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Bertram, S.

Publications and source records attributed to Bertram, S..

2 recordsLinked to original sources

The disadvantage of having a big mouth: the relationship between insect body size and microplastic ingestion

Plastic pollution is ubiquitous, and animals are exposed to diverse plastic shapes and sizes. When plastics enter natural environments, they break down into microplastics (MPs; <5 mm) and likely become more accessible to smaller animals. Insects play critical environmental and economic roles, ingest plastics in the wild, and can physically degrade ingested MPs into smaller and more harmful nanoplastics. While particle size and body size undoubtedly impact plastic ingestion, we have no predictive understanding of how these factors interact to influence which plastics are a threat to which animals. To uncover these potential interactions, we studied how a model cricket species (Gryllodes sigillatus) interacts with plastics of differing sizes throughout a twentyfold change in body size during growth and development. We fed crickets a range of MP sizes of 38 to 500 {micro}m with clearly defined particle size thresholds. We investigated whether crickets would avoid MPs when given a choice and found that they do not; instead they gradually began to consume more of the plastic diet over time. We then studied how MP ingestion is influenced by body size and mouth size, and the extent of breakdown that occurs once MPs are ingested. We found that crickets would only consume whole beads when their mouth size was larger than the MP. While small MPs were more likely to be excreted whole, larger MPs were more extensively broken down as crickets grew. We conclude that crickets do not exhibit avoidance behaviour towards plastic and ingest it once a particle can be consumed whole. These effects of insect behaviour and body size on the likelihood of plastic ingestion and the degree to which MPs are degraded have important implications for regulating the size classes of plastic particles entering natural environments and how plastics move through those environments once discarded.

physiology↗

Super-enhancer-driven CACNA2D2 is an EWSR1::WT1 signature gene encoding a diagnostic marker for desmoplastic small round cell tumor (DSRCT)

Desmoplastic small round cell tumor (DSRCT) is a highly aggressive cancer predominantly occurring in male adolescents and young adults. The lack of a comprehensive understanding on the biology of the disease is paralleled by its dismal survival rates (5-20%). To overcome this challenge, we first identified and prioritized urgently needed resources for clinicians and researchers. Thus, we established genome-wide single-cell RNA-sequencing and bulk proteomic data of in vitro and in vivo-generated knockdown models of the pathognomonic DSRCT fusion oncoprotein (EWSR1::WT1) and combined them with an original systems-biology-based pipeline including patient data and the largest histology collection of DSRCTs and morphological mimics available to date. These novel tools were enriched with curated public datasets including patient- and cell line-derived ChIP-seq, bulk and single-cell RNA-seq studies resulting in a multi-model and multi-omic toolbox for discovery analyses. As a proof of concept, our approach revealed the alpha-2/delta subunit of the voltage-dependent calcium channel complex, CACNA2D2, as a highly overexpressed, super-enhancer driven, direct target of EWSR1::WT1. Single-cell and bulk-level analyses of patient samples and xenografted cell lines highlighted CACNA2D2 as a critical component of our newly established EWSR1::WT1 oncogenic signature, that can be employed to robustly identify DSRCT in reference sets. Finally, we show that CACNA2D2 is a highly sensitive and specific single biomarker for fast, simple, and cost-efficient diagnosis of DSRCT. Collectively, we establish a large-scale multi-omics dataset for this devastating disease and provide a blueprint of how such toolbox can be used to identify new and clinically relevant diagnostic markers, which may significantly reduce misdiagnoses, and thus improve patient care.

cancer biology↗