bioRxiv Science⌕ Search

bioRxiv · 10.1101/2025.11.18.689007

Microfluidics based exploration for quorum quenching genes in Antarctic microbiomes

Abstract

Quorum sensing (QS) is a form of microbial communication that enables each cell in a population to sense the total population density, so that gene expression can be modified accordingly. Quorum quenching (QQ) is the antagonistic disruption of this communication by competing organisms, with potential use in the ongoing human effort to control microbial populations. Previous studies have taken advantage of functional metagenomics to retrieve new QS/QQ genes, but the frequency of obtaining positive clones remained very low, suggesting the need for increased screening efficiency. Here, a new ultrahigh-throughput screening method was developed to search for genes encoding novel QQ genes based on functional metagenomics, microfluidics, and the development of an Escherichia coli reporter strain whose fluorescence is repressed in the presence of AHLs but restored by the expression of any gene that interferes with the QS system. This strain was transformed with a metagenomic short-insert library collected from Antarctic plant rhizospheres; an understudied extreme environment. The library was encapsulated in droplets containing single clones and sorted using fluorescence-activated cell sorting (FACS). After screening approximately 7,000,000 clones, around 200 were recovered and one positive hit was confirmed, showing a previously unreported mode of action that would have been difficult to detect using rational computational methods. These findings underline the potential of microfluidics to dramatically increase screening efficiency, while reducing costs and processing time, and they act as a proof of concept for the discovery of more genes involved in QS and other molecular mechanisms of interest in microbial ecology. IMPORTANCEQuorum sensing (QS) regulates essential microbial behaviours, including virulence, biofilm formation, and symbiotic interactions, making it a key target for ecological and applied microbiology. Disrupting QS through quorum quenching (QQ) has major potential in agriculture, medicine, and biotechnology as an alternative to antibiotics or chemical treatments. However, the discovery of QQ genes through brute-force approaches is limited by large screening efforts, resulting in high costs and long processing times. Our study introduces a microfluidics-based, ultrahigh-throughput functional screening platform that strongly improves screening efficiency. It allowed us to identify a novel QQ gene, predicted to be involved in a previously undescribed mechanism of QS disruption, from an under-explored extreme environment (Antarctic rhizosphere). These results demonstrate how microfluidics can optimise screening technologies, while unlocking the hidden functional diversity of microbial communities useful for biotechnological applications in microbial control.

Explore related subjects

Keep this discovery

Explore connections, maps & timelines

BibTeXRIS

White, J. J., Diaz-Rullo, J., Morgante, V., Gonzalez-Pastor, J. E., Hidalgo, A., Sanchez-Costa, M.. 2025-11-18. Microfluidics based exploration for quorum quenching genes in Antarctic microbiomes. https://doi.org/10.1101/2025.11.18.689007

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

KEEP EXPLORING

Related preprints

A G-Quadruplex Containing First Intron Harbors a Functional Polyadenylation Signal in TP53

First introns of mammalian genes are often longer than other introns and may contain regulatory elements, suggesting that they may have roles in gene regulation. We detected a previously unannotated, low abundance intronic transcript, TP53-INT1, using long-read direct RNA sequencing data. TP53-INT1 has low coding potential and terminates within the first and longest intron of TP53. The transcript structure and 3'-end were validated by independent experimental and in silico evidence. We identified a canonical polyadenylation signal upstream of the transcript termination site and demonstrated its functionality using reporter assays. Furthermore, a potential G-quadruplex (G4)-forming sequence was identified upstream of this polyadenylation signal. The G4-forming potential was confirmed using spectroscopic and thermal stability analyses. Complementing the in vitro characterizations, treatment with Pyridostatin, a G4-stabilizing drug, was associated with decreased TP53 expression. Together, these findings characterize a previously unannotated TP53 intronic transcript and reveal a local genomic context combining accessible chromatin, a functional polyadenylation signal, and a potential G4-forming sequence that may influence full-length transcription.

molecular biology↗

LOca-1: A minimal calcium-activated arginyl-specific orthocaspase from the Loki's Castle hydrothermal vent field

Orthocaspases are prokaryotic homologs of metacaspases within the C14 family of cysteine proteases, yet their biochemical properties and cellular roles remain poorly understood. Here, we report the discovery and comprehensive characterization of LOca-1, a metagenome-derived orthocaspase from the Loki's Castle hydrothermal vent field. LOca-1 consists primarily of a single, conserved p20 catalytic domain and undergoes calcium-dependent activation through cleavage at a conserved arginine residue. Once activated, LOca-1 displays strict arginyl-specific proteolytic activity and strong selectivity for residues surrounding the cleavage site. The enzyme is both thermoactive and thermostable, exhibiting maximal activity at 65 {degrees}C and a melting temperature of approximately 72 {degrees}C. Structural modelling revealed conservation of the catalytic core relative to plant metacaspases despite substantial sequence divergence. To our knowledge, LOca-1 is only the second biochemically characterized orthocaspase and the first reported from a deep-sea hydrothermal vent environment. LOca-1 expands the known biochemical diversity of prokaryotic metacaspase homologs and provides insights into the properties of a minimal p20-domain orthocaspase. Together, our findings establish LOca-1 as a thermostable, calcium-activated arginyl-specific orthocaspase and provide a foundation for future studies of orthocaspase function in prokaryotes.

molecular biology↗

A TMEM175 Mutation Disrupts the Lysosomal-Mitochondrial Axis Causing Short QT Syndrome and Sudden Cardiac Death

Short QT Syndrome (SQTS) is a rare cardiac channelopathy characterized by abnormally short QTc intervals and increased sudden cardiac death (SCD) risk. Only 20-30% of SQTS cases have been linked to genetic mutations, typi-cally in surface membrane ion channels. We identified a novel lysosomal TMEM175 gene mutation (p.Arg377His) in 7 patients in a family with SQTS and SCD. Genetic analyses, including whole exome sequencing in the family and rare-variant burden testing in [~]118,000 UK Biobank participants, sug-gested an association between TMEM175 rare variants and QT interval short-ening. Functional studies in CRISPR-engineered mice and patient-specific induced pluripotent stem cell-derived cardiomyocytes (iPSC-CMs) revealed that TMEM175R377H causes shortened QT intervals and hastened repolariza-tion, respectively, as well an increased arrhythmia susceptibility. Isolated TMEM175R377H cardiomyocytes showed action potential duration (APD) abbre-viation, confirmed in whole TMEM175R377H mouse hearts and patient-specific iPSC-CM monolayers. In silico and electron microscopy studies showed that TMEM175R377H disrupts lysosomal-mitochondrial interactions, leading to mito-chondrial dysfunction, as evidenced by the reduced maximal respiration and spare respiratory capacity, with reduced ATP production, IKATP activation, and APD shortening. This mutation represents the first non-sarcolemmal ion chan-nel defect associated with SQTS and high SCD risk, potentially expanding the genetic landscape of the disease.

molecular biology↗