Ribosomal biogenesis defects trigger subunit specific developmental checkpoints via TOR signaling and gap junction in C. elegans.

Molecular characterization of two phenotypes of Mixta calida isolated from post-liver transplant drainage fluid.

Background: Gastrointestinal nematode infections represent a major threat to the health of both wild and domestic animals, including captive deer. However, data on their prevalence and molecular characteristics in Indonesia remain limited. Understanding parasite diversity is crucial for establishing effective control and health management programs. Objectives: This study aimed to detect, identify, and analyze the phylogenetic relationships of gastrointestinal nematodes infecting captive deer in West Java, Indonesia. Methods: Fecal samples were obtained from 13 breeding centers for parasitological and molecular analyses. Parasitological analyses involved flotation and McMaster techniques to detect strongyle-type eggs, while polymerase chain reaction (PCR) targeting the ITS2 ribosomal DNA region was performed to amplify nematode DNA. Positive amplicons were sequenced; species identification was confirmed through BLAST analysis. Phylogenetic trees were constructed using maximum likelihood methods to assess the genetic relationships of the identified nematodes with reference sequences. Results: The overall prevalence of gastrointestinal nematode infection was 18.1%, with egg counts consistently below 50 EPG, indicating mild infection levels. Molecular analysis identified two nematode species: Trichostrongylus axei, detected across multiple locations, indicating widespread presence, and Spiculopteragia houdemeri, found only in three specific sites. Phylogenetic analysis revealed high genetic similarity between Indonesian isolates and reference sequences from Europe and Asia, highlighting the potential global conservation of these species. Conclusion: This study presents the first molecular detection of T. axei and S. houdemeri in captive deer populations in Indonesia, thereby providing critical baseline data to support future epidemiological surveillance and the development of health management strategies.

Liver fibrosis significantly burdens global health, and increased protein synthesis during hepatic stellate cell (HSC) activation plays a crucial role in its progression. Ribosome is the site of protein synthesis. RNA polymerase I (Pol I) is a protein that regulates the transcription of ribosomal DNA (rDNA) genes into ribosomal RNA (rRNA) in ribosomal biogenesis. Therefore, we investigated the role and mechanism of Pol I-regulated ribosome biogenesis in HSCs activation and liver fibrosis progression. Initially, we assessed the expression levels of Pol I in the serum of patients diagnosed with liver fibrosis. Then, we assessed Pol I-regulated ribosome biogenesis levels in mouse models of metabolic dysfunction-associated steatohepatitis (MASH) and carbon tetrachloride (CCl4). Finally, we employed overexpression or knockdown of the Pol I gene in LX2 cells or utilised the Pol I inhibitor CX-5461 invivo and invitro, assessing the levels of ribosome biogenesis and HSCs activation. Pol I levels were elevated in the serum of patients with liver fibrosis. Additionally, Pol I-regulated ribosome biogenesis levels were significantly increased in both MASH and CCl4 mouse models, as well as in HSCs activated by transforming growth factor beta 1 (TGFβ1). The overexpression of Pol I was found to enhance the activation of HSCs and promote ribosome biogenesis, while the knockdown of Pol I or the inhibitor CX-5461 inhibited these processes. Pol I-regulated ribosome biogenesis is significantly increased during HSCs activation and liver fibrosis progression. Pol I may serve as a potential target for the diagnosis and treatment of liver fibrosis.

Identification, safety evaluation and probiotic potential of lactic acid bacteria isolated from wheat.

Zebrafish yolk high phosphoprotein-derived peptide Pt5-1c inhibits methicillin-resistant Staphylococcus aureus by targeting the cell membrane with associated ribosomal perturbation.

Trichophyton (T.)tonsurans is an anthropophilic dermatophyte known as 'mat fungus' among wrestlers. Dermatomycoses caused by this pathogen have recently been diagnosed more frequently in Germany. Anew route of infection is the transmission of T.tonsurans in barbershops. In this article, the laboratory diagnostic detection of T.tonsurans is assessed. Skin and hair samples, preferably from Saxony, Saxony-Anhalt and Thuringia and from all over Germany, were analysed. The mycological detection of T.tonsurans from skin scales, hair roots and swabs were based on culture methods. From 2011, diagnostics were supplemented by polymerase chain reaction-enzyme linked immunosorbent assay (PCR-ELISA). Selected dermatophyte strains were identified by sequencing the internal transcribed spacer (ITS) region of the ribosomal DNA in order to differentiate them from morphologically similar dermatophytes, in particular T.quinckeanum, which has also increased in prevalence during the period under investigation. From 2022, real-time (RT)-PCR with melting curve analysis was also used. Multiple isolates from one patient were only statistically considered once. If there were more than 3months between two fungal detections, this was categorised as anew infection. For years, T.tonsurans was ararely diagnosed dermatophyte. Until 2014, amaximum of 12isolates were found per year. The detection rate rose to 20/year for the first time in 2015. Asignificant increase was observed from 2017 onwards. Asignificant increase was recorded from 2017 to 2019, with 38-71 cases of T.tonsurans annually. This was accompanied by asustained outbreak of dermatophytosis caused by T.tonsurans at the Leipzig wrestling club. From 2020, there was an even more significant increase in T.tonsurans. The detection figures rose from 101/year to 347 in 2023. The provisional peak was reached in 2024 with 538 T.tonsurans infections. The increase is continuing. Two to three times more boys and men are affected than girls and women. The average age of patients is15-20years. The antimycotic treatment of tinea capitis, tinea barbae and tinea faciei should almost always be combined topical and systemic (oral). The drug of choice for oral treatment is terbinafine, but itraconazole is also effective. Fluconazole can also be used successfully in individual cases, especially as apowder for oral suspension as an alternative to tablets or capsules.

Abstract San Francisco Bay, California, typically has chlorophyll a (chl- a ) concentrations below 10 µg L −1 , despite nutrient loadings exceeding those in many estuaries with recurring harmful algal blooms (HABs). However, in August 2022 there was a Heterosigma akashiwo (raphidophyte) bloom with chl- a concentrations exceeding 450 µg L −1 , resulting in widespread hypoxia and fish die-off. We used protist community (18S ribosomal ribonucleic acid gene metabarcoding) and environmental data collected 2–3 times per month from 2015–2023 to assess differences between 2022 and other years, and capture dynamics pre-, during, and post-bloom. The 2022 protist community clustered separately from other years in non-metric multidimensional scaling and hierarchical cluster analyses. A diatom bloom in June generated the highest median June chl- a concentration (15 µg L −1 ) recorded between 1977–2023 and drew down nutrients (nitrogen, silicate), leading to the establishment of a heterotrophic community in July with low dinoflagellate abundance (0.9% of protists versus 5.9% average in other years). The absence of dinoflagellates, potentially including H. akashiwo predators , plus suitable habitat (13–14 daylight hours, temperatures 17–21˚C, nitrate concentrations 17–24 µmol L −1 , neap tides) likely provided opportunity for H. akashiwo to proliferate from 0.03% to 48% of protists between July 20 and August 25. As the bloom collapsed, the genus Gyrodinium (dinoflagellate predator of H. akashiwo ) increased from 3.0% to 52% of protists between August 25 and August 31, likely exerting grazing pressure. Results show that antecedent protist community dynamics play important roles in shaping HABs, and interactions between biotic and abiotic factors govern the development of blooms.

This study aimed to characterize the effects of Prochristianella sp. infection (Cestoda: Trypanorhyncha) in the Octopus maya, with focus on tissue pathology, immune response, and potential implications for host health. Molecular analyses of 28S ribosomal DNA were performed to confirm the identity of collected parasites from the buccal mass of octopus hosts. Macro- and microscopic observations of O. maya tissues, hemocyte counts, and histological analyses were conducted to assess the damage caused by the infection. Comparisons were made between naturally infected octopuses from Río Lagartos, Yucatán (the affected group), and minimally infected octopuses from Campeche (the control group) to establish a reference baseline for health and tissue morphology. Prochristianella sp. 1 was the only parasitic species infecting the buccal mass of octopuses collected from Río Lagartos, contrasting with the absence of the parasite in octopuses from Campeche, which were used as a reference group to characterize the infection. The affected group exhibited an undescribed capsular structure on the superior mandibular muscle of the buccal mass, containing cestodes and mucus and associated with tissue alterations, such as fibrosis, hemocyte infiltration, and focal necrosis. These findings led to the provisional designation of this condition as "myocestodiasis in cephalopods." This work provides new findings on helminth-induced pathologies, generating hypotheses about the underlying mechanisms in infected cephalopods. The study highlights the importance of multidisciplinary approaches to understanding host-parasite interactions. Furthermore, it lays the groundwork for managing and conserving the O. maya, an important marine resource of the Yucatán Peninsula.

Endocrine-disrupting chemicals (EDCs) are pervasive environmental hazards that have been linked to osteoporosis (OP), though causal mechanisms remain elusive. Employing an integrated multiomics framework, this study combined bidirectional Mendelian randomization (MR), network toxicology, machine learning, molecular simulations, and ovariectomized rat models to elucidate causal relationships between EDCs and osteoporosis, and to identify the molecular underpinnings of these relationships. MR analyses leveraging European GWAS data identified methylparaben (MP; OR = 0.973, p < 0.001) and monomethyl phthalate (MMP; OR = 0.984, p = 0.006) as causal agents reducing bone mineral density (BMD), validated across two independent cohorts. Network toxicology revealed CYP3A4 as a shared target for both EDCs, with HSPA5-driven endoplasmic reticulum (ER) stress implicated in MP-induced bone loss and CRP-mediated inflammation central to MMP pathology. Molecular dynamics simulations confirmed stable binding of MP/MMP with hub targets. Crucially, ribosomal genes (RPL9/RPL37A/RPS19) altered by MP were mechanistically linked to ER stress-induced osteotoxicity rather than direct EDC binding. In vivo validation demonstrated that MP and MMP exposure in OVX rats significantly exacerbated trabecular degradation, suppressed osteogenic markers, and elevated osteoclastic activity. This work establishes CYP3A4 as a high-value therapeutic target for countering EDC-induced osteoporosis and resolves longstanding controversies regarding the osteotoxic mechanisms of parabens and phthalates.

The transcription of ribosomal genes (rDNA) and precursor rRNA (pre-rRNA) processing are crucial biological processes in ribosome biogenesis. Yet, the specific impact of ribosome biogenesis on the first lineage differentiation during early mouse embryonic development remains unclear. Nucleolar proteinLy-1 antibody reactive clone (LYAR) can accelerate ribosome production, regulating rDNA transcription and pre-rRNA maturation. Our study employed immunofluorescence and quantitative polymerase chain reaction (qPCR) to investigate the presence and localization of LYAR during early mouse embryonic development. The interference fragments and mRNA of LYAR were separately injected into embryos at the pronuclear stage, and the embryo development was statistically analysed. The impact of regulating LYAR expression on the first lineage differentiation was determined by immunofluorescence staining, At the 2-cell stage, regulatory fragments and RFP mRNA were injected into a single blastomere. By immunofluorescence staining to determine the proportion of blastomeres with regulated LYAR expression contributing to the ICM. The influence of interfering with LYAR expression at the pronuclear stage on the overall level of newly synthesised rRNA was detected by EU staining. Finally, qPCR was used to further determine the impact of regulating LYAR expression on rDNA transcription and pre-rRNA processing. The results demonstrate that LYAR is detectable at various stages of preimplantation development. Importantly, as embryonic development progresses, LYAR gradually translocates from the cytoplasm and nucleus into the nucleolus. Knockdown of LYAR during the pronuclear stage results in a reduction in the number of ICM following the first lineage differentiation of embryonic development. Furthermore, modulating the expression of LYAR in individual blastomeres at the 2-cell stage affects their contribution to the ICM, altering the proportion of cells that contribute to the blastocyst. Our study hints a link between ribosome biogenesis and the first lineage differentiation, contributing to a better understanding of the mechanisms underlying mouse embryonic development.

Aberrant ribosome biogenesis promotes gastric cancer (GC) progression and contributes to chemoresistance by sustaining protein synthesis, upon which GC cell survival depends. However, the regulatory role of cancer-testis-associated long noncoding RNAs (CT-lncRNAs) in modulating ribosome biogenesis in GC remains largely unexplored. First, we performed a screening of lncRNAs and identified CT-lncRNA LINC01940 on the basis of integrated expression and survival analyses using The Cancer Genome Atlas (TCGA) data. Subsequently, the impact of LINC01940 on GC progression and chemosensitivity was evaluated using in vitro cell functional assays, patient-derived organoid models, and in vivo subcutaneous tumor xenograft experiments. To further elucidate the underlying mechanisms, we employed a comprehensive approach combining bioinformatics analyses, RNA sequencing, fluorescence in situ hybridization, translation assays, ribosomal DNA (rDNA) transcription assays, methylated RNA immunoprecipitation, co-immunoprecipitation mass spectrometry, fluorescence multiplex immunohistochemistry, and RNA pull-down mass spectrometry. Normally, testis-specific LINC01940 is aberrantly upregulated in GC and associated with poor prognosis. Functional assays demonstrated that LINC01940 promotes GC cell proliferation and invasion and confers resistance to cisplatin. Mechanistically, LINC01940 is stabilized by methyltransferase 16 (METTL16)/ insulin-like growth factor 2 messenger RNA binding protein 3 (IGF2BP3)-mediated N6-methyladenosine (m6A) modification, which enhances its ability to act as a scaffold promoting the interaction between the small ubiquitin-like modifier 2 (SUMO2) E3 ligase TATA-box binding protein associated factor 15 (TAF15) and Nucleolar protein 11 (NOL11), promoting the SUMOylation of NOL11 and enhancing its protein stability. This, in turn, increases ribosomal DNA transcription and ribosome biogenesis, thereby promoting GC progression and chemoresistance. LINC01940 is a cancer-testis lncRNA that promotes GC progression and cisplatin resistance by enhancing ribosome biogenesis via the METTL16/IGF2BP3-TAF15-NOL11 axis. These findings suggest its potential as a prognostic biomarker and therapeutic target in GC.

The type III secretion system (T3SS) is a syringe-like machine that pathogenic bacteria use to inject effector proteins into host cells. Its ability to mediate targeted protein delivery has prompted efforts to adapt it for diverse biotechnological applications. However, the influence of bacterial host culture conditions on the performance of the T3SS-based circuits, which has never been systematically studied, is addressed in this study. In this study, we developed and characterized an IPTG-inducible, refactored T3SS circuit (iT3SS) in Salmonella enterica, in which the prgH gene, encoding a protein of the basal body complex, was fused to the coding sequence of GFP in order to monitor the expression of the secretion system. The engineered system was shown to secrete efficiently the effector protein SptP. The dynamics of expression of the PrgH-GFP fusion was assessed in rich LB medium and in glucose minimal medium under various IPTG concentrations. Interestingly, secretion efficiency was maintained across IPTG concentrations in cells grown in glucose minimal medium, but not in cells grown in rich LB medium. In cells grown in LB medium, secretion and invasion efficiencies did not increase proportionally with increasing IPTG concentrations. Both PrgH abundance and SptP secretion efficiency were lower at high IPTG concentration than at low and medium IPTG concentrations. Since RNA-seq analysis of cells grown in LB medium revealed that the transcription of iT3SS genes increased proportionally to inducer level, this indicated that transcription was not the limiting factor for iT3SS expression. This suggested that the limiting factor might be due to a translational and/or post-translational burden of iT3SS component mRNAs. Indeed, uneven (not stoichiometric) translation of the iT3SS components and/or their imperfect folding might impair their assembly and insertion in the membrane. Consequently, one cannot exclude that the iT3SS components not properly assembled or integrated are being degraded, giving the wrong impression of a low translation level. Interestingly, RNA-seq revealed that in LB cultures at high IPTG concentration, stress-response genes were up-regulated whereas ribosomal protein-coding genes were down-regulated. This feature might contribute to limiting iT3SS translation. Several hypotheses are proposed in the discussion to explain how culture conditions could influence the functionality of iT3SS. Our findings demonstrate that the nature of the growth medium has an impact on the performance of programmable secretion systems that might be due to host's resource-allocation strategy that would have a negative impact on the translational efficiency of the iT3SS components, compromising their correct assembly and thus their membrane insertion. This insight provides a medium-aware framework for optimizing engineered secretion platforms for synthetic biology applications.

Background: In wildlife, the identification of parasitic infections should be pursued seriously in countries facing endangered species of animals in their geographical territories. We aimed to increase understanding of the possible role of wildlife herbivore reservoirs in the emergence of helminth infections in Kermanshah Province, western Iran. Methods: Sixty-five feces from Gazelle (Gazella subgutturosa) (N = 36 samples) and wild goat (Capra aegagrus) (N = 14 samples) were investigated. The samples were microscopically examined for gastrointestinal helminth eggs, and genomic DNA was extracted from the identified eggs. The internal transcribed spacer 2 (ITS2) region of ribosomal DNA was amplified and sequenced. Phylogenetic analysis of the nucleotide sequences confirmed the species identity. Results: The most common species circulating in the hosts were Teladorsagia circumcincta, Marshallagia spp., and Nematodirus oiratianus, all of which are reported in the wildlife in western Iran for the first time. Conclusion: These findings emphasize the importance of continuously assessing the parasite status of wildlife and similar routine surveillance in domestic environments to detect and manage potential zoonotic parasite species.

The intestine plays a key role in the initiation of sepsis. The gut barrier impedes the translocation of commensal bacteria to the liver in sepsis. Previous studies have reported that angiotensin-(1-7) [Ang-(1-7)] attenuated sepsis-induced organ injury and mortality. However, its role in sepsis-induced intestinal barrier dysfunction remains unclear. Here we have investigated therapeutic effects of Ang-(1-7) on the intestinal barrier dysfunction and dysbiosis in a murine model of sepsis. We used a model of sepsis in C57BL/6 mice with caecal ligation and puncture (CLP), to assess mortality and histological and biochemical changes in the gut and liver tissues. Faecal microbiota transplantation (FMT) was used to assess the role of the gut microbiome. 16-s rDNA and metabolomics analyses were performed to characterize differences in the gut microbiome signatures and metabolic profiles. Plasma Ang-(1-7) was decreased in patients with sepsis. In CLP mice, exogenous Ang-(1-7) attenuated intestinal barrier dysfunction and liver damage. FMT experiments showed that the protective effects of Ang-(1-7) on the gut depended on the gut microbiota. Furthermore, 16-s ribosomal DNA analysis revealed that Ang-(1-7) treatment increased the abundance of Lactobacillus gasseri (L. gasseri) among commensal bacteria. Mechanistically, L. gasseri regulated the production of antimicrobial peptides in intestinal epithelia by activating NLRP6 inflammation. Ang-(1-7) protected against sepsis-induced intestine barrier dysfunction and liver injury in mice by modulating gut homeostasis and NLRP6 inflammasome. Ang-(1-7) is a promising candidate drug for protecting intestinal homeostasis in sepsis, offering new insights for clinical treatment.

SummaryPedigree analysis remains the gold standard for rare disease diagnostics, yet whole genome sequencing studies typically omit critical regions like centromeres, telomeres, and acrocentric chromosome p-arms. Here, we present telomere-to-telomere (T2T) reference genomes for four self-identified African American individuals of admixed ancestry spanning three generations. Our parent-of-origin assigned, chromosome-level assemblies revealed precise meiotic recombination breakpoints in previously inaccessible regions, including recombination events across acrocentric and subtelomeric sequences. Centromeric regions were highly stable, with multi-megabase arrays inherited intact across three generations, while the position of kinetochore assembly sites remained consistent and predominantly associated with the p-arm proximal region. The relative lengths of telomeres on individual chromosomes were maintained across generations. Using a targeted rDNA assembly approach, we reconstructed a complete megabase-scale ribosomal DNA (rDNA) array corresponding to the paternal chromosome 14. This openly available pedigree provides a benchmark dataset for studying recombination and genetic and epigenetic variation across the complete genome.

MYC-driven medulloblastoma (MB) is a highly aggressive brain tumor with poor prognosis and limited treatment options. Through CRISPR-Cas9 screening, we identify the Mediator-associated kinase CDK8 as a critical regulator of MYC-driven MB. Both genetic loss and pharmacological inhibition of CDK8 impair MB tumor growth. Moreover, we find that CDK8 cooperates with MYC to sustain the MYC-mediated translational program, as CDK8 depletion induces pronounced transcriptional changes in translation-associated gene sets, reduces ribosome biogenesis, and impairs protein synthesis. Mechanistically, CDK8 regulates the occupancy of RNA polymerase II at specific chromatin loci, facilitating epigenetic alterations that promote the transcription of ribosomal genes. Furthermore, combined inhibition of CDK8 and mTOR synergistically enhances therapeutic efficacy in vivo, leading to more pronounced tumor growth suppression. Overall, our findings establish a functional link between CDK8-mediated transcriptional regulation and mRNA translation, suggesting a promising therapeutic approach targeting protein synthesis for MYC-driven MB.

The potential of schistosomiasis to spread across borders, coupled with the considerable delay by which infected travellers and migrants are diagnosed in Europe, calls for better surveillance of the distribution of this disease. This study explored the geographical origin and genetic profiles of Schistosoma infections imported into Europe and diagnosed in a network of 11 European centres specialized in traveller and migrant health. Genetic profiles were obtained from DNA extracted from concentrated Schistosoma eggs or Schistosoma-positive samples (faeces, urine, biopsy) collected during routine diagnostic procedures. The species-specific cytochrome oxidase sub-unit 1 (cox1) diagnostic region and the standard complete internal transcribed spacer (ITS)1 + ITS2 (ITS1 + 2) ribosomal DNA region were amplified and sequenced, together with a partial region of 18S ribosomal DNA in selected cases. Prevalences of the different genetic profiles within the whole patient cohort and by country/geographical area of possible infection were analysed. A phylogenetic analysis was performed using the larger cox1 (~ 956base pairs) sequences dataset. A total of 94 samples were available for analysis, 36 from patients with a diagnosis of intestinal schistosomiasis and 58 with urinary schistosomiasis, all acquired in a sub-Saharan African country. Mitochondrial (mt) cox1, nuclear ITS1 + 2 and/or 18S (mt/nuclear) genotypes were successfully obtained from 51/94 (54%) samples; while for 43/94 (46%) samples, only a partial mt genotype was obtained. Infections with Schistosoma haematobium and Schistosoma mansoni were identified in the majority of cases (66/94; 70%), while mixed Schistosoma spp. genetic profiles, which were identified in 30% (28/94) of the samples, were almost exclusively (27/28; 96%) associated with cases of urinary schistosomiasis. Among the urinary infections, almost half (27/58; 47%) could be identified as having a mixed genetic profile. These mostly (26/28; 93%) included genetic traits of S. haematobium and Schistosoma bovis, and all were from patients probably infected in West Africa. Infections with S. haematobium and S. mansoni represent the majority of cases of schistosomiasis currently being diagnosed in Europe; however, mixed Schistosoma genetic profiles (mostly S. haematobium/S. bovis) were identified in at least 30% of samples. Our results call for a coordinated effort encompassing prompt diagnosis and treatment of Schistosoma infections, together with monitoring of the possible introduction of species of Schistosoma and establishment of their autochthonous transmission under suitable conditions in Europe.

ABSTRACT This study describes a novel parasitic fungus that infects the benthic and epiphytic dinoflagellate Ostreopsis cf. ovata during a coastal microalgal bloom in the Mediterranean Sea. Microscopic observations revealed a distinctive, irregularly shaped zoosporangium during the mature stages and spherical, posteriorly uniflagellate zoospores. This supports its affiliation within the phylum Chytridiomycota. Concatenated phylogenetic analysis based on 18S, 5.8S, and 28S ribosomal DNA placed the fungus within the order Lobulomycetales, thus establishing it as a distinct lineage separate from previously described species. Additional phylogenetic analyses including environmental DNA sequences revealed a close phylogenetic relationship with previously reported freshwater sequences. This suggests a possible ecological link between marine and freshwater habitats. Cross-infection experiments confirmed the ability of the fungus to infect healthy cells of both dinoflagellate and diatom species, rendering it the first known chytrid with a broad phytoplankton host range. Additionally, it is the first member of this order known to parasitize dinoflagellate species and only the second known to parasitize marine algae. Infection prevalence was higher in dinoflagellates than in diatoms. Furthermore, under laboratory conditions, the chytrid also developed zoosporangia on pollen grains, using them as an alternative nutrient source. Based on these findings, this study describes a new genus and species of zoosporic fungus, Algophthora mediterranea, within the order Lobulomycetales.

This study describes a new species of Sedum (Crassulaceae), Sedum qingyuanense sp. nov. discovered in Qingyuan City, Guangdong Province, China. Morphologically, S. qingyuanense resembles S. alfredii and S. emarginatum. The new species may have previously been misidentified as S. alfredii. However, the new species can be readily distinguished from S. alfredii by its creeping sterile stems, opposite leaves, emarginate leaf apices, and smaller sepals. Compared to S. emarginatum, it is differentiated by its creeping sterile stems, smaller sepals, and conspicuous pseudopetioles. Phylogenetic analysis based on the nuclear ribosomal DNA internal transcribed spacer (ITS) region revealed that the new species forms a sister clade to S. emarginatum within Sedum sect. Sedum, supported by moderate to strong bootstrap support (> 80%). Integrating both morphological evidence and the phylogenetic tree, we establish it as an independent lineage.