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Biology subjects

Baars, I.

Publications and source records attributed to Baars, I..

4 recordsLinked to original sources

A combinatorial DNA origami platform for biologically replicable, thermostable data storage and molecular authentication

DNA origami is becoming an attractive platform for data storage, yet current approaches rely on the limited stability of DNA hybridization, preventing them from fully utilizing the stability and cost-effective copying inherent to classical sequence-based storage. Here we introduce DNA Origami for Combinatorial data Storage (DOCS), where we encode information into the scaffold molecule using a combinatorial enzymatic approach. This enables text encoding that is biologically cloneable, stable at high temperatures, and randomly accessible. We further demonstrate the DOCS platforms combinatorial power by creating a stochastic molecular authentication system. Finally, we show using simulations that expanding the information capacity of data carriers allows for the storage and recovery of large files up to several hundred kilobytes in size. DOCS provides a robust, scalable strategy for molecular data storage and security that bridges the gap between classical DNA data storage strategies and DNA nanostructure-based methods.

bioengineering↗

Leishmaniamajor co-opts IL-7 feedback in monocytes to suppress CD4⁺ T-cell immunity

During immune responses, pro-and anti-inflammatory mechanisms must be balanced to ensure pathogen clearance while limiting tissue damage. Monocyte-derived cells contribute to both processes, yet the underlying regulatory circuits remain incompletely defined. Here, we show that a subset of PDPN+IL-7R+ monocyte-derived cells that impair effector CD4 T cell-mediated control of intracellular pathogens, and thus perpetuate the infection. Fibroblast-derived IL-7 drives this immunosuppressive program, which is up-regulated in response to IFN{gamma}. We thus uncover a cytokine-dependent feedback circuit in which elevated IFN{gamma} induces IL-7 production by fibroblasts, licensing immunosuppressive monocyte-derived cells that restrain CD4 T cell responses. This mechanism links excessive inflammation to immune suppression at the expense of pathogen control. Targeting this feedback loop may enable therapeutic strategies that enhance antimicrobial immunity while preserving tissue integrity.

immunology↗

An error correction strategy for image reconstruction by DNA sequencing microscopy

By pairing adjacent molecules in-situ and then mapping these pairs, DNA microscopy could significantly reduce workload in spatial omics methods by directly inferring geometry from sequencing data alone. However, experimental artefacts can lead to errors in the adjacency data which distort the spatial reconstruction. Here, we describe a method to correct two such errors: spurious crosslinks formed between any two nodes, and fused nodes that are formed out of multiple molecules. We build on the principle that spatially close molecules should be connected and show that these errors violate this principle, allowing for their detection and correction. Our method corrects errors in simulated data, even in the presence of up to 20% errors, and proves to be more efficient at removing errors from experimental data than a read count filter. Integrating this method in DNA microscopy will significantly improve the accuracy of spatial reconstructions with lower data loss.

bioinformatics↗

Clustering of death receptor for apoptosis using nanoscale patterns of peptides

The nanoscale spatial organization of transmembrane tumor necrosis factor (TNF) receptors has been implied as a regulator of cellular fate. Accordingly, molecular tools that can induce specific arrangements of these receptors on cell surfaces would give us an opportunity to study these effects in detail. To achieve this, we introduce DNA origami nanostructures, that precisely scaffold the patterning of TNF-related apoptosis-inducing ligand (TRAIL)-mimicking peptides at nanoscale level. Stimulating human breast cancer cells with these patterns, we find that around 5 nm is the critical inter-ligand distance of hexagonally patterned peptides to induce death receptor clustering and a resulting apoptosis. We thus offer a strategy to reverse the non-efficacy of current ligand- and antibody-based methods for TNF superfamily (TNFRSF) activation.

bioengineering↗