Biology subjects

Sahu, P.

Publications and source records attributed to Sahu, P..

16 recordsLinked to original sources

bioRxiv2026

Integrated miRNA-protein profiling of small extracellular vesicle cargo reveals dynamic cargo remodelling during tissue repair in UV-C-damaged C. elegans

Ultraviolet-C (UV-C) radiation is a potent environmental stressor that induces DNA damage, accumulation of reactive oxygen species (ROS), and cellular dysfunction. This also initiates coordinated molecular responses to regulate cellular adaptation and recovery. Small extracellular vesicles (sEVs) have emerged as key mediators of intercellular communication through the selective incorporation of microRNAs (miRNAs), proteins, and lipids. However, the temporal changes of sEV-associated cargo during the progression from UV-C-induced damage to recovery remain uncharacterized. We hypothesised that UV-C exposure induces stage-specific changes in sEV cargo (miRNA and proteins) that promote the transition of cells from damage to the response and recovery phases. To examine this, a time-resolved UV-C exposure model was established using Caenorhabditis elegans (C. elegans). In this paper, we studied 2.5 hours of UV-C exposure, including cellular damage, intracellular ROS levels, and DNA integrity, to define the damage and repair state. Based on these temporal variations, samples were collected: i) immediately after exposure, ii) 6 hours post-exposure, and iii) 16 hours post-exposure were designated as damage, response, and recovery conditions, respectively. sEVs isolated from whole-worm preparations were characterised using biophysical and molecular approaches, followed by miRNA sequencing and proteomic analyses. Integrative analysis further identified miRNA-protein associations and associated them with pathways involved in stress adaptation, metabolism, signal transduction, and cellular homeostasis. Collectively, these findings provide a temporal molecular framework of sEV cargo associated with UV-C-induced damage, response, and recovery in C. elegans. Overall, this study identified candidate molecular signatures and miRNA-protein associations that underlie the temporally selective packaging of sEV-associated cargo following UV-C-induced damage, providing a basis for future tissue-specific and mechanistic investigations.

molecular biology↗

bioRxiv2026

Sequence-Dependent DNA Base Selection Fidelity: A Kinetics-based Model and its validation

DNA replication achieves error rates as low as 10-9-10-11 per base pair through the combined contribution of base selection, exonuclease proofreading, and mismatch repair. Among those processes, base selection determines the initial level of accuracy and is strongly modulated by local sequence context. Existing models address this dependence either by fitting individual rate constants for each sequence context or by invoking the global template properties, neither of which derives sequence dependence from the underlying thermodynamics and kinetics of base pair formation. Here we present a mechanism for sequence-dependent base selection fidelity, built from two physical properties: nearest-neighbor stacking thermodynamics and directional kinetic asymmetry. The model fits the experimentally observed mutation spectra from three mismatch repair-deficient organisms well (r=0.74, 0.70, and 0.63), and predicts that base-selection accuracy varies non-monotonically with temperature in a sequence-dependent manner. Our model, therefore, provides a framework that connects sequence-dependent thermodynamic and kinetic effects during nucleotide incorporation to experimentally observed mutation rates.

biochemistry↗

bioRxiv2026

TAS2R10 Suppresses ABCG2 Transporter-Associated Chemoresistance and Enhances Cisplatin Sensitivity in Head and Neck Squamous Cell Carcinoma

Cisplatin resistance remains a major barrier in head and neck squamous cell carcinoma (HNSCC) treatment. ATP-binding cassette (ABC) transporters contribute to chemoresistance by limiting intracellular drug accumulation. Bitter taste receptor 10 (T2R10) has been implicated in ABC transporter regulation, but its role in HNSCC remains undefined. HNSCC cell lines were treated with T2R10-agonist caffeine (100 or 200 M), cisplatin, or a combination, and viability was assessed by crystal violet assay. T2R10 promoter activity and expression following caffeine exposure were evaluated using a promoter-driven mCherry reporter and RT-qPCR. ABC transporter expression was measured after caffeine treatment and T2R10 gene (TAS2R10) knockdown or overexpression. Associations between tumor TAS2R10 expression and survival were assessed using TCGA data through GEPIA2. Caffeine enhanced the cisplatin-associated reduction in viability in a cell line- and concentration-dependent manner, with the strongest effect seen in UM-SCC47. A significant effect was observed in FaDu at 200 M of caffeine, and minimal response in RPMI 2650. RPMI 2650 cells and FaDu cells exhibited lower baseline TAS2R10 expression and RPMI 2650 cells did not demonstrate enhanced cisplatin sensitivity following caffeine treatment. Caffeine treatment increased TAS2R10 promoter activity and expression and was associated with decreased ABCG2 expression. TAS2R10 knockdown increased ABCG2 and ABCF1 expression, whereas TAS2R10 overexpression reduced ABCG2 and ABCC1 expression. High tumor TAS2R10 expression was associated with improved disease-free survival (log-rank p=0.0071; HR=0.61) but not overall survival. Caffeine enhances cisplatin sensitivity in selected HNSCC models. Caffeine exposure is associated with increased TAS2R10 expression and reduced expression of chemoresistance-associated transporters, particularly ABCG2.

cancer biology↗

bioRxiv2026

Directional purine pyrimidine asymmetry in CRISPR repeats facilitates spacer acquisition

Spacer acquisition is the primary and essential step of CRISPR-Cas adaptive immunity in most prokaryotes and occurs preferentially at the leader-repeat junction of the CRISPR array. Despite the conservation of the adaptation machinery, spacer acquisition efficiencies and site-specificity vary markedly across CRISPR-Cas systems, suggesting that the local sequence architecture of the repeat and leader-repeat junction may contribute to the variation in the adaptation efficiency. To investigate this possibility, we systematically analyzed the direct repeat sequences and the terminal base pairs at the 3' end of leader regions adjacent to the integration site. We identify a conserved asymmetric purine-pyrimidine (RY) distribution within direct repeats, characterized by a 5' pyrimidine-rich half and a 3' purine-rich half, together with purine enrichment at the 3' end of leader sequences. Building on these observations, we develop a mechanistic model for spacer acquisition by demonstrating the importance of the sequence motif of the first direct repeat and the leader-repeat junction, using the sequence-dependent asymmetric cooperativity model that captures DNA unzipping kinetics. According to our model, sequences with such directional RY-asymmetric nucleotide distribution as direct repeats have high unzipping propensity and thus can promote efficient spacer integration. Consistent with this mechanism, experimental data from previous studies show that repeats with stronger asymmetry and appropriately positioned pyrimidine-to-purine transition sites are associated with larger spacer counts within CRISPR arrays. These findings reveal a conserved architectural feature of CRISPR repeats and provide a mechanistic model connecting DNA sequence organization to efficiency.

genomics↗

bioRxiv2026

Ineffectual Genomic Error Correction Under Environmental Perturbation Dynamically Regulates Mutational Supply and Robustness

Adaptive evolution depends on the supply of heritable variation, yet excessive mutation threatens viability by degrading essential molecular functions. Here, we show that this trade-off emerges naturally from the kinetic proofreading mechanism that controls replication fidelity. In our model, environmental shifts alter the optimal driving rate constant of proofreading enzymes, transiently elevating replication error rates and triggering rapid evolutionary change until a new fidelity optimum is reached. This produces alternating periods of stasis and rapid adaptation, consistent with punctuated equilibrium. We further show that coding-region length and population size jointly determine whether adaptation succeeds or mutational collapse occurs, reflecting the balance between mutation supply and error tolerance predicted by the drift-barrier principle. These results provide a molecular mechanistic basis for nearly neutral evolutionary dynamics and illustrate how genomic organization constrains long-term evolutionary resilience.

evolutionary biology↗

bioRxiv2026

Precursor-Dependent Routing of Aromatic Amino Acids Determines Lignin Structure in Grasses by Sensitivity-Enhanced Solid-State NMR

Lignin biosynthesis in grasses exhibits unique metabolic flexibility, yet the precursor-specific routing of carbon into lignin polymers remains poorly resolved in planta. Here, we combine 13C-isotope labeling with solid-state NMR under sensitivity-enhancement by dynamic nuclear polarization (DNP), to directly track phenylalanine- and tyrosine-derived carbon incorporation into the lignin polymer in Brachypodium distachyon. Precursor-specific 13C labeling reveals that phenylalanine is the dominant contributor to canonical guaiacyl and syringyl lignins, whereas tyrosine preferentially enriches hydroxyphenyl lignin and hydroxycinnamates, including ferulates characteristic of grass cell walls. Two-dimensional 13C-13C correlation NMR resolves distinct lignin moieties arising from each precursor. Disruption of p-coumarate 3-hydroxylase (C3H) selectively impairs phenylalanine-derived lignification, while tyrosine-derived lignin remains comparatively unchanged, maintaining polymer assembly through alternative metabolic routes. These findings show precursor-dependent control of lignin composition and reveal tyrosine-mediated lignification as a compensatory pathway in grasses. This work also establishes precursor-resolved solid-state NMR and DNP as a powerful framework for dissecting lignin biosynthesis and metabolic plasticity in plant cell walls. SIGNIFICANCE STATEMENTLignin is a complex plant polymer that strengthens cell walls but also limits the efficiency of biomass processing for agriculture and bioenergy. Grasses possess a unique lignin biosynthetic flexibility that is not well understood. By combining stable isotope labeling with solid-state NMR spectroscopy, we directly traced how the aromatic amino acids, phenylalanine and tyrosine, contribute differently to lignin formation in intact grass cell walls. We show that phenylalanine primarily builds conventional lignin structures, whereas tyrosine supplies alternative phenolic components and maintains lignin synthesis even when a key biosynthetic enzyme is disrupted. This metabolic flexibility helps explain the unique structural aspects of grass cell walls and identifies precursor-level control as a promising strategy for engineering lignin composition to improve biomass utilization.

plant biology↗

bioRxiv2025

Genome size and nucleotide skews as predictors of bacterial growth rate

Bacterial growth rates are constrained by genome replication, yet the role of replication kinetics in bacterial growth rates remains incompletely understood. Here, we examine if genome size, replichore organization, and nucleotide compositional asymmetry are reasonable predictors of bacterial doubling times. In free-living bacteria, both genome size and the length of the longest replichore are found to correlate positively with doubling time, pointing to an influence of replication dynamics on bacterial growth rates. Moreover, fast-growing bacteria are shown to exhibit stronger nucleotide compositional skew. Incorporating skew into the model substantially improves predictive accuracy, suggesting that compositional asymmetry in genomes may facilitate replication fork progression and thereby enhance growth rates. Based on these observations, we speculate that nucleotide skew may play a potential adaptive role in bacterial genome replication. To assess whether the observed association between genome architecture and growth rate reflects an evolutionary signature or a mechanistic link, we reconstructed ancestral states and found that the model fits ancestral traits more strongly, with predictive strength (R2) decreasing progressively along the evolutionary tree as successive speciations occur. We speculate that this association has been stronger early in bacterial evolution and became subsequently screened as organisms diversified and increased in ecological and physiological complexity.

genomics↗

bioRxiv2025

Cross-species analysis identifies genotype-driven vulnerabilities in lung adenocarcinoma

While three major genetic alteration subsets, characterized by mutations in STK11, KRAS, and EGFR, are seminal in driving tumorigenesis in LUAD, their distinct effects on tumor cells and the tumor microenvironment are not fully understood. Here, we map critical oncogenic subset-specific vulnerabilities by identifying conserved cell-type-specific reprogrammings between human and mouse LUAD. Through harmonized scRNA-seq analysis of 57 human and 18 mouse specimens, we unveil that genetic alterations impose genotype-specific immune imprints on the tumor microenvironment: KRAS is associated with a transitional immune state, whereas STK11 and EGFR mutations define discrete and contrasting immune phenotypes. We find that STK11-mutant tumors exhibit complement and interferon-rich immune microenvironments while EGFR-mutant tumors harbor a naive T cell-rich phenotype accompanied by a global HLA downregulation, stress-responsive alveolar macrophages marked by MARCO. In the epithelial compartments, cross-species analysis reveals metabolic dependencies, including OGDH in EGFR- and PDE4D in STK11-mutant cells. Statement of SignificanceThis study delineates oncogenotype-specific molecular and immune imprints in lung adenocarcinoma, revealing STK11-, KRAS-, and EGFR-mutated tumors as transcriptionally and immunologically discrete ecosystems. By mapping epithelial vulnerabilities alongside immune imprints, we unveil genotype-imposed dependencies that inform the rational development of precision therapies with direct translational relevance.

cancer biology↗

bioRxiv2025

Replication rate-information storage trade-off shapes genome architecture across domains

Genome size varies widely among organisms, from compact genomes of bacteria to vast and complex genomes of eukaryotes. In this study, we theoretically identify the evolutionary pressures that may have driven this divergence in genome size. We use a parameter-free model to study genome size evolution under selection pressure to minimize replication time and maximize information storage capacity. We substantiate this choice by demonstrating a correlation between replication time and genome size using literature data. We show that bacteria tend to reduce genome size, constrained by a single replication origin, while eukaryotes expand their genomes by incorporating multiple replication origins. We propose a connection between genome size and cellular energetics, suggesting that endosymbiotic organelles, mitochondria and chloroplasts, evolutionarily regulate the number of replication origins, thereby influencing genome size in eukaryotes. We substantiate this claim by showing a correlation between organelle count and genome size data. We argue that nucleotide skews, present in nearly all genomes studied, and are used to identify replication origins, directly influence DNA unzipping kinetics, and hence its replication time. This connection enables us to derive nearly universal observations, such as Chargaffs second parity rule and replichore symmetrization, as adaptive consequences. We argue that high skews lead to faster replication, and substantiate it by showing a correlation between skews and replication speed in bacteria. The model reproduces more evolutionary genomic observations, such as a general preference for deletions over insertions across domains, and elongation and high variance of genome size under reduced selection pressure for replication rate, an integral component of C-value paradox. We highlight the possibility of regulation of the firing of latent replication origins in response to cues from the extracellular environment, leading to the regulation of cell cycle rates in multicellular eukaryotes. Significance StatementUnderstanding the forces shaping genome architecture is a long-standing challenge in evolutionary biology. Our study demonstrates that the balance between replication speed, influenced by nucleotide skews, and information storage, constrained by cellular energetics, drives the divergence in genome size between bacteria and eukaryotes. By quantifying selection pressure as the ratio of replication time to genomic information storage capacity, we show that this pressure enforces adaptive constraints, giving rise to observed features such as symmetric replichores and Chargaffs second parity rule. These insights not only help us resolve an enduring evolutionary puzzle, but also offer a unified framework linking genome organization, cellular specialization, and even potential mechanisms underlying carcinogenesis.

genomics↗

bioRxiv2025

Non-enzymatic error correction in self-replicators without extraneous energy supply

Accurate propagation of sequence information in nucleic acids is central to the evolutionary dynamics of self-replicating systems. Modern biological systems achieve high fidelity using enzymes that actively correct errors through energy-driven mechanisms. However, such complex machinery was absent under prebiotic conditions. Here, we present a theoretical model of error correction in self-replicating heteropolymers that requires neither enzymes nor an extraneous energy supply. The model relies solely on the free-energy gradient driving strand growth and requires asymmetric cooperativity -- a kinetic asymmetry known to promote unidirectional elongation. Despite its simplicity, we demonstrate that this minimal model facilitates kinetic discrimination between correct and incorrect base pair incorporations, and for specific set of parameters, reproduces the error ratio of [~] 10-4, experimentally observed in passive base selection processes. It replicates key features observed in DNA error correction, including stalling, fraying, next-nucleotide effects, and the speed-accuracy trade-off. Our results provide plausible answers for longstanding questions, such as the energy source for the enhanced base selectivity of passive DNA polymerases and the role of thermodynamics and kinetics of phosphodiester bond formation in error correction. We show that catalysis of the phosphodiester bond plays a central role in error correction, even without explicit enzymatic structural discrimination. This observation points to a plausible pathway for accurate oligomer synthesis under prebiotic conditions, driven solely by the thermodynamic gradient favoring strand elongation. More broadly, the model highlights how persistent molecular order can emerge from non-equilibrium dynamics - a central requirement for emergence of life.

biochemistry↗

bioRxiv2025

Eukaryotes evade information storage-replication rate trade-off with endosymbiont assistance leading to larger genomes

Genome length varies widely among organisms, from compact genomes of prokaryotes to vast and complex genomes of eukaryotes. In this study, we theoretically identify the evolutionary pressures that may have driven this divergence in genome length. We use a parameter-free model to study genome length evolution under selection pressure to minimize replication time and maximize information storage capacity. We show that prokaryotes tend to reduce genome length, constrained by a single replication origin, while eukaryotes expand their genomes by incorporating multiple replication origins. We propose a connection between genome length and cellular energetics, suggesting that endosymbiotic organelles, mitochondria and chloroplasts, evolutionarily regulate the number of replication origins, thereby influencing genome length in eukaryotes. We show that the above two selection pressures also lead to strict equalization of the number of purines and their corresponding base-pairing pyrimidines within a single DNA strand, known as Chagraffs second parity rule, a hitherto unexplained observation in genomes of nearly all known species. This arises from the symmetrization of replichore length, another observation that has been shown to hold across species, which our model reproduces. The model also reproduces other experimentally observed phenomena, such as a general preference for deletions over insertions, and elongation and high variance of genome lengths under reduced selection pressure for replication rate, termed the C-value paradox. We highlight the possibility of regulation of the firing of latent replication origins in response to cues from the extracellular environment leading to the regulation of cell cycle rates in multicellular eukaryotes. Significance StatementUnderstanding the forces shaping genome architecture is a long-standing challenge in evolutionary biology. Our study demonstrates that the balance between replication speed and information storage, constrained by cellular en-ergetics, drives the divergence in genome lengths between prokaryotes and eukaryotes. By quantifying selection pressure as the ratio of replication time to genomic information content, we show that this pressure enforces adaptive constraints, giving rise to features such as symmetric replichores and Chargaffs second parity rule. These insights not only help us resolve an enduring evolutionary puzzle, but also offer a unified framework linking genome organization, cellular specialization, and even potential mechanisms underlying carcinogenesis.

evolutionary biology↗

bioRxiv2025

Rapid High-Resolution Analysis of Polysaccharide-Lignin Interactions via Proton-Detected Solid-State NMR with Application to Eucalyptus and Spruce

The plant secondary cell wall, a complex matrix composed of cellulose, hemicellulose, and lignin, is crucial for the mechanical strength and water-proofing properties of plant tissues, and serves as a primary source of biomass for biorenewable energy and biomaterials. Structural analysis of these polymers and their interactions within the secondary cell wall has been heavily relying on 13C-based solid-state NMR techniques. In this study, we explore the application of 1H-detected solid-state NMR techniques for rapid, high-resolution structural characterization of polysaccharides and lignin, demonstrated on the stems of hardwood eucalyptus and softwood spruce. We employed several strategies, including the use of synthesized 2D spectra to resolve central 1H resonances and the combined application of 3D hCCH and hCHH experiments for complete resonance assignment and unambiguous identification of lignin-carbohydrate interactions. Our findings emphasize the central role of acetylated three-fold xylan conformers, rather than two-fold, in stabilizing the carbohydrate-lignin interface, with glucuronic acid sidechains in eucalyptus glucuronoxylan colocalizing with lignin, revised cellulose-lignin interactions involving uncoated microfibril surfaces, and pectin-lignin interactions indicative of early-stage lignification. We also carefully evaluated the interference from tannins in softwood species. These results present a novel approach for rapid structural analysis of lignocellulosic biomaterials without the need for solubilization or extraction.

biophysics↗

bioRxiv2024

Biomechanics of stem cell fate decisions in multilayered tissues

Tissue homeostasis relies on a precise balance of fate choices between renewal and differentiation, which is dysregulated during tumor initiation. Although much progress has been done over recent years to characterize the dynamics of cellular fate choices at the single cell level, their underlying mechanistic basis often remains unclear. In particular, although physical forces are increasingly characterized as regulators of cell behaviors, a unifying description of how global tissue mechanics interplays with local cellular fate choices is missing. Concentrating on skin epidermis as a paradigm for multilayered tissues with complex fate choices, we develop a 3D vertex-based model with proliferation restrained in the basal layer, showing that mechanics and competition for space naturally gives rise to homeostasis and neutral drift dynamics that are seen experimentally. We then explore the effect of introducing mechanical inhomogeneities, whereby subpopulations have differential tensions. We uncover that relatively small mechanical disparities can be sufficient to heavily tilt cellular towards symmetric renewal and exponential growth. Importantly, the simulations predict that such mechanical inhomogeneities are reflected by distinct morphological changes in single-cell shapes. This led us to derive a master relationship between two very different experimentally measurable parameters, cell shape and long-term clonal dynamics, which we validated using a model of basal cell carcinoma (BCC) consisting in clonal Smoothened overexpression in mouse tail epidermis. Altogether, we propose a theoretical framework to link mechanical forces, quantitative cellular morphologies and cellular fate outcomes in complex tissues.

biophysics↗

bioRxiv2023

Identification of post-transcriptional modifications in nucleic acid sequences using propose-designed molecular beacons

Post-transcriptional RNA modifications (PTxMs) present in small RNA species, specifically circulating extracellular RNAs, were recently identified as clinically relevant readouts, often more indicative of disease severity than the classical "up and down" changes in their copy number alone. While identification of PTxMs requires multiple and complex sample preparation steps, microgram-range amounts of RNA, followed by expensive and protracted bioinformatics analyses, the clinically relevant information is usually a yes/no for a particular genetic variant(s), and an up/down answer for relevant biomarkers. We have previously shown that molecular beacons (MBs) can identify specific nucleic acid sequences with picomolar sensitivity and single nucleotide specificity by exploiting the target-dependent change in their electrophoretic mobility profile. We now present a method for direct identification of miRNAs and isomiRs in cells and extracellular vesicles using gel electrophoresis, without the need for RNA isolation and purification. The detection is based on discreet changes in the hydrodynamic surface profile, the overall size, charge and charge distribution of the MB-target hybrid. Furthermore, using an RNA tertiary structure prediction algorithm (iFoldRNA) and a custom molecular dynamics simulation (DMD), we designed modified MBs specific for m6A-modified nucleotides in target RNA sequences. The sample preparation method coupled to the software package affords the design of specific MBs and sensitive, multiplex-type detection of targets in a wide variety of biofluids and cells, in a simple mix and read approach.

molecular biology↗

bioRxiv2022

Prioritization of driver genes in cancer-associated copy number alterations identifies B4GALT5 as a glycooncogene

Cancer is a disease resulting from aberrant communication between cells of a multicellular organism. The glycan coat that surrounds the cells is an important player in cellular communication. While altered cell surface glycans are known biomarkers for cancer, glycan biosynthesis itself has not been considered a potential oncogenic pathway. So, to understand the oncogenic potential of the glycan biosynthetic pathways we have analyzed the copy number alterations (CNA) of genes encoding for glycosylation regulators (glycogenes) in cancer genome datasets and identify novel glyco-oncogenes and glyco-tumor suppressor genes (TSGs). CNA of oncogenes and TSGs is an important cancer-associated genetic alteration that associates with worst prognosis. Nevertheless, identity of the driver genes in the copy number altered segments of the genome remains obscure in most cases. We developed a prioritization pipeline based on bioinformatic and experimental criteria to identify putative driver genes. In addition to correctly identifying several well-established oncogenes/TSGs, this pipeline discerns several novel oncogenes and TSGs, some of which are glycogenes. Further, among glyco-oncogenes there is an enrichment for glycosphingolipid biosynthetic pathway and trans-Golgi associated lysosomal sorting machinery and among glyco-TSGs there is an enrichment for early N-glycan biosynthetic enzymes. As a proof-of-principle we show that one of the identified glycooncogene B4GALT5, encoding a key enzyme in the glycosphingolipid pathway exhibits oncogenic property of promoting increased growth of hepatocellular carcinoma cells. Thus, this study identifies glycosylation pathways with oncoregulatory properties and opens up a new group of enzymes as potential therapeutic targets for cancer.

cancer biology↗

bioRxiv2019

Retrograde Transport of Golgi Enzymes by GOLPH3 Across Maturing Cisternae Regulates Glycan Assembly on Sphingolipids and CellGrowth

Glycans are ubiquitous sugar polymers with major biological functions that are assembled by glyco-enzymes onto cargo molecules during their transport through the Golgi complex. How the Golgi determines glycan assembly is poorly understood. By relying on the Golgi cisternal maturation model and using the glyco-enzyme adaptor and oncoprotein GOLPH3 as a molecular tool, we define the first example of how the Golgi controls glycosylation and associated cell functions. GOLPH3, acting as a component of the cisternal maturation mechanism, selectively binds and recycles a subset of glyco-enzymes of the glycosphingolipid synthetic pathway, hinders their escape to the lysosomes and hence increases their levels through a novel lysosomal degradation-regulated mechanism. This enhances the production of specific growth-inducing glycosphingolipids and reprograms the glycosphingolipid pathway to potentiate mitogenic signaling and cell proliferation. These findings unravel unforeseen organizing principles of Golgi-dependent glycosylation and delineate a paradigm for glycan assembly by the Golgi transport mechanisms. Moreover, they indicate a new role of cisternal maturation as a regulator of glycosylation, and outline a novel mechanism of action for GOLPH3-induced proliferation.

cell biology↗