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Biology subjects

Larsen, N. B.

Publications and source records attributed to Larsen, N. B..

5 recordsLinked to original sources

Transient matrix remodeling during direct cell-fate reprogramming enables self-assembly of dense neuronal niches

Native tissues are characterized by high cellular density and continuous reciprocal interactions between cells and the extracellular matrix (ECM), yet recreating these features in vitro remains a major challenge. Current three-dimensional (3D) culture systems typically capture either dense cell-cell interactions or a defined ECM environment, but rarely both. Here, we introduce a strategy that exploits direct fibroblast-to-neuron reprogramming to decouple microenvironment formation from final cell identity. Human dermal fibroblasts were embedded in collagen microgels, where their intrinsic matrix-remodeling capacity drove rapid ECM compaction. Concurrently, the contractile fibroblasts were converted into induced neurons (iN), generating densely packed neuronal microcultures within a remodeled collagen matrix. This approach transforms a defining function of the starting cell type into a mechanism for engineering the microenvironment of the target cell type. The resulting iN-microgels combine high cell density, defined ECM composition, and tunable biophysical properties in a scalable microscale format. By coupling matrix remodeling with cell-fate conversion, our platform establishes a general framework for engineering tissue-like microenvironments and reveals how dynamic 3D extracellular contexts can be integrated into direct cell reprogramming.

bioengineering↗

SARS-CoV-2 sequencing artifacts associated with targeted PCR enrichment and read mapping

Protocols and pipelines for SARS-CoV-2 genome sequencing were rapidly established when the COVID-19 outbreak was declared a pandemic. The most widely used approach for sequencing SARS-CoV-2 includes targeted enrichment by PCR, followed by shotgun sequencing and reference-based genome assembly. As the continued surveillance of SARS-CoV-2 worldwide is transitioning towards a lower level of intensity, it is timely to re-visit the sequencing protocols and pipelines established during the acute phase of the pandemic. In the current study, we have investigated the impact of primer scheme and reference genome choice by sequencing samples with multiple primer schemes (Artic V3, V4.1 and V5.3.2) and re-processing reads with multiple reference genomes. We have also analysed the temporal development in ambiguous base calls during the emergence of the BA.2.86.x variant. We found that the primers used for targeted enrichment can result in recurrent ambiguous base calls, which can accumulate rapidly in response to the emergence of a new variant. We also found examples of consistent base calling errors, associated with PCR artifacts and amplicon drop-out. Similarly, misalignments and partially mapped reads on the reference genome resulted in ambiguous base calls, as well as defining mutations being omitted from the assembly. These findings highlight some key limitations of using targeted enrichment by PCR and reference-based genome assembly for sequencing SARS-CoV-2, and the importance of continuously monitoring and updating primer schemes and bioinformatic pipelines.

bioinformatics↗

Embedded 3D printing in self-healing annealable composites for functional patterning of human neural constructs

Human in vitro models of neural tissue with controllable cellular identity, tunable microenvironment, and defined spatial arrangement are needed to facilitate studies of brain development and disease. Towards this end, embedded printing in jammed microgel supports (i.e., granular gels) holds great promise as it allows precise and programmable patterning of extremely soft and compliant tissue constructs. However, in contrast to the vast material landscape available for bulk hydrogels, granular printing support formulations are restricted to a handful of materials without the ability for facile adjustment of biofunctional properties of the cellular microenvironment. Therefore, there has been a need for novel materials that take advantage of versatile biomimicry of bulk hydrogels while providing high-fidelity support for embedded printing akin to granular gels. To address this need, we present a modular platform for bioengineering of neuronal networks via direct embedded 3D printing of human stem cells inside Self-Healing Annealable Particle-Extracellular matrix (SHAPE) composites. SHAPE composites consist of soft microgels immersed in viscous extracellular-matrix solution to enable precise freeform patterning of human stem cells and consequent generation and long-term maintenance of mature subtype-specific neurons that extend projections within the volume of the annealed support. The developed approach further allows multi-ink deposition, live spatial and temporal monitoring of oxygen levels, as well as creation of vascular channels. Due to its modularity, SHAPE biomanufacturing toolbox not only offers a solution for functional modeling of mechanically sensitive neural constructs, but also has potential to be applied to a wide range of biomaterials with different crosslinking mechanisms to model tissues and diseases where recapitulation of complex architectural features and topological cues is essential.

bioengineering↗

Mechanism of replication-coupled DNA-protein crosslink proteolysis by SPRTN and the proteasome

DNA-protein crosslinks (DPCs) are bulky DNA lesions that interfere with DNA metabolism and therefore threaten genomic integrity. Recent studies implicate the metalloprotease SPRTN in S-phase removal of DPCs, but how SPRTN activity is coupled to DNA replication is unknown. Using Xenopus egg extracts that recapitulate replication-coupled DPC proteolysis, we show that DPCs can be degraded by SPRTN or the proteasome, which act as independent DPC proteases. Proteasome recruitment requires DPC polyubiquitylation, which is triggered by single-stranded DNA, a byproduct of DNA replication. In contrast, SPRTN-mediated DPC degradation is independent of DPC polyubiquitylation but requires polymerase extension of a nascent strand to the lesion. Thus, SPRTN and proteasome activities are coupled to DNA replication by distinct mechanisms and together promote replication across immovable protein barriers.\n\nHighlightsO_LIThe proteasome, in addition to SPRTN, degrades DPCs during DNA replication\nC_LIO_LIProteasome-dependent DPC degradation requires DPC ubiquitylation\nC_LIO_LIDPC ubiquitylation is triggered by ssDNA and does not require the replisome\nC_LIO_LISPRTN-dependent DPC degradation is a post-replicative process\nC_LI

molecular biology↗

The CMG helicase bypasses DNA protein cross-links to facilitate their repair

Covalent and non-covalent nucleoprotein complexes impede replication fork progression and thereby threaten genome integrity. Using Xenopus laevis egg extracts, we previously showed that when a replication fork encounters a covalent DNA-protein cross-link (DPC) on the leading strand template, the DPC is degraded to a short peptide, allowing its bypass by translesion synthesis polymerases. Strikingly, we show here that when DPC proteolysis is blocked, the replicative DNA helicase (CMG), which travels on the leading strand template, still bypasses the intact DPC. The DNA helicase RTEL1 facilitates bypass, apparently by translocating along the lagging strand template and generating single-stranded DNA downstream of the DPC. Remarkably, RTEL1 is required for efficient DPC proteolysis, suggesting that CMG bypass of a DPC normally precedes its proteolysis. RTEL1 also promotes fork progression past non-covalent protein-DNA complexes. Our data suggest a unified model for the replisomes response to nucleoprotein barriers.

biochemistry↗