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Biology subjects

Boroviak, K.

Publications and source records attributed to Boroviak, K..

3 recordsLinked to original sources

A novel chemogenomic screening platform for scalable antimalarial drug target identification

Large-scale chemical-genetic screening, or chemogenomics, can faciliate rapid and scalable drug target identification. To establish a chemogenomic screen for antimalarial drug target identification, we leveraged [~]600 Plasmodium berghei artificial chromosomes (PbACs) encoding potential drug targets to generate a systematic overexpression library. PbACs were engineered with DNA barcodes, enabling their quantification within mixed pools using next generation sequencing (barcode sequencing or BarSeq). Pooled transfection of PbACs into the highly genetically tractable Plasmodium knowlesi demonstrated efficient vector uptake and transcription of encoded P. berghei genes. Parasite pools were exposed to antimalarial candidates, with pilot screens probing for known gene-compound associations identifying their targets with high sensitivity. Screening antimalarial inhibitors with unknown mechanisms of action successfully identified pi4k as the target for one novel compound, which was subsequently validated using in vitro evolution in Plasmodium falciparum parasites. This sensitive and scalable chemogenomics platform therefore represents a valuable early-stage tool for antimalarial target identification.

microbiology↗

A genetic variant of the Wnt receptor LRP6 accelerates synapse degeneration during ageing and in Alzheimer's disease

Synapse loss strongly correlates with cognitive decline in Alzheimers Disease (AD), but the underlying mechanisms are poorly understood. Studies suggest that deficient Wnt signalling, a pathway required for neuronal connectivity, contributes to synapse dysfunction and loss in AD. Consistent with this idea, a variant of Lrp6, (Lrp6-val), which confers reduced Wnt signalling, has been linked to late onset AD. However, the impact of Lrp6-val on synapses in the healthy and AD brain has not been examined. Using CRISPR/Cas9 genome editing, we generated a novel knock-in mouse model carrying this Lrp6 variant to study its role in synaptic integrity. Lrp6-val mice develop normally and do not exhibit morphological brain abnormalities. Hippocampal neurons from Lrp6-val mice do not respond to Wnt7a, a Wnt ligand that promotes synaptic assembly through the Frizzled-5 (Fz5) receptor. Activation of the Wnt pathway by Wnt ligands leads to the formation of a complex between LRP6 and Fz5. In contrast, LRP6-Val impairs the formation of the LRP6-Fz5 complex elicited by Wnt7a, as detected by proximity ligation assay (PLA). We demonstrate that Lrp6-val mice exhibit structural and functional synaptic defects that become more pronounced with age, consistent with decreased canonical Wnt signalling during ageing. To investigate the contribution of this variant to AD, Lrp6-val mice were crossed to hAPPNL-G-F/NL-G-F (NL-G-F), a knock-in AD mouse model. The presence of the Lrp6-val variant significantly exacerbates synapse loss around amyloid-{beta} plaques in NL-G-F mice. Our findings uncover a novel role for the Lrp6-val variant in synapse vulnerability during ageing and its contribution to synapse degeneration in AD.

neuroscience↗

No unexpected CRISPR-Cas9 off-target activity revealed by trio sequencing of gene-edited mice

Introduction Introduction Results and Discussion Conclusion Author Contributions Competing Financial Interests 1. gRNA choices and... 2. Zygote injection 3. DNA extraction from... 4. Amplicon sequencing and... 5. Whole Genome Sequencing 6. Probability of detecting... 7. Variant calling, Trio... 8. Intersection of all... 9. Comparison of SNVs... 10. Validation with PCR... 11. Re-analysis of De... Supplementary Figure Supplementary tables References CRISPR-Cas technologies have transformed genome-editing of experimental organisms and have ...

bioengineering↗