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Biology subjects

Escandell, J. M.

Publications and source records attributed to Escandell, J. M..

4 recordsLinked to original sources

Development of a Serum-Free Producer Cell Line Generation Process for Scalable and Efficient rAAV Production for gene therapy applications

1.The growing field of recombinant Adeno-Associated Virus (rAAV) gene therapy demands scalable and efficient production platforms. Manufacturing platforms based on producer cell lines (PCL) hold substantial promise due to their capacity for high productivity and scalability. However, the generation of stable cell lines for rAAV production is typically performed using serum-containing processes, which pose a risk due to safety and regulatory concerns related to animal-derived components. In this study, we established a fully serum-free process for PCL generation for rAAV production, optimizing critical stages of this process, including transfection methodologies for stable plasmid integration, isolation of highly productive cell pools, and media supplementation to support single-cell cloning. The developed serum-free process generated clonally derived PCLs with productivity and product quality on par with traditional serum-based methods. This approach significantly reduced the cell line generation timeline and eliminated the challenge related to serum supplementation, adapting it to industry requirements. The reported advances overcome a critical step in cell line development for rAAV production, facilitating the implementation of scalable and efficient production platforms to support the development of rAAV-based gene therapies.

bioengineering↗

Pot1 promotes telomere DNA replication via the Stn1-Ten1 complex in fission yeast

Telomeres are nucleoprotein complexes that protect the chromosome-ends from eliciting DNA repair while ensuring their complete duplication. Pot1 is a subunit of telomere capping complex that binds to the G-rich overhang and inhibits the activation of DNA damage checkpoints. In this study, we explore new functions of fission yeast Pot1 by using a pot1-1 temperature sensitive mutant. We show that pot1 inactivation impairs telomere DNA replication resulting in the accumulation of ssDNA leading to the complete loss of telomeric DNA. Recruitment of Stn1 to telomeres, an auxiliary factor of DNA lagging strand synthesis, is reduced in pot1-1 mutants and overexpression of Stn1 rescues loss of telomeres and cell viability at restrictive temperature. We propose that Pot1 plays a crucial function in telomere DNA replication by recruiting Stn1-Ten1 and Pol-primase complex to telomeres, thus promoting lagging-strand DNA synthesis at stalled replication forks.

genetics↗

SSU72 phosphatase is a telomere replication terminator

Telomeres, the protective ends of eukaryotic chromosomes, are replicated through concerted actions by conventional DNA polymerases and telomerase, though the regulation of this process is not fully understood. Telomere replication requires (C)-Stn1-Ten1, a telomere ssDNA-binding complex that is homologous to RPA. Here, we show that the evolutionarily conserved phosphatase Ssu72 is responsible for terminating the cycle of telomere replication in fission yeast. Ssu72 controls the recruitment of Stn1 to telomeres by regulating Stn1 phosphorylation at S74, a residue that lies within the conserved OB fold domain. Consequently, ssu72{Delta} mutants are defective in telomere replication and exhibit long 3 overhangs, which are indicative of defective lagging strand DNA synthesis. We also show that hSSU72 regulates telomerase activation in human cells by controlling the recruitment of hSTN1 to telomeres. Thus, in this study, we demonstrate a previously unknown yet conserved role for the phosphatase SSU72, whereby this enzyme controls telomere homeostasis by activating lagging strand DNA synthesis, thus terminating the cycle of telomere replication.

cell biology↗

Molecular basis of mitotic decline during human aging

Aneuploidy, an abnormal chromosome number, has been linked to aging and age-associated diseases, but the underlying molecular mechanisms remain unknown. Supported by direct live-cell imaging of young, middle-aged and old-aged primary human dermal fibroblasts, we found that aneuploidy increases with aging due to general dysfunction of the mitotic machinery. Increased chromosome segregation defects in elderly mitotic cells correlated with an early senescence-associated secretory phenotype (SASP) and repression of Forkhead box M1 (FoxM1), the transcription factor that drives expression of most G2/M genes. By restoring FoxM1 levels in elderly and Hutchison-Gilford Progeria Syndrome fibroblasts we prevented aneuploidy and, importantly, ameliorated cellular phenotypes associated with aging. Moreover, senescent fibroblasts isolated from elderly donors cultures were mostly aneuploid, suggesting that aneuploidy is a key player in the progression into full senescence phenotypes. Based on this feedback loop between cellular aging and aneuploidy, we propose modulation of mitotic efficiency through FoxM1 as a potential strategy against aging and progeria syndromes.

cell biology↗