Unterholzner, Jonas J.

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Unterholzner, Jonas J.
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jonas.unterholzner@hs-bremen.de
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2025 - 20263

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    Item-typ:Veröffentlichung,
    Wound-induced reactivation of developmental cuticle programmes in mature insects
    (The Royal Society, 2026-06)
    Unterholzner, Jonas J.
    ;
    Dirks, Jan-Henning
    The insect cuticle exoskeleton is among the most abundant and versatile biological structures. During ontogeny, the cuticle undergoes extensive modification, enabling insects to adapt to a wide range of ecological niches. In contrast, cuticular remodelling is generally thought to cease after adult emergence, raising the question of how mature insects respond to damage to their exoskeleton. To address this fundamental issue, we used an interdisciplinary experimental approach combining biomechanics, quantitative image analysis and molecular biology to investigate the response of mature Locusta migratoria to cuticular injury. We show that deep tibial wounds penetrating the epidermis trigger a coordinated repair programme that integrates rapid sclerotization of the perilesional cuticle with the local deposition of newly synthesized, layered cuticle beneath the wound site. These structural responses are accompanied by a strong but transient reactivation of the developmental enzyme chitin synthase 1 and the induction of the antimicrobial peptide defensin 3 in the vicinity of the injury. In contrast, superficial injuries that do not reach the epidermis fail to elicit cuticle deposition and sclerotization. Together, our results demonstrate that mature insects retain the capacity to locally reactivate developmental cuticle pathways to restore exoskeletal integrity, thereby directly linking structural repair with immune activation.
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      35
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    Advancing Research on Biomaterials and Biological Materials with Scanning Electron Microscopy under Environmental and Low Vacuum Conditions
    (Wiley, 2025-12)
    Riedel, Jendrian
    ;
    Dierker, Lea
    ;
    Kwame, Antoine Eyram
    ;
    Wagner, Kim Nora
    ;
    Unterholzner Jonas J
    In this article, a general introduction to the fundamental principles of environmental scanning electron microscopy (ESEM) is given and its advantages in comparison to conventional SEM is illustrated through selected application examples from life sciences, focusing on biomaterial research and biology. Conventional SEM is a well-established and widely used technique to characterize material properties and surface structures in a variety of research fields. However, due to the high vacuum conditions used in conventional SEM, imaging delicate, nonconductive, and/or wet samples—which are particularly prevalent in life sciences—normally requires extensive sample preparation, such as critical point drying and sputter-coating, which can alter the sample properties. Here, ESEM offers a convenient solution, where nonconductive and wet biological samples can be imaged in their near-native state almost without sample preparation. The advantages of ESEM compared to conventional SEM for life sciences based on examples from literature and new application examples from biomaterials science and zoology are illustrated. Finally, recent advances in automated imaging and AI-based image processing are beginning to extend the current limits of resolution and sample stability in ESEM, potentially enabling more precise, real-time, and less damaging imaging of hydrated and beam-sensitive materials in future studies.
    Wissenschaftlicher Artikel
      96
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    The Gb3-synthase A4GALT is an epigenetically regulated driver of tumor invasiveness in gastrointestinal cancer
    (Springer Science and Business Media LLC, 2026-01-27)
    Hirsch, Noah-David
    ;
    Perl, Markus
    ;
    Holzinger, Simon
    ;
    Barz, Christoph
    ;
    Enßle, Stefan
    Background Tumor lipid metabolism has emerged as a critical, yet underexplored, determinant of cancer progression with clinical and prognostic importance. A membrane lipid species of particular interest is globotriaosylceramide (Gb3/CD77), a glycosphingolipid that serves as cellular receptor for the bacterial Shiga toxins, and is upregulated in various malignancies. While preclinical studies have suggested a pro-tumorigenic role for Gb3, the regulatory drivers of its biosynthesis in human tumors have remained elusive. Methods The glycosyltransferase A4GALT, responsible for Gb3 biosynthesis, and the degrading enzyme α-galactosidase A (α-GLA) are two essential molecular determinants of Gb3 cell surface expression. Expression of these enzymes was analyzed on mRNA level in tissues from colorectal cancer, published datasets from gastric, pancreatic, esophageal and colorectal cancer (1213 patients) and in human cell lines. Pharmacological manipulation in vitro using the hypomethylating agent 5-Aza-2-deoxycytidine and histone deacetylase (HDAC) inhibitors induced A4GALT expression in DLD1 colon cancer cells and Gb3 biosynthesis. A4GALT deficiency was induced by CRISPR-Cas9 mutagenesis in human HCT116 colon cancer cells, and its putative effects tested for proliferation, cell migration and invasion. Results A4GALT deficiency in HCT116 cells confirmed its essential role for Gb3 biosynthesis, leading to resistance against Shiga toxin 1a, and to reduced cancer cell migration and invasion. Gene enrichment analyses revealed that high A4GALT and low α-GLA expression is associated with a distinct gene expression program in gastric, pancreatic and colorectal cancer, including increased signatures of epithelial–mesenchymal transition. A4GALT expression is regulated by chromatin accessibility and DNA methylation at a defined intronic enhancer. In accordance, pan‑cancer analysis of TCGA datasets validated the A4GALT‑high/α‑GLA‑low signature as a negative prognostic indicator across gastrointestinal tumor entities. Conclusions Our study uncovers an epigenetically regulated lipid metabolic axis involving A4GALT and Gb3 that contributes to aggressive tumor behavior. Of note, this pathway may be therapeutically targetable using natural or synthetic Shiga toxin B-subunit derivatives.
    Wissenschaftlicher Artikel
    Band:26
      17