Search bioRxiv⌕ Search

bioRxiv · 10.1101/2019.12.18.881748

Testing Hormone-specific Antibody Probes for Presumptive Detection and Separation of Contributor Cell Populations in Trace DNA Mixtures

Abstract

"Touch" or trace DNA evidence represent a significant proportion of samples analyzed by forensic science laboratories. Because these samples frequently contain multiple contributors and are often challenging to analyze due to low DNA concentrations and frequent degradation, front end techniques to simplify the mixture prior to DNA profiling could significantly impact case processing and enhance success rates. The goal of this study was to investigate whether targeting hormone molecules within the cell with antibody probes could be used to selectively label and then physically isolate contributor cell populations in trace biological samples. The separation of male and female cells into distinct fractions could reduce the complexity of the mixture prior to DNA profiling. To accomplish this, we first tested the specificity of fluorescently labelled anti-testosterone and anti-dihydrotestosterone antibody probes to epidermal cells from both male and female individuals. Results show that male and female cell populations can be effectively labeled using anti-testosterone and anti-dihydrotestosterone antibody probes and that distinct differences in binding efficiency and resulting median fluorescence of cell populations were observed between several individuals. These differences were then used to design sorting criteria for physically isolating each cell population in two-person epidermal cell mixtures using fluorescence activated cell sorting (FACS). DNA profiling of separated fractions in combination with probabilistic modeling demonstrated that some cell mixtures could be enriched for one contributor in separated cell fractions and yielded statistically more discriminating profiles compared to those generated from the original mixtures. Other mixtures tested showed less evidence of effective cell separation possibly due to a number of factors including imbalance of contributor DNA ratio, intra-sex variation of antibody binding efficiency, and contributions of extracellular or cell-free DNA in the mixture sample. Screening and separation of trace DNA samples with this approach may be presumptive and ultimately constrained by specific parameters of the original mixture, however, antibody binding optimization may mitigate some of these influences.

Explore related subjects

Keep this discovery

Explore connections, maps & timelines

BibTeXRIS

Miller, J. A., Brocato, E. R., Yadavalli, V. K., Greenspoon, S. A., Ehrhardt, C. J.. 2019-12-19. Testing Hormone-specific Antibody Probes for Presumptive Detection and Separation of Contributor Cell Populations in Trace DNA Mixtures. https://doi.org/10.1101/2019.12.18.881748

Cite the original work for its findings. Save a collection to share your selection of sources.

KEEP EXPLORING

Related preprints

Fatty Acid Synthase Binds Cellular mRNAs and its Depletion Reduces Translational Efficiency

Metabolic enzymes with non-canonical RNA binding activity have drawn a growing interest, due to their implications for basic biology and disease. Here we present the first endogenous RNA interactome of fatty acid synthase (FASN), an emerging oncological and virological target. Utilizing crosslinking-based approaches, we characterize the direct RNA association of FASN in two human cell lines, identifying over 6000 binding sites across over 3500 protein-coding genes, with a striking preference for the 5' UTR. We provide a functional cross-screen on the effects of FASN depletion on cellular translation. This integration with ribosome profiling indicated a preferential reduction in the translational efficiencies of FASN-associated mRNAs - an effect shown to be dependent on binding location and site number. Associated transcripts were enriched for morphogenic and cell division-related functions, as well as palmitoylated proteins. This correlative work primes further investigation of FASN as a regulator of translation of its target mRNAs.

molecular biology↗

Genomic features and instability of linezolid resistance in vancomycin-resistant Enterococcus faecalis ST525

This study investigated the mechanisms of oxazolidinone resistance and genomic background in clinical ST525 Enterococcus faecalis isolates, a poorly characterized lineage reported in Brazilian hospitals as either vancomycin-resistant (VRE) or linezolid- and vancomycin-resistant (LVRE). Five LVREfs from intensive care unit patients (linezolid MICs, 8-32 mg/L; vancomycin MICs, >256 mg/L) carried only G2576T and G2505A (in three of four rrl copies) as known linezolid resistance determinants, despite variable linezolid MICs. During serial in vitro passages without antibiotic pressure, isolates with initial MICs of 8-16 mg/L exhibited progressive MIC reductions accompanied by reversion of mutant to wild-type rrl copies, whereas the isolate with an initial MIC of 32 mg/L maintained high-level resistance without reversion. Additional domain V substitutions emerged during MIC decline, while growth kinetics remained broadly similar. Whole-genome sequencing of a representative isolate (LVREfs L7) revealed a ~2.8-Mb chromosome enriched in mobile genetic elements (~8.6%), lacking a functional CRISPR-Cas system. A plasmid-borne prototype Tn1546 carrying vanA, devoid of internal insertion sequences, was found inserted into a Tn3-family transposase gene, a platform not typically associated with vanA mobilization. Together, these findings indicate that ST525 LVREfs, whose genomic features are consistent with long-term persistence in hospitals, may pose a challenge to routine susceptibility testing. A single mutational mechanism can yield variable linezolid MICs, and the ratio of mutated vs wild-type rrl copies can become heterogeneous in the absence of antibiotic pressure, without correlating directly with these values, contrary to the well-documented copy number-MIC correlation.

molecular biology↗

Global repression of mesenchymal genes in epithelial cells by the histone demethylase LSD1

Epithelial-mesenchymal transition (EMT) is an essential process in development, tissue repair, and tumour metastasis, and is triggered by SNAI, ZEB and TWIST transcription factors, that recruit lysine-specific demethylase 1 (LSD1) to repress epithelial genes such as E-cadherin. In mesenchymal cells, LSD1 inhibition restores E-cadherin expression and reduces migration and invasion, consistent with LSD1 inhibition reverting EMT, and offering a therapeutic modality for EMT-associated disease. Recent data, however, suggest context-dependent roles for LSD1, as its inhibition in epithelial cells increases mesenchymal marker expression, potentially promoting EMT. To investigate this discrepancy, we mapped genome-wide binding of LSD1 in HCT116 epithelial cells and used rapid degron-mediated ablation of endogenous LSD1 to measure changes in nascent and steady-state transcription and chromatin accessibility. In epithelial cells, LSD1 binds constitutively-accessible, primed mesenchymal promoters. These are rapidly derepressed after LSD1 ablation, with activation of SNAI2 and ZEB1, which repress epithelial hallmarks such as E-cadherin. Re-introduction of LSD1 downregulates SNAI2 and ZEB1 but, surprisingly, further represses E-cadherin, indicating sustained loss of epithelial characteristics. Collectively, our results show that LSD1 maintains epithelial identity by repressing mesenchymal genes, questioning the therapeutic utility of LSD1 inhibition for EMT control.

molecular biology↗