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Biology subjects

Jadhav, H.

Publications and source records attributed to Jadhav, H..

3 recordsLinked to original sources

Make it so: Rapid and affordable plasmid sequencing on ONT platforms with PICARD-seq

Plasmid construction underpins molecular biology and synthetic biology, yet validation is often limited to the inserted fragment rather than the whole plasmid, and around a third of laboratory-made plasmids carry sequence errors that can affect function. Sanger sequencing scales poorly across whole plasmids, while short-read approaches cannot resolve the repeated DNA parts, such as promoters, that are common in synthetic constructs. We present PICARD-seq, a rapid nanopore-based protocol that uses off-the-shelf Tn5 rapid barcoding reagents and a MinION to sequence pools of whole plasmids in under a day, and we systematically benchmark the computational pipelines available for analysing the resulting data. Using a curated set of 25 plasmids of known sequence spanning 3.0-20.6 kbp, including various dilution series and repetitive multi-part constructs, we ran five independent replicates of each pipeline. The ONT EPI2ME Clone Validation workflow was fast (13-18 min) but stochastic, varying between replicates for both plasmids assembled and what sequence was returned; Canu outperformed the default Flye assembler, and reducing the minimum coverage parameter from 60x to 20x substantially improved assembly of large, repetitive, and dilute samples. The ensemble assembler Autocycler was slower (81-111 min) but gave the highest and most consistent rate of recovering the expected sequence. Complementary read mapping with minimap2 distinguished genuine sequence differences from assembly artefacts. Applying PICARD-seq to problematic plasmids revealed backbone concatemers, a misincorporated promoter part, and a mixed population of rearranged molecules in a repetitive construct. PICARD-seq makes routine whole-plasmid validation practical and affordable for individual laboratories.

bioinformatics↗

CREation of an expanded plant memory gene circuit toolkit

Genetic circuits rely on modular, well-characterized genetic parts to achieve predictable cellular behaviour. Despite their widespread adoption, biological parts are complex and when used in a new molecular context can result in unexpected outcomes. Site-specific recombinases have been widely used due to their unique ability to induce precise, irreversible changes to a DNA sequence, making them ideal tools for memory logic operations. However, unexpected context-specific failures of even the most widely used recombinase, Cre, has limited the expansion and complexity of synthetic gene circuits in diverse species. Here, through a systematic analysis of Cre failure in plant gene circuits, we uncovered multiple unexpected post-recombination interactions within the transcriptional unit between the promoter region, recombinase, and their cognate recognition sites. These significantly inhibit transcriptional activity, preventing circuit functionality. Specifically, post-recombination Cre recombinase exhibits an inhibitory property by binding to lox sites, with the remaining lox site repressing transcription. By thoroughly characterizing these dynamics, we restored Cre functionality and expanded the plant-based recombinase toolkit for Cre-related recombinases, developing combinations of recombinases and cognate sites with different activation levels for constructing logic gates with stable memory functions. We further developed multiple functional split-recombinase systems for simultaneous logic using a range of dimerization domains and constructed complex logic gates, including 3-input and 6-input AND gates. Together, this exploration of component context dependency in genetic circuits, even with commonly used parts like the Cre/lox system, has implications extending beyond plant systems, and significantly expands plant memory circuit capabilities.

synthetic biology↗

STING agonism enhances anti-tumor immune responses and therapeutic efficacy of PARP inhibition in BRCA-associated breast cancer

Poly (ADP-ribose) polymerase (PARP) inhibitors exert their efficacy by inducing synthetic lethal effects, as well as cGAS/STING-mediated immune responses in BRCA- and other homologous recombination repair-deficient cancer cells. Here we investigated whether the immunologic and therapeutic effects of PARP inhibition in BRCA-deficient breast cancer models could be augmented by synthetic cyclic dinucleotide agonists of STING. Combined PARP inhibition and STING agonism induced a greater degree of STING pathway activation and proinflammatory cytokine production compared to monotherapies in BRCA1-deficient human and mouse triplenegative breast cancer cell lines. In a mouse model of BRCA1-deficient TNBC, the combination also induced an improved immune response compared to either monotherapy alone, evidenced by a greater degree of cytotoxic T cell recruitment and activation, and enhanced dendritic cell activation and antigen presentation. Nanostring mRNA analysis indicated that combinatorial effects were the result of augmented interferon signaling and antigen processing, as well as of heightened leukocyte and dendritic cell functions. Finally, the combination markedly improved anti-tumor efficacy in vivo compared to monotherapy treatment, with evidence of complete tumor clearance and prolongation of survival. These results support the development of combined PARP inhibition and STING agonism in BRCA-associated breast cancer.

cancer biology↗