bioRxiv Science⌕ Search

Biology subjects

Bohra, D.

Publications and source records attributed to Bohra, D..

3 recordsLinked to original sources

deepthought: domain driven design for microscopy with applications in DNA damage responses

Analysis-in-the-loop microscopy has been demonstrated many times, but it is rarely used outside the laboratories that build it. Each demonstration constructs its own acquisition infrastructure, so little transfers between them, and it has remained unclear which parts of the problem are already solved. In this work, the microscopy acquisition stack was itself treated as the object of study, and was investigated by construction. A minimal stack was built end to end, and four applications were then driven through it as test conditions. These were fixed-cell high-throughput immunofluorescence, live time-lapse imaging of an unsynchronized population, fluorescence anisotropy imaging, and autonomous focus and exposure. Each element of the stack was then classified by how it varied across these applications. Device access, sequencing, data storage and viewing held constant, and mature implementations of each were adopted unchanged. Interpretation, or how an image becomes a set of entities, differed with the application and belongs behind an interface. Two elements had nothing available to adopt and were therefore built. These are a geometric representation of the sample that a plan can traverse, and a representation of a run that yields detected objects rather than images. With those two in place, feedback from analysis into acquisition was ordinary control flow. The system was applied to the DNA damage response, where 22,000 cells were acquired and analyzed without operator intervention, and cells were followed through mitosis over 24 hours in an unsynchronized population without chemical synchronization. One element, targeting, or the choice of where to observe next, varies between applications and remains unabstracted in this implementation. It is identified here as the next requirement. Codehttps://github.com/ndsystems/deepthought (acquisition client), https://github.com/ndsystems/hard-link (instrument access server)

bioinformatics↗

HP1α-driven Phase Separation and Repair Pathway Choice in Response to Heterochromatin Damage

Double-strand breaks (DSBs) pose significant threat to genomic stability and need immediate attention from DNA Damage Response (DDR) machinery involved in Homologous Recombination (HR) or Non-homologous end joining (NHEJ). DDR in heterochromatin is challenging owing to the distinct chromatin organization. Heterochromatin Protein 1 (HP1) isoforms that contribute significantly to the organization of heterochromatin, have been shown to be involved in DDR. Mammalian HP1 has three isoforms, HP1, HP1{beta}, and HP1{gamma}, which possess significant homology and yet have distinct functions. HP1 is the only isoform known to undergo liquid-liquid phase separation. We show that the minute-scale dynamics of HP1 and HP1{beta} differ dramatically and they promote differential recruitment of HR vs. NHEJ factors at the sites of laser-induced clustered DSBs. Perturbing HP1 phase-separation abrogates both the recruitment of HR factors and readouts of HR. Our study provides a link between phase-separation and DDR-centric roles of HP1 and hints at spatial partitioning of repair pathways in response to damage in heterochromatin.

cell biology↗

Acute Activation of Genes Through Transcriptional Condensates Impact Non-target Genes in a Chromatin Domain

Transcription activation of genes by estrogen is driven by enhancers, which are often located within the same Topologically Associating Domain (TAD) as non-targeted promoters. We investigated how acute enhancer-driven activation affects neighbouring non-target genes within the same TAD. Using single-molecule RNA FISH (smFISH), we tracked the transcription of TFF1 (enhancer-target gene) and TFF3 (non-target gene) during estrogen stimulation. We observed mutually exclusive expression patterns: TFF1 expression peaked at 1 hour, while TFF3 reached its peak at 3 hours, after TFF1 activation had diminished. Chromatin looping data indicated that the enhancer loops with TFF1 but not TFF3, suggesting that TFF3 upregulation is not due to direct enhancer-promoter interactions. CRISPR deletion of the enhancer, affected TFF1 transcription more acutely than TFF3. 1,6-hexanediol (HD) exposure suggested that the TFF1 enhancer:promoter undergo a potential ER-mediated condensate formation, which sequesters the transcriptional machinery and inhibits TFF3 expression. As estrogen signalling fades at 3h, TFF1 expression declines while TFF3 expression increases. Our findings reveal that enhancer-driven activation can indirectly repress neighbouring genes within the same TAD, highlighting a dynamic shift in gene expression as signalling progresses.

molecular biology↗