Biology subjects

Mair, M.

Publications and source records attributed to Mair, M..

4 recordsLinked to original sources

bioRxiv2026

COLLEMBOT: AI-Based Counting of Collembola for OECD 232 Tests

Ecotoxicological tests with soil organisms, such as the collembolan Folsomia candida, are essential for assessing chemical risks in terrestrial ecosystems. However, the current Organization for Economic Co-operation and Development (OECD) 232 reproduction tests rely on manual counting of juvenile and adult Collembola, a process that is costly, labor-intensive, time-consuming and prone to operator bias. These limitations restrict data availability and hinder robust risk assessments. We therefore developed COLLEMBOT, an automated counting tool based on a YOLOv11 convolutional neural network, designed to integrate seamlessly into OECD workflows without protocol modifications. The model was trained on high-resolution images (n = 3207) from multiple laboratories and validated using 22 independent datasets (n = 1704 images) from Amsterdam (Netherlands), Basel (Switzerland), Bayreuth (Germany), Coimbra (Portugal) and Aarhus (Denmark). Datasets consisted of relevant standard soils (OECD artificial soils with 2.5%, 5% and 10% sphagnum peat; LUFA 2.2) and the springtail Folsomia candida. Automated counts showed strong agreement with manual counts (R{superscript 2} = 0.88-0.99). Dose-response curves derived from automated and manual counts strongly overlapped and effect concentrations (EC and EC) differed minimally (Median %{Delta} 6.2 {+/-} 23 and EC10 - EC90 R2 [≥] 0.977), remaining within acceptable limits for regulatory risk assessment and confirming reliability. Time efficiency improved significantly: a test with [~]300 images and up to 1,500 individuals per image was processed in less than 3 hours, compared to [~]137 hours needed for manual counting, a reduction of approximately 97%. By reducing labor and improving reproducibility, COLLEMBOT enables broader hazard data generation for collembolans, supporting science-based chemical risk assessment. The code and workflow are publicly available to facilitate adoption and community-driven development. O_FIG O_LINKSMALLFIG WIDTH=200 HEIGHT=187 SRC="FIGDIR/small/697653v1_ufig1.gif" ALT="Figure 1"> View larger version (131K): org.highwire.dtl.DTLVardef@1d3ddc5org.highwire.dtl.DTLVardef@84c90aorg.highwire.dtl.DTLVardef@1aaf06aorg.highwire.dtl.DTLVardef@18ddfcd_HPS_FORMAT_FIGEXP M_FIG C_FIG

ecology↗

bioRxiv2025

Modeling the effects of Huntington disease on age-related genes reveals CXXC4 as an epigenetic target to restore health and excitability of Drd1-expressing striatal neurons

Neurons adapt gene expression to counter aging, yet the mechanisms by which they harness age- related genes to resist neurodegenerative disease remain elusive. We found that transcriptionalaging inversion (TAGI) in the Drd1-expressing striatal neurons (Drd1 SNs) of Huntingtons disease (HD) knock-in (Hdh) mice exhibits discrete patterns against a TAG-like (TAGL) signature. Strikingly, TAGI dynamics may explain disease progression more accurately than TAGL. Moreover, in Drd1 SNs, genes affected by 3UTR accumulation during aging are predisposed to downregulation in aging and deregulation in Hdh mice. By integrating age-related 3UTR data and Hdh-mice data, we identified a CAG-repeat-dependent network of upregulated genes with compensatory potential. This network features (i) Atad-5, a P CNA unloader that modifies CAG expansion in human HD plasma samples, and (ii) CXXC4 (IDAX), an epigenetic regulator whose early-stage upregulation is lost as behavioral symptoms worsen in Hdh mice. Functionally, CXXC4 reduces the senescence marker p16INK4a and restores glutamate excitability in human HD iPS cell-derived SNs. Collectively, these findings suggest that Drd1 SN resilience capacity against HD relies on discrete age-related patterns and responses transiently activated in early disease stages. The reactivation of specific age-related genes such as CXXC4 may notably restore cortico-striatal function in HD.

neuroscience↗

bioRxiv2025

Status of Florida's pillar coral population: in situ declines and ex situ successes

The population of the pillar coral, Dendrogyra cylindrus, in Florida was decimated from 2013-2020, primarily by the emergence of stony coral tissue loss disease (SCTLD). Monitoring of survivors from 2021 - early 2025 showed that the population underwent an additional 96% decline in live tissue, 78% loss in living colonies, and 57% loss of genotypes. SCTLD continued to be the primary cause of these losses. Though some surviving tissue isolates exhibited small amounts of growth, the population remains extremely small, with only an estimated 9.6 square meters of tissue remaining on 23 colonies (15 genotypes). Additionally, colonies are far too dispersed to successfully fertilize spawned gametes. The further declines in the population since 2020 highlight the instability of the remnant population, as well as the value of the pillar coral rescue program and ongoing propagation efforts. As of February 2025, eight different in situ and ex situ facilities were caring for rescued D. cylindrus. Experimental fragmentation at one in situ nursery identified variable, but continually increasing, growth rates across multiple fragmentation events. Sexual propagation efforts at an ex situ nursery documented 105 different rescue fragments spawning across five years. The smallest fragment was 9 x 7 x 9 cm, establishing a potential "minimum colony size" for reproductive capacity for this species. From these spawning events, 82 juveniles were being raised ex situ in early 2025. Two of these sexually propagated juveniles spawned six years after settlement, thus establishing a potential minimum age for reproduction.

ecology↗

bioRxiv2020

Modulating glial genes involved in synaptic function mitigates pathogenesis and behavioral deficits in a Drosophila model of Huntington's Disease

Most research on neurodegenerative diseases has focused on neurons, yet glia help form and maintain the synapses whose loss is so prominent in these conditions. To investigate the contributions of glia to Huntingtons disease (HD), we studied transcriptomic changes in HD human, HD mice, and Drosophila expressing human mutant Huntingtin (mHTT) in either glia, neurons or both. A large portion of conserved genes are concordantly dysregulated across the three species; we tested these genes in a high-throughput behavioral assay and found that downregulation of genes involved in synapse assembly mitigated pathogenesis and behavioral deficits. To our surprise, mitigating glial pathogenesis by dNRXN3 knockdown was sufficient to improve the phenotype of flies expressing mHTT in neurons, suggesting that mHTTs toxic effects in glia ramify throughout the brain. This supports a model in which dampening synaptic function is protective because it attenuates the excitotoxicity that characterizes HD.

systems biology↗