Biology subjects

Burczyk, S.

Publications and source records attributed to Burczyk, S..

4 recordsLinked to original sources

bioRxiv2026

Comprehensive Characterization of the Human Neural Stem Cell Line HNSC.100 as a Versatile Model for Neurobiological Research

Studying neural-related questions is inherently challenging due to the limited number of suitable cell models. Here, we characterize a previously reported immortalized human neural stem cell line, HNSC.100, serving as a robust model for a wide range of neurobiological research questions. The cell line expresses key neural stem cell markers, including SOX2, vimentin, nestin, and allows for efficient genetic manipulation. Furthermore, HNSC.100 cells can be differentiated into neurons, astrocytes, and oligodendrocytes, thereby covering a wide spectrum of major neural cell types. We adapted corresponding differentiation protocols and established a comprehensive panel of molecular markers to validate successful differentiation, enabling precise characterization of the resulting cell population. In addition, we provide a complete dataset of RNA expression levels for all detectable genes in HSNC.100 cells. Based on this dataset, we assembled a list of expressed genes implicated in neural disorders that can be studied with this cell line. Together, we present a detailed characterization of the HNSC.100 cell line and provide new tools and reference data to facilitate its use. This resource enables researchers to evaluate the lines suitability for specific applications and to rapidly integrate HNSC.100 cells into their experimental workflows. O_FIG O_LINKSMALLFIG WIDTH=200 HEIGHT=130 SRC="FIGDIR/small/700829v2_ufig1.gif" ALT="Figure 1"> View larger version (28K): org.highwire.dtl.DTLVardef@1eef4e5org.highwire.dtl.DTLVardef@1100f62org.highwire.dtl.DTLVardef@1621481org.highwire.dtl.DTLVardef@305d5b_HPS_FORMAT_FIGEXP M_FIG C_FIG

cell biology↗

bioRxiv2025

SEVI Fibrils are Induced by Bacterial Surface Molecules and Exert Antimicrobial Activity Against ESKAPE Pathogens

The semen-derived enhancer of viral infection (SEVI) is an amyloid fibril formed by the self-assembly of the PAP248-286 peptide, a cleavage product of prostatic acid phosphatase, which is naturally present in human seminal plasma. Beyond its previously described role in HIV transmission, findings highlight a physiological function for SEVI in innate immunity. As many amyloids display antimicrobial effects, we tested SEVI fibrils for antibacterial activity against microbial ESKAPE pathogens and urogenital bacteria, including Pseudomonas aeruginosa, Klebsiella quasipneumoniae, Escherichia coli, Acinetobacter baumannii, Staphylococcus aureus, Streptococcus agalactiae and Listeria monocytogenes. SEVI exhibited direct dose-dependent antibacterial effects in radial diffusion and survival assays, with activity observed at physiologically relevant concentrations. Bacterial surface molecules such as lipopolysaccharides and lipoteichoic acid induced the formation of SEVI fibrils, as confirmed by kinetic assays. Preincubation with epigallocatechin gallate, a fibril disruptor, abolished SEVIs antibacterial activity, pointing to the importance of its fibrillar structure. Mechanistic studies and electron microscopy revealed limited bacterial membrane disruption and the intracellular accumulation of polyphosphate granules in P. aeruginosa, indicating a stress response. In conclusion, SEVI exerts a potent antibacterial activity against pathogens found in the urogenital tract, indicating a potential physiological role in vaginal mucosal immunity.

microbiology↗

bioRxiv2022

Human TRMT2A methylates different components of the translation machinery and contributes to translation fidelity

Methyl-5-uridine (m5U) is one of the most abundant RNA modifications found in cytosolic tRNA. tRNA methyltransferase 2 homolog A (hTRMT2A) is the dedicated mammalian enzyme of m5U formation at tRNA position 54. However, its RNA binding specificity and functional role in the cell are not well understood. Here we dissected structural and sequence requirements for binding and methylation of its RNA targets. Specificity of tRNA modification by TRMT2A is achieved by a combination of modest binding preference and presence of a uridine in position 54 of tRNAs. Mutational analysis together with crosslinking experiments identified a large hTRMT2A-tRNA binding surface. Furthermore, complementing hTRMT2A interactome studies revealed that TRMT2A interacts with proteins involved in RNA biogenesis. Finally, we addressed the question of the importance of TRMT2A function by showing that its knockdown reduces translation fidelity. These findings extend the role of hTRMT2A beyond tRNA modification towards a role in translation.

biochemistry↗

bioRxiv2022

Depletion of the RNA-binding protein PURA triggers changes in posttranscriptional gene regulation and loss of P-bodies

The RNA-binding protein PURA has been implicated in the rare, monogenetic, neurodevelopmental disorder PURA Syndrome. PURA binds both DNA and RNA and has been associated with various cellular functions. Only little is known about its main cellular roles and the molecular pathways affected upon PURA depletion. Here, we show that PURA is predominantly located in the cytoplasm, where it binds to thousands of mRNAs. Many of these transcripts change abundance in response to PURA depletion. The encoded proteins suggest a role for PURA in immune responses, mitochondrial function, autophagy and processing (P)-body activity. Intriguingly, reduced PURA levels decrease the expression of the integral P-body components LSM14A and DDX6 and strongly affect P-body formation in human cells. Furthermore, PURA knockdown results in stabilization of P-body-enriched transcripts, whereas other mRNAs decrease. Hence, reduced PURA levels, as reported in patients with PURA Syndrome, influence the formation and composition of this phase-separated RNA processing machinery. Our study proposes PURA Syndrome as a new model to study the tight connection between P-body-associated RNA regulation and neurodevelopmental disorders. Graphical Abstract O_FIG O_LINKSMALLFIG WIDTH=200 HEIGHT=150 SRC="FIGDIR/small/479353v2_ufig1.gif" ALT="Figure 1"> View larger version (49K): org.highwire.dtl.DTLVardef@5712f9org.highwire.dtl.DTLVardef@9eb133org.highwire.dtl.DTLVardef@83b7b2org.highwire.dtl.DTLVardef@1912e5c_HPS_FORMAT_FIGEXP M_FIG C_FIG

molecular biology↗