenic Protein pathway, are found to be associated with juvenile idiopathic arthritis. Identified ACVR1 variants map to critical protein domains. AlphaFold modeling predicts that the ACVR1 interaction with its inhibitor OGT is disrupted by these variants, indicating that the patient-mutated protein has a gain-of-function phenotype. Drosophila melanogaster expressing either a wild-type or patient-mutated version of ACVR1 exhibit embryonic lethality, with the mutant exhibiting 1.4-fold greater lethality than wild-type. The combination of family-based cohorts for gene discovery, AI-based computational tools, and animal model studies for tests of variant function underscores shared disease pathogenesis between JIA and monogenic disorders of immunity and connective tissue.

Arthritis, Juvenile