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bioRxiv2018

Effects of P16 DNA Methylation on Proliferation, Senescence, and Lifespan of Human Fibroblasts

The aim is to study the effects of P16 DNA methylation on lifespan of normal cells. An expression-controllable pTRIPZ vector expressing P26-specific zinc finger binding protein-based methyltransferase (P16-Dnmt) was used to induce P16 methylation in primary CCD-I8C0 fibroblasts via stable transfection. Long-term dynamic IncuCyte analysis showed that CCD-I8C0 fibroblasts expressing baseline P16-Dnmt continued proliferating until passage-26 in the 53th post-transfection week, while vector control cells stopped proliferating at passage-6 and completely died 2 weeks later. The proliferation rate of baseline P16-Dnmt cells was significantly higher than that of vector control cells. The proportion of P-galactosidase-positive staining cells was significantly decreased in baseline P16-Dnmt cells compared to vector control cells. The P16 expression was lost in baseline P16-Dnmt cells at and after passage-6. The average telomere length in baseline P16-Dnmt cells also gradually decreased. In conclusion, P16 methylation could prevent senescence, promote proliferation, and expand lifespan of human fibroblasts, which may play a role in cancer development.\n\nSummaryA zinc finger protein-based DNA methyltransferase (P16-Dnmt) expressed at the baseline level could specifically methylate P16 promoter CpG islands. P16 methylation induced by baseline P16-Dnmt could significantly prevent senescence, promote proliferation, and expand lifespan of primary human fibroblasts.

cell biology↗
bioRxiv2018

ECM deposition is driven by caveolin1-dependent regulation of exosomal biogenesis and cargo sorting

The composition and physical properties of the extracellular matrix (ECM) critically influence tumour cell behaviour, and ECM deposition and remodelling by stromal fibroblast populations is therefore pivotal for tumour progression. The molecular mechanisms by which stromal and tumour cell populations regulate ECM layering are poorly understood. Tumour-stroma interaction is critically dependent on cell-cell communication mediated by exosomes, small vesicles secreted by most cell types and generated within multivesicular bodies (MVBs). Here, we show that caveolin-1 (Cav1), an essential regulator of stromal remodelling and tumour cell fate, plays a central role in modulating both exosome biogenesis and exosomal protein cargo sorting through cholesterol-dependent mechanisms. Quantitative proteomics profiling revealed that a major share of Cav1-dependent exosomal cargoes are compsed of ECM proteins, one of the most important components being tenascin-C (TnC). Comparative functional assays demonstrated that Cav1 is required for fibroblast-derived exosomes to depose ECM and promote tumour cell invasiveness. Exosomes purified from Cav1WT cells, but not those from Cav1-null cells, were able to nucleate distant stromal niches in different organs in vivo. These findings suggest a key role for Cav1 as a cholesterol rheostat in MVBs, and seems to determine ECM deposition by eliciting ECM component sorting into specific exosome pools. These results, together with previous work, support a model in which Cav1 is a central regulatory hub for tumour-stroma interactions through a novel exosome-dependent ECM deposition mechanism.

cell biology↗
bioRxiv2018

β-actin mRNA interactome mapping by proximity biotinylation

The molecular function and fate of mRNAs are controlled by RNA binding proteins (RBPs). However, identification of the interacting proteome of a specific mRNA in vivo is still very challenging. Based on the widely-used RNA tagging with MS2 aptamers for RNA visualization, we developed a novel RNA proximity biotinylation (RNA-BioID) method by tethering biotin ligase (BirA*) via MS2 coat protein (MCP) at the 3UTR of endogenously MS2 tagged {beta}-actin mRNA in mouse embryonic fibroblasts (MEFs). We demonstrate the dynamics of the {beta}-actin mRNA interactome by characterizing its changes upon serum-induced localization of the mRNA. Apart from the previously known interactors, we identified over 60 additional {beta}-actin associated RBPs by RNA-BioID, among them the KH-domain containing protein FUBP3/MARTA2 has shown to be required for {beta}-actin mRNA localization. This protein binds to the 3-untranslated region of {beta}-actin mRNA, is essential for {beta}-actin mRNA localization but does not interact with the characterized {beta}-actin zipcode element. RNA-BioID provides a tool to identify new mRNA interactors and to study the dynamic view of the interacting proteome of endogenous mRNAs in space and time.

cell biology↗
bioRxiv2018

Icariin induces MC3T3-E1 cell proliferation and differentiation via the BMP-2/Smads/Runx2 signal pathway

Icariin, the main active ingredient of Epimedium, has played an important role in bone anabolism. However, the molecular mechanism for this effect was not convincingly reported yet. In this paper, the role of icariin on cell morphology, viability, cell cycling and the activity of alkaline phosphatase (ALP) were studied, and the molecular mechanism of icariin induced osteogenic effect was also investigated. Icariin with different concentrations (10, 20 and 40 ng/ml) was used to modify the pre-osteoblastic MC3T3-E1 cells for 48, 72 and 96 h, and the proliferation, morphology, and the cell cycle of the cells were evaluated by Cell Counting Kit-8 (CCK-8), microscopy and flow cytometry, respectively. Bone morphogenic protein-2 (BMP-2), bone morphogenic protein receptor-2 (BMPR-2), Smad4, Smadl/5/8 proteins expression levels were obtained by Western blotting and the expression levels of runt-related transcription factor 2 (Runx2) mRNA was examined by reverse transcription-polymerase chain reaction (RT-PCR). In this study, we found that icariin could promote the proliferation and differentiation of MC3T3-E1 cells in a dose - and time-dependent manner. Icariin could stimulate the expression of the BMP-2, BMPR-2, Smad4 and Smadl/5/8 proteins. Furthermore, icariin could upregulate the expression of Runx2 mRNA. These results showed that icariin played an important role in upregulating BMP-2 expression to activate the BMP-2/Smads/Runx2 signal pathway for increasing both the proliferation and differentiation of the MC3T3-E1 cells. However, the osteogenic effects of icariin can be suppressed by the BMP-2 antagonist (Noggin). In conclusion, we demonstrate that icariin is an osteoinductive factor that exerts its osteogenic effect by regulating the BMP-2/Smads/Runx2 signal pathway in MC3T3-E1 cells.

cell biology↗
bioRxiv2018

Yes-associated protein (YAP) is required in maintaining normal ovarian follicle development and function

Yes-associated protein (YAP) is one of the major components of the Hippo signaling pathway, also known as the Salvador/Warts/Hippo (SWH) pathway. Although the exact extracellular signal that controls the Hippo pathway is currently unknown, increasing evidence supports a critical role of the Hippo pathway in embryonic development, regulation of organ size, and carcinogenesis. The ovary is one of few adult tissues that exhibit cyclical changes. Ovarian follicles, the basic units of ovary, are composed of a single oocyte surrounded by expanding layers of granulosa and theca cells. Granulosa cells (GCs) produce sex steroids and growth factors, which facilitate the development of the follicle and maturation of the oocyte. It has been reported that YAP is highly expressed in human GC tumors, but the role of YAP in normal ovarian follicle development is largely unknown. In current study, we examined YAP expression in bovine ovaries. We demonstrate that downstream hippo signaling effector protein, YAP and transcription co-activator, TAZ, are present and localization of both YAP and TAZ are density-dependent. Likewise, YAP and TAZ are critically involved in granulosa cell proliferation. Furthermore, reducing YAP in granulosa cells inhibits FSH-induced aromatase expression and estradiol biosynthesis. The data suggest that YAP plays an important role in the development of ovarian follicles and estradiol synthesis, which are necessary for maintaining normal ovarian function.

cell biology↗
bioRxiv2018

TANGO1 and SEC12 are co-packaged with procollagen I to facilitate the generation of large COPII carriers

Large COPII-coated vesicles serve to convey the large cargo procollagen I (PC1) from the endoplasmic reticulum (ER). The link between large cargo in the lumen of the ER and modulation of the COPII machinery remains unresolved. TANGO1 is required for procollagen (PC) secretion and interacts with PC and COPII on opposite sides of the ER membrane, but evidence suggests that TANGO1 is retained in the ER, and not included in normal size (<100nm) COPII vesicles. Here we show that TANGO1 is exported out of the ER in large COPII-coated PC1 carriers, and retrieved back to the ER by the retrograde coat, COPI, mediated by the C-terminal RDEL retrieval sequence of HSP47. TANGO1 is known to target the COPII initiation factor SEC12 to ER exit sites through an interacting protein, cTAGE5. SEC12 is important for the growth of COPII vesicles, but it is not sorted into small budded vesicles. We found both cTAGE5 and SEC12 were exported with TANGO1 in large COPII carriers. In contrast to its exclusion from small transport vesicles, SEC12 was particularly enriched around ER membranes and large COPII carriers that contained PC1. We constructed a split GFP system to recapitulate the targeting of SEC12 to PC1 via the luminal domain of TANGO1. The minimal targeting system enriched SEC12 around PC1 and generated large PC1 carriers. We conclude that TANGO1, cTAGE5, and SEC12 are co-packed with PC1 into COPII carriers to increase the size of COPII thus ensuring the capture of large cargo.

cell biology↗
bioRxiv2018

DNA replication-mediated error correction of ectopic CENP-A deposition maintains centromere identity

Chromatin assembled with the histone H3 variant CENP-A is the heritable epigenetic determinant of human centromere identity. Using genome-wide mapping and reference models for 23 human centromeres, CENP-A is shown in early G1 to be assembled into nucleosomes within megabase, repetitive -satellite DNAs at each centromere and onto 11,390 transcriptionally active sites on the chromosome arms. Here we identify that DNA replication acts as an error correction mechanism to sustain centromere identity through the removal of the sites of CENP-A loading on the chromosome arms, while maintaining centromere-bound CENP-A with the same DNA sequence preferences as in its initial loading.

cell biology↗
bioRxiv2026

Proteolytic Remodeling of Cargo Receptor Networks by RHBDL4 Tunes Secretory Pathway Flux

Cargo receptors are central organizers of the secretory pathway, yet the mechanisms controlling their abundance remain poorly understood. The endoplasmic reticulum (ER)-resident intramembrane protease RHBDL4 promotes substrate turnover via a non-canonical branch of ER-associated degradation and has recently been implicated in regulating secretory pathway components. We previously identified the p24 cargo receptor TMED7 as an RHBDL4 substrate, suggesting that cargo receptor turnover contributes to secretory pathway regulation. Here, quantitative proteomics identify members of the ER-Golgi intermediate compartment (ERGIC) cargo receptor family as endogenous RHBDL4 substrates, demonstrating that RHBDL4 targets multiple cargo receptor families within the early secretory pathway. Accordingly, RHBDL4 modulates multiple ERGIC-dependent transport pathways. In addition, unbiased secretome analysis reveals increased secretion of lysosomal precursor proteins upon RHBDL4 ablation. Mechanistically, we show that this phenotype is mediated, at least in part, by RHBDL4-dependent cleavage of the lysosomal cargo receptor sortilin/SORT1. Together, these findings identify cargo receptors as a major class of RHBDL4 substrates and establish proteolytic remodeling of cargo receptor networks as a mechanism for regulating secretory pathway flux.

cell biology↗
bioRxiv2026

Red and blue light cues drive contrasting remodeling of lipophilic metabolites and photophysiology in natural benthic diatom biofilms

Intertidal mudflats are low hydrodynamic energy environments hosting microphytobenthic communities that experience strong spatiotemporal variability in light regimes, including changes in spectral quality and light intensity that can lead to cellular photooxidative stress. To cope with these fluctuations, autotrophs exhibit diverse and highly plastic adaptations that are often species-dependent and shaped by their ecological niches. This study investigates photophysiological responses and metabolic remodeling in a diatom assemblage originating from a natural winter microphytobenthic biofilm under contrasting red and blue light intensities. To this end, photosynthetic parameters were monitored alongside changes in lipophilic metabolites, including untargeted lipids and lipophilic pigments. While few metabolites showed temporal remodeling, rapid and contrasting changes were observed within 30 minutes in response to both spectral quality and light intensity. Red light treatments induced broader remodeling of lipophilic metabolites than blue light, whereas blue light appeared to have a greater impact on photosynthetic parameters. Moreover, red light induced xanthophyll-cycle responses comparable to those observed under blue light at equivalent incident intensity. We discuss these metabolic responses in relation to diatom photoadaptive strategies, placing these findings within the intertidal environmental framework. This work further underlines the importance of understanding rapid metabolic plasticity in coping with light fluctuations, providing new insights into the photoregulatory strategies of natural microphytobenthic communities.

cell biology↗
bioRxiv2026

GDF15 contributes to inflammasome-associated excessive mechanoresponses of hyperlipidemic PdL fibroblasts

Orthodontic tooth movement relies on a tightly regulated pro-inflammatory and pro resorptive mechanoresponse of local periodontal ligament fibroblasts (PdLFs). Dysregulation is linked to complications such as root resorption and tooth loss. Hyperlipidemic conditions promote excessive PdL mechanoresponses, with growth differentiation factor 15 (GDF15) acting as potential regulator. This study examined the contribution of the inflammasome/pyroptosis pathway as underlying mechanism for dysregulated mechanoresponses. Human PdLFs were treated with palmitic acid (PA) or oleic acid (OA) for six days before 24 hours of compressive loading. PA increased CASP1, CASP4, and CASP3 activity, secretion of IL-1{beta}, IL-18, and HMGB1, and LDH release. Pharmacological blockade and siRNA-mediated knockdown of inflammasome- and pyroptosis-related targets revealed that NLRP3, CASP1, CASP4, and GSDMD partially contributed to monocyte and osteoclast overactivation. Silencing PA-increased GDF15, partially normalized the phenotype, at least in part by inflammasome/pyroptosis regulation. GDF15 acted through extracellular, and a nuclear signaling route, each accounting partially to this phenotype. Together, GDF15 partially regulates the PA-induced, pyroptosis-associated overactivated mechanoresponse alongside pyroptosis-independent mechanisms suggesting it as an interesting target for potential clinical interventions.

cell biology↗
bioRxiv2026

POU2AF2/OCA-T1 coactivates POU2F2 and defines a lineage-specific dependency in diffuse large B-cell lymphoma

Lineage-restricted transcriptional programs establish cell identity and can create selective dependencies in cancer. Here, we identify POU2AF2, encoding the transcriptional co-activator OCA-T1, as a critical lineage-specific dependency in a subset of diffuse large B-cell lymphoma (DLBCL). Pan-cancer dependency analyses and patient cohorts reveal elevated POU2AF2 expression in genetically aggressive DLBCL, where its depletion markedly suppresses tumor growth in vitro and in vivo. Mechanistically, POU2AF2 cooperates with the B-cell lineage-defining transcription factor POU2F2 (OCT2) to activate lymphocyte activation gene programs through direct chromatin engagement, thereby sustaining malignant transcriptional networks. We further identified a key epigenetic regulatory axis composed of the lineage-specific transcription factor TCF3 and the histone methyltransferase SET1A-COMPASS that drives POU2AF2 expression downstream of B-cell receptor signaling. Single-cell transcriptomic analysis reveals that POU2AF2 marks and sustains an innate-like B1 B-cell population in vivo, a candidate cell of origin for lymphoma. Together, these findings define a lineage-restricted POU2AF2/POU2F2 transcriptional module, controlled by a TCF3/SET1A epigenetic network, that sustains both innate-like B-cell identity and malignant fitness in DLBCL. Our study uncovers a previously unrecognized lineage-specific transcriptional dependency and highlights POU2AF2 and its associated regulatory circuitry as potential therapeutic targets in aggressive B-cell malignancies.

cell biology↗
bioRxiv2026

Glutaminase contributes to MYC-induced cell-autonomous autophagy and to RasV12-dependent non-autonomous autophagy in the Drosophila wing disc epithelium

MYC-driven metabolic reprogramming supports rapid cell growth but also creates metabolic demands that require adaptive mechanisms to maintain cellular homeostasis. Here, combining clonal analysis in Drosophila wing imaginal discs with studies in Schneider S2 cells, we identify glutamine metabolism as a component of Myc-induced autophagy. Myc increased the expression of genes involved in glutamine utilization, including glutaminase (GLS), and enhanced ammonia production, a metabolic by-product of glutaminolysis. Genetic depletion of GLS in clones suppressed the accumulation of Myc-induced Atg8a-positive structures and reduced autophagic flux, demonstrating that glutaminase contributes to the autophagic response elicited by Myc. Exogenous NHCl was sufficient to induce Atg8a-positive structures and partially restored their accumulation following GLS depletion, supporting ammonia as a downstream contributor to this response. Mechanistically, Myc-induced autophagy in clones required the core autophagy factor Atg5 but was not suppressed by depletion of Rheb or Atg1, consistent with an autophagic program that can operate independently of canonical TOR-Atg1 signaling. We further found that Myc activity is required for RasV12-driven epithelial overgrowth and that RasV12 cells induce a pronounced non-cell-autonomous accumulation of Atg8a-positive structures in wild-type cells surrounding RasV12 clones. Depletion of either Myc or GLS in RasV12 cells strongly reduced this neighboring autophagic response, linking Myc-dependent glutamine metabolism in transformed cells to autophagy in the surrounding tissue. Together, our findings identify GLS-dependent glutamine metabolism as a previously unrecognized component of Myc-induced autophagy and extend this relationship to Ras-transformed epithelia, where Myc and Gls contribute to non-cell-autonomous autophagic responses in neighboring cells.

cell biology↗
bioRxiv2026

Arterial Elastin Abundance, Rather Than Orthologue Origin, Modulates Medial Arterial Calcification in Matrix Gla Protein-Deficient Mice

Abstract Calcific deposits in the arterial media have been associated with a number of metabolic and genetic disorders including diabetes, chronic kidney disease and generalized arterial calcification of infancy. While medial calcification and physiologic hard tissue mineralization in the skeleton are both regulated by several common determinants, emerging data suggest that there might be fundamental differences in the mechanisms underlying these two processes. Objective: We previously demonstrated that elastin haploinsufficiency delays medial calcification in MGP-deficient mice. Here, using mice in which a human ELN transgene rescues mouse elastin deficiency, we investigated whether the origin and abundance of arterial elastin differentially affect the initiation and progression of medial calcification. Approach and Results: We pursued a transgenic approach to alter the arterial elastin scaffold in MGP-deficient mice. Our analyses of a humanized MGP-deficient model with 40% reduction of medial elastin content showed a complete absence of the early-stage vascular calcification. Additionally, we showed that mouse and human elastin orthologues affect vascular calcification in a comparable manner. Conclusion: Arterial elastin abundance, rather than orthologue origin, modulates the initiation and progression of medial calcification in MGP-deficient mice. A further reduction in arterial elastin beyond that achieved by elastin haploinsufficiency profoundly delays mineral deposition and maturation, whereas restoration of elastin abundance through transgenic human ELN expression restores arterial calcification.

cell biology↗
bioRxiv2026

Non-invasive forecasting of skin cancer evolution through longitudinal hair sampling

The ability to longitudinally track clonal evolution non-invasively would transform cancer interception strategies, long before late-stage disease when most cancer genomes are analysed. Here, we demonstrate that repeated hair sampling from the same individual followed by exome sequencing enables tracking of somatic evolution in vivo over several months after chemically induced skin carcinogenesis. We found that hair follicles accumulate a higher mutation burden than spatially-matched skin and harbour mutations that spread into surrounding epidermis and persist throughout tumour progression. DNA-damaged follicles enter sustained quiescence that delays replication and repair, creating a reservoir for long-lived mutations. During premalignant progression, carcinogen-associated mutations become enriched as follicular clones expand into adjacent skin. Mutation tracking identified genes that may govern tumour predisposition and initiation, many of which are mutated at high incidence in human cutaneous squamous cell carcinoma cohorts. Hair follicles therefore provide a non-invasive readout to forecast the early development of skin cancer, enabling patient risk stratification.

cell biology↗
bioRxiv2026

Replication stress at centromeres biases the segregation of DNA damage

Replication-associated errors can cause DNA damage to accumulate on the newly synthesized strand over time. In specific cases such as stem cells, retention of the immortal strand used as template preserves one daughter cell into pluripotency while correlating with terminal differentiation of the damage one. In somatic cells, DNA damage distribution after mitosis remains unclear. Here, we uncovered a mechanism of non-random segregation of the DNA damage marker gH2AX occurring during a single cell division cycle. Replication stress using hydroxyurea (HU) upon release into S phase in RPE-1, BJ, hCEC D29 and fibroblasts showed reproducible Non-Random Segregation (NRS) of gH2AX in the ensuing G1, a phenotype not observed in any of the cancer cell lines analyzed. Notably, removal of R-loops led to a reduction of cells with NRS, whether RNaseH1 was over-expressed globally or exclusively targeted to centromeres, indicating that centromeric DNA-RNA hybrids contribute to NRS of the damage. In line with our previous evidence of centromeric chromatin disruption leading to R-loops, rapid removal of the histone H3 variant CENP-A causes damage and NRS, although to a lower extent than HU alone. This implies that additional mechanisms contribute to centromeric R-loops and NRS of damage in the daughter cells upon mitotic exit. Mechanistically, chemical inhibition of the catalytic activity of Rad51 led to a significant drop in NRS without a change in the total amount of damaged cells, implying involvement of the Homologous Recombination (HR) pathway to accumulation of gH2AX to only one chromatid. In turn, this affects the spindle-kinetochore with a measurable length asymmetry, inducing mechanical and/or epigenetic signals that affect the orientation of the sister chromatids on the metaphase plate to bias segregation. Altogether, we found replication-induced asymmetric segregation of DNA damage during mitosis that is influenced by centromeric R-loops, Rad51 activity and spindle dynamics, with implications on cell fate, chromosome and genome stability in the daughter cells.

cell biology↗
bioRxiv2026

Data-driven spectroscopic dictionaries and detector-calibrated inference for photon-limited Raman hyperspectral imaging of living cells

Label-free Raman imaging of living cells is photon limited: at exposures compatible with cellular dynamics, single-pixel spectra carry about one count per channel on a dominant smooth background. We present an unmixing framework in which the decoder of a physics-constrained autoencoder is restricted to a data-driven spectroscopic dictionary: band centers,widths, and pseudo-Voigt shapes are measured from the dataset and fixed, and the network learns only nonnegative band amplitudes, a smooth B-spline background, and a per-pixel gain.First, on slit-scanning images of HeLa cells (532 nm) the dictionary yields spike-free component spectra that read as band tables, including a resonance-enhanced cytochrome-c-associated component matching literature spectra, and the most stable decomposition against the component number. Second, the dictionary and initialization calibrated at 1 s exposure perline transfer to 100 ms per line (12 s sweeps): cytochrome-c spectral identity survives a single sweep (correlation 0.92) while its map remains photon limited; the dictionary provides spectral physicality, and the transferred initialization prevents a structural collapse that global map correlations miss; in a measurement-derived phantom the dictionary estimator holds thecytochrome-c spectrum to 17-19{degrees} spectral angle at 100 ms, where classical factorizations and free decoders lose it (55-64{degrees}). Estimation on the count-equivalent detector output uses a calibrated shifted-Poisson quasi-likelihood. Third, evaluation must be time matched:correlation against a separately acquired reference saturates through slow specimen drift and acquisition mismatch rather than photon noise, and the self-consistency of learned denoisers is inflated by shared bias; time-matched self-consistency and independent cross-checks areproposed.

cell biology↗
bioRxiv2026

Lipogenic gene expression and substrate sensitivity in the bovine mammary gland shape milk fat composition

Milk fat is produced by mammary epithelial cells (MEC) through a conserved mechanism shared among all fat-producing cells across biological kingdoms. Although highly conserved, different tissues and organisms produce distinctive fat compositions. Notably, ruminant milk fat is characterized by enrichment in short and medium chain fatty acids. We hypothesized that this unique profile is driven by MEC-specific metabolic characteristics related to their response to lipogenic substrates. To study this, we compared bovine MEC and udder-derived fibroblasts in terms of their lipogenic capacity and fatty acid composition when exposed to lipogenic building blocks. When exposed to acetate, MEC showed coordinated upregulation of acyl-CoA short-chain synthetase 1 (ACSS1) and diacylglycerol transferase (DGAT), while expression of acyl-CoA synthetase long-chain 1 (ACSL1) decreased. Medium chain fatty acids were also elevated in acetate-treated MEC and not in fibroblasts. The role of ACSS1 in the production of medium chain fatty acids in MEC was confirmed by knockdown experiments. Metabolomics analysis showed that in MEC acetate treatment triggered a broad metabolic response, primarily amino acids catabolism, energy and polar lipid metabolism. Collectively, these findings demonstrate effective utilization of acetate for de novo fatty acid synthesis in MEC with preferred tendency to produce medium chain fatty acids.

cell biology↗