Biology subjects

Schott, M.

Publications and source records attributed to Schott, M..

6 recordsLinked to original sources

bioRxiv2026

Microplastics Disrupt Predator-Induced Plasticity in Daphnia across Behavioral, Morphological and Molecular Levels

Microplastics (MP) are widespread in aquatic ecosystems and pose a threat to freshwater biodiversity. While numerous studies examine physiological effects on aquatic organisms, less is known about how MP alter chemically mediated interactions that regulate predator-prey dynamics. Predator-induced defenses in Daphnia depend on detecting kairomones and represent an important form of adaptive phenotypic plasticity. Whether MP interfere with these responses, and through which mechanisms, remains unclear. Here, we show that polystyrene MP impair predator-induced defenses across Daphnia species by disrupting predator-cue-mediated plasticity at the behavioral, morphological, and molecular levels. In D. longicephala, chronic exposure to PS fragments weakened Notonecta-induced morphological defenses, whereas additive-containing PS fragments nearly suppressed defense formation and reduced body size. Consistent with these phenotypic effects, proteomic analyses revealed alterations in pathways related to molting and chitin metabolism, linking MP exposure to impaired defense formation. In D. magna, PS particles attenuated fish kairomone-induced diel vertical migration, with stronger effects for larger particles, consistent with reduced effective availability or perception of predator cues. Natural limestone particles caused only minor effects, indicating particle-specific rather than general particle-driven responses. Our findings demonstrate that MP can disrupt adaptive predator-prey interactions with potential cascading consequences for freshwater food webs.

zoology↗

bioRxiv2026

Chemical toxicity of microplastics is stronger than particle effects in D. magna

Microplastics (MP) are ubiquitous environmental contaminants with diverse physicochemical characteristics. Many studies have shown that size, shape, and polymer type are responsible for their toxicity, but this also seems to differ among MP from the same plastic type. One parameter likely contributing to these differences is plastic chemicals, a broad class of compounds intentionally or unintentionally added to plastics during their production and manufacturing. However, knowledge on the composition of plastic chemicals and their effects remains scarce. Therefore, to elucidate the chemical aspect of MP toxicity, we exposed Daphnia magna individuals to MP (PET, PBS, and PDLLA), cellulose, extracted particles (eMP), and methanol-based extracts of these particles for 10 days. Chemicals within such extracts were analyzed via GC-MS. This study was conducted with reduced food availability to investigate plastic effects in an environmentally relevant scenario. The introduction of a high-food control suggests that a more realistic feeding regime might exacerbate the plastic effects of the selected treatments. Our results indicated that, depending on the polymer type, plastic chemicals determine MP toxicity, which varies according to the endpoint investigated (i.e., body length, reproduction, levels of ROS and LPO). Body length, in particular, was significantly impaired by PET and PDLLA extracts, whereas reproduction was affected by most treatments. The investigated biochemical parameters (ROS and LPO) were not affected by the exposure. These results suggest that MP toxicity strongly depends on their chemical composition, whereas adverse effects due to physical properties are present independently of chemical composition across all MP types. Graphical Abstract O_FIG O_LINKSMALLFIG WIDTH=200 HEIGHT=80 SRC="FIGDIR/small/724551v1_ufig1.gif" ALT="Figure 1"> View larger version (23K): org.highwire.dtl.DTLVardef@b6ecc8org.highwire.dtl.DTLVardef@17366d7org.highwire.dtl.DTLVardef@164d3f4org.highwire.dtl.DTLVardef@973af0_HPS_FORMAT_FIGEXP M_FIG C_FIG

ecology↗

bioRxiv2025

Lineage origin and microenvironment shape neuroblastoma transcriptional state and plasticity

Neuroblastoma, a neural-crest-derived malignancy of the peripheral nervous system, is a devastating pediatric disease characterized by high intra- and intertumoral heterogeneity. While several tumor expression programs correlate with patient outcome, the developmental and contextual determinants of their emergence remain incompletely understood. Here, we systematically dissected neuroblastoma transcriptional heterogeneity and measured how tumor expression programs are associated with lineage history and developmental context. To achieve this, we combined single-cell transcriptomics with high-throughput lineage tracing and tumor cell transplantation in zebrafish models of MYCN-driven neuroblastoma. We identified developmental cell-state-associated programs that align with sympathoadrenal development, as well as general cellular-process programs. Clonal analysis showed that developmental programs are preferentially clone-associated, whereas cellular-process programs are more context-responsive. Transplantation into an embryonic environment reshaped the activation of several initially clone-associated programs, consistent with developmentally determined state reconfiguration and/or selection of state-competent cells. Together, our results show that lineage history and developmental context jointly shape tumor-state architecture in vivo.

cancer biology↗

bioRxiv2025

Spatiotemporal dynamics of tumor microenvironment remodelling

During tumorigenesis, interactions between tumor and stromal cells progressively remodel the tumor microenvironment (TME) towards pro-tumoral functions. Understanding early TME remodeling dynamics is therefore crucial for developing interceptive therapies. However, clinical samples typically provide isolated, late tumorigenesis snapshots. To overcome this limitation, we generated triple-negative breast cancer mice that develop multifocal, asynchronous tumors along a continuous luminal-to-basal transdifferentiation trajectory. Ordering spatial transcriptomes from 100+ ducts along this trajectory reveals the spatiotemporal dynamics of TME remodeling and underlying molecular mechanisms. Cancer-associated myofibroblasts (myCAFs) emerge as key players in advanced tumors, where they orchestrate pro-invasive remodeling of the tumor-stromal interface. myCAFs are conserved in patient-derived xenograft models and steer tumor trajectories towards invasive phenotypes when co-injected with tumor cells in syngeneic mice. Our study shows that temporal ordering of spatially-resolved disease snapshots unravels some of the molecular "forces" that, starting from the cell-of-origin, propel cells/microenvironments along a disease trajectory.

cancer biology↗

bioRxiv2025

AKAP12 variant 1 knockout enhances vascular endothelial cell motility

In this study, we examined the role of AKAP12, in endothelial cell motility, with a specific focus on AKAP12 variants AKAP12v1 and AKAP12v2. Previous work has shown that AKAP12, a multivalent A-kinase anchoring protein that binds to PKA and several other proteins regulating protein phosphorylation, is expressed at low levels in most endothelia in vivo but at higher levels in cells in vitro. Here, we found that AKAP12 expression in endothelial cell (HUVEC) cultures was cell density-dependent, with the expression being highest in subconfluent cultures and lowest in confluent cultures. AKAP12 expression was also elevated in cells at the wound edge of wounded endothelial cell monolayers. Knockdown of variants 1 and 2 inhibited cell migration, whereas CRISPR/Cas9 knockout of AKAP12v1 enhanced migration, indicating that the absence of this variant and the presence of AKAP12v2 may shift the signaling pathways. Further analysis using bulk RNA sequencing revealed that the loss of AKAP12v1 affects genes associated with cell migration and intercellular junctions. We propose that AKAP12v1 and AKAP12v2 work together to modulate endothelial cell migration, providing insights into their distinct yet complementary roles in endothelial function and potential implications for cardiovascular health.

cell biology↗

bioRxiv2023

Open-ST: High-resolution spatial transcriptomics in 3D

Spatial transcriptomics (ST) methods have been developed to unlock molecular mechanisms underlying tissue development, homeostasis, or disease. However, there is a need for easy-to-use, high-resolution, cost-efficient, and 3D-scalable methods. Here, we report Open-ST, a sequencing-based, open-source experimental and computational resource to address these challenges and to study the molecular organization of tissues in 3D. In mouse brain, Open-ST captured transcripts at subcellular resolution and reconstructed cell types. In primary tumor and patient-matched healthy/metastatic lymph nodes, Open-ST captured the diversity of immune, stromal and tumor populations in space. Distinct cell states were organized around cell-cell communication hotspots in the tumor, but not the metastasis. Strikingly, the 3D reconstruction and multimodal analysis of the metastatic lymph node revealed spatially contiguous structures not visible in 2D and potential biomarkers precisely at the 3D tumor/lymph node boundary. We anticipate Open-ST to accelerate the identification of spatial molecular mechanisms in 2D and 3D.

systems biology↗