Biology subjects

Laurent, L.

Publications and source records attributed to Laurent, L..

6 recordsLinked to original sources

bioRxiv2026

Stony coral tissue loss disease outbreak altered reef communities of Carrie Bow Cay, Belize

Stony coral tissue loss disease (SCTLD) has caused one of the most damaging coral epizootics on record, impacting about half of coral species across most of the reef systems of the Caribbean and Florida. To evaluate its impact on the coral reefs surrounding Carrie Bow Cay, Belize, we monitored seven fixed transects before and at two time points during the outbreak using three different methods. We estimated species-specific mortality rates by fate tracking tagged colonies, quantified reef-wide lesion prevalence and resulting changes to colony density and community composition using in situ transect surveys, and finally calculated changes to total coral cover using benthic photoquadrats. SCTLD quickly led to mortality of infected corals. Between October 2019 and May 2022, 32% of the 102 fate-tracked coral colonies had developed lesions consistent with SCTLD and an additional 30% had suffered complete mortality likely due to SCTLD. By December of 2022, 21% of the 33 colonies that had been observed with lesions had died. We documented patterns of species susceptibility largely confirming previous reports in other locations. We documented sharp abundance declines in several species, including the total loss of Meandrina meandrites from survey transects, leading to a significant shift in community composition. Cover of several species declined between October 2019 and May 2022, but only Siderastrea siderea experienced sustained declines into December of 2022. Overall cover of scleractinian corals decreased from 13.2 to 7.9% during the monitoring period. The ecological impacts of SCTLD in the area surrounding Carrie Bow Cay are consistent with reports from elsewhere in the Caribbean, underscoring the magnitude of colony density and coral cover loss caused by SCTLD across the region.

ecology↗

bioRxiv2026

Epithelial density controls cell migration through an adhesion-nucleus mechanotransduction pathway

Cell density is thought to regulate tissue growth, homeostasis, and regeneration, yet how cells sense and respond to density remains poorly understood. To investigate density-dependent mechanotransduction, we combined genetically encoded biosensors with quantitative fluorescence microscopy in epithelial cells subjected to genetic, pharmacological, and mechanical perturbations. We found that low epithelial density promotes focal adhesion growth, causing mechanical relaxation of vinculin and release of its competitive binding with FAK and ERK. This enables FAK to bind and activate ERK in the cytoplasm. Cytoskeletal tension transmitted through LINC complexes drives their nuclear translocation, where low density induces ERK-dependent chromatin decondensation and increased nuclear envelope tension. This recruits and activates cPLA2, leading to arachidonic acid production and enhanced cell migration. Together, these findings identify a mechanochemical pathway linking cell density to epithelial migration via ERK, cPLA2, and mechanically regulated signaling from adhesions to the nucleus. Significance statementIn multicellular organisms, cells constantly experience crowding, yet how they detect changes in cell density and convert them into biological responses is not well understood. Here, we show how low cell density mechanically triggers signaling inside epithelial cells to promote migration. When cells are sparse, adhesion sites grow and release key signaling proteins that move into the nucleus stretched by the cytoskeleton. These mechanical and biochemical inputs alter nuclear structure, activates lipid signaling, and boosts cell migration. By revealing how mechanical forces, cell adhesions, and nuclear signaling work together, this study provides a clear mechanistic link between cell density and migration, a process central to tissue growth, repair, and disease progression.

cell biology↗

bioRxiv2025

MECP2 Mutations Rewire Human ESC Fate and Bias Cortical Lineage Commitment

Rett syndrome arises from loss-of-function mutations in the X-linked chromatin regulator MECP2, yet the earliest molecular derailments in human development remain poorly defined. Using isogenic hESC models carrying three patient-derived MECP2 mutations, we followed the transcriptome from pluripotency through neuro-ectoderm, neural stem, and neural progenitor stages and into three-month cerebral organoids. Stage dominated transcriptional variance, but mutants shared a secondary program enriched for synaptic-membrane and extracellular-matrix genes. Single-cell profiling revealed a naive-like, hyper-proliferative state marked by up-regulation of ZFP42 at ESC stage. Strikingly, EMX1, a cortical radial-glia determinant, was consistently suppressed from the earliest stage onward, and cerebral organoids subsequently generated fewer excitatory neurons in favour of inhibitory and glial lineages. These data chart a continuous developmental trajectory for MECP2-mutant human cells and nominate ZFP42 and EMX1 dysregulation as tractable entry points for dissecting Rett pathogenesis.

neuroscience↗

bioRxiv2021

Comparison of heat-inactivated and infectious SARS-CoV-2 across indoor surface materials shows comparable RT-qPCR viral signal intensity and persistence

Environmental monitoring in public spaces can be used to identify surfaces contaminated by persons with COVID-19 and inform appropriate infection mitigation responses. Research groups have reported detection of Severe Acute Respiratory Syndrome Coronavirus 2 (SARS-CoV-2) on surfaces days or weeks after the virus has been deposited, making it difficult to estimate when an infected individual may have shed virus onto a SARS-CoV-2 positive surface, which in turn complicates the process of establishing effective quarantine measures. In this study, we determined that reverse transcription-quantitative polymerase chain reaction (RT-qPCR) detection of viral RNA from heat-inactivated particles experiences minimal decay over seven days of monitoring on eight out of nine surfaces tested. The properties of the studied surfaces result in RT-qPCR signatures that can be segregated into two material categories, rough and smooth, where smooth surfaces have a lower limit of detection. RT-qPCR signal intensity (average quantification cycle (Cq)) can be correlated to surface viral load using only one linear regression model per material category. The same experiment was performed with infectious viral particles on one surface from each category, with essentially identical results. The stability of RT-qPCR viral signal demonstrates the need to clean monitored surfaces after sampling to establish temporal resolution. Additionally, these findings can be used to minimize the number of materials and time points tested and allow for the use of heat-inactivated viral particles when optimizing environmental monitoring methods. ImportanceEnvironmental monitoring is an important tool for public health surveillance, particularly in settings with low rates of diagnostic testing. Time between sampling public environments, such as hospitals or schools, and notifying stakeholders of the results should be minimal, allowing decisions to be made towards containing outbreaks of coronavirus disease 2019 (COVID-19). The Safer At School Early Alert program (SASEA) [1], a large-scale environmental monitoring effort in elementary school and child care settings, has processed > 13,000 surface samples for SARS-CoV-2, detecting viral signals from 574 samples. However, consecutive detection events necessitated the present study to establish appropriate response practices around persistent viral signals on classroom surfaces. Other research groups and clinical labs developing environmental monitoring methods may need to establish their own correlation between RT - qPCR results and viral load, but this work provides evidence justifying simplified experimental designs, like reduced testing materials and the use of heat-inactivated viral particles.

microbiology↗

bioRxiv2021

Gene regulatory networks underlying human microglia maturation

The fetal period is a critical time for brain development, characterized by neurogenesis, neural migration, and synaptogenesis1-3. Microglia, the tissue resident macrophages of the brain, are observed as early as the fourth week of gestation4 and are thought to engage in a variety of processes essential for brain development and homeostasis5-11. Conversely, microglia phenotypes are highly regulated by the brain environment12-14. Mechanisms by which human brain development influences the maturation of microglia and microglia potential contribution to neurodevelopmental disorders remain poorly understood. Here, we performed transcriptomic analysis of human fetal and postnatal microglia and corresponding cortical tissue to define age-specific brain environmental factors that may drive microglia phenotypes. Comparative analysis of open chromatin profiles using bulk and single-cell methods in conjunction with a new computational approach that integrates epigenomic and single-cell RNA-seq data allowed decoding of cellular heterogeneity with inference of subtype- and development stage-specific transcriptional regulators. Interrogation of in vivo and in vitro iPSC-derived microglia models provides evidence for roles of putative instructive signals and downstream gene regulatory networks which establish human-specific fetal and postnatal microglia gene expression programs and potentially contribute to neurodevelopmental disorders.

genomics↗

bioRxiv2018

An Atlas of Human and Murine Genetic Influences on Osteoporosis

Osteoporosis is a common debilitating chronic disease diagnosed primarily using bone mineral density (BMD). We undertook a comprehensive assessment of human genetic determinants of bone density in 426,824 individuals, identifying a total of 518 genome-wide significant loci, (301 novel), explaining 20% of the total variance in BMD--as estimated by heel quantitative ultrasound (eBMD). Next, meta-analysis identified 13 bone fracture loci in ~1.2M individuals, which were also associated with BMD. We then identified target genes from cell-specific genomic landscape features, including chromatin conformation and accessible chromatin sites, that were strongly enriched for genes known to influence bone density and strength (maximum odds ratio = 58, P = 10-75). We next performed rapid throughput skeletal phenotyping of 126 knockout mice lacking eBMD Target Genes and showed that these mice had an increased frequency of abnormal skeletal phenotypes compared to 526 unselected lines (P < 0.0001). In-depth analysis of one such Target Gene, DAAM2, showed a disproportionate decrease in bone strength relative to mineralization. This comprehensive human and murine genetic atlas provides empirical evidence testing how to link associated SNPs to causal genes, offers new insights into osteoporosis pathophysiology and highlights opportunities for drug development.

genomics↗