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Tudela, J.

Publications and source records attributed to Tudela, J..

3 recordsLinked to original sources

eRREMS expands regulatory CpG coverage in reduced representation methylome sequencing

Profiling the regulatory DNA methylation landscape remains technically challenging. Reduced-representation bisulfite sequencing (RRBS) misses distal enhancers and non-canonical regulatory elements, while whole-genome bisulfite sequencing (WGBS) distributes reads genome-wide, limiting consistent recovery of informative CpGs across sample collections. Here we present eRREMS (enhanced Reduced Representation Enzymatic Methylation Sequencing), addressing both limitations by combining MspI and HaeIII digestion with enzymatic cytosine conversion. eRREMS approximately doubles regulatory CpG recovery relative to standard RRBS, outperforming TaqI-based extended protocols, with gains concentrated in dynamically regulated enhancers, alternative promoters, and splicing-associated regions. HaeIII-specific CpGs capture additional complex trait heritability beyond standard RRBS. At modest, comparable sequencing depths, eRREMS achieves greater cohort-level completeness for regulatory and dynamically variable CpGs than WGBS and requires substantially fewer reads. CpG capture is stable across enzymatic conversion kits and library preparation conditions, supporting broad adoption. eRREMS provides a cost-efficient and reproducible strategy for scalable methylome profiling of regulatory CpGs across cohorts.

genomics↗

Kaposi Sarcoma Herpes Virus Reprograms Mesenchymal Cell Glycosylation to control platelet-derived growth factor receptor A signaling

Kaposi sarcoma-associated herpesvirus (KSHV) reprograms host cellular pathways to promote viral persistence and tumor development by supporting the survival and expansion of infected and bystander cells. Among the signaling axes implicated in this process, oncogenic activation of receptor tyrosine kinases, particularly platelet-derived growth factor receptor alpha (PDGFRA), is a well-established hallmark of Kaposi sarcoma pathogenesis. However, the impact of virus-driven cell surface glycosylation changes in PDGFRA-associated signaling remains uncertain. Here, we identified a critical role for KSHV in reshaping the glycosylation landscape of mesenchymal stromal cells (MSCs), thereby reprogramming PDGFRA signaling. We show that KSHV infection enhances a unique glycan profile in human and mouse MSCs, enriched in branched complex N-glycans with limited (2-6) sialylation, Transcriptomic analyses of KSHV-infected MSCs and Kaposis Sarcoma patient samples revealed a coordinated dysregulation of pathways involved in carbohydrate metabolism, nucleotide-sugar transport, and sialic acid turnover, with a particular focus on sialic acid turnover (NPL/NEU3), the UDP-N-acetylglucosamine transporters SLC35A3/B4, and complex N-glycan elongation (MGAT5/B3GNT2/B4GALT1) as critical nodes underlying reduced (2-6) sialylation and increased N-glycan branching. This remodeled glycan landscape contributes to create a permissive context for galectin-1 (Gal-1) binding, which in turn enhances PDGFRA activation and downstream signaling. These findings identify an integral component of KSHV-driven mesenchymal cell reprogramming, unveiling a lectin-dependent mechanism of RTK activation in Kaposi sarcoma pathogenesis.

Cancer Biology↗

The transcriptional landscape of metastatic hormone-naive prostate cancer

Metastatic hormone-naive prostate cancer (mHNPC) is an infrequent form of this tumour type that is characterized by metastasis at the time of diagnosis and accounts for 50% of prostate cancer-related deaths. Despite the extensive characterization of localized and metastatic castration resistant prostate cancer (mCRPC), the molecular characteristics of mHNPC remain largely unexplored. Here we provide the first extensive transcriptomics characterization of mHNPC. We generated discovery and validation bulk and single-cell RNA-Seq datasets and performed integrative computational analysis in combination with experimental studies. Our results provide unprecedented evidence of the distinctive transcriptional profile of mHNPC and identify stroma remodelling as a predominant feature of these tumours. Importantly, we discover a central role for the transcription factor SOX11 in triggering a heterotypic communication that is associated to the acquisition of metastatic properties. Our study will constitute an invaluable resource for a profound understanding of mHNPC that can influence patient management.

cancer biology↗