Dokument: Host mechanisms controlling bacterial colonization in the sea anemone Nematostella vectensis
Titel: | Host mechanisms controlling bacterial colonization in the sea anemone Nematostella vectensis | |||||||
URL für Lesezeichen: | https://docserv.uni-duesseldorf.de/servlets/DocumentServlet?id=70593 | |||||||
URN (NBN): | urn:nbn:de:hbz:061-20250904-134843-3 | |||||||
Kollektion: | Dissertationen | |||||||
Sprache: | Englisch | |||||||
Dokumententyp: | Wissenschaftliche Abschlussarbeiten » Dissertation | |||||||
Medientyp: | Text | |||||||
Autor: | Kaya, Nida Hatice [Autor] | |||||||
Dateien: |
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Beitragende: | Prof. Dr. Fraune, Sebastian [Betreuer/Doktorvater] Prof. Dr. Axmann, Ilka Maria [Gutachter] | |||||||
Dewey Dezimal-Klassifikation: | 500 Naturwissenschaften und Mathematik » 570 Biowissenschaften; Biologie | |||||||
Beschreibung: | Animals exist as dynamic ecosystems, shaped by intricate partnerships between hosts and their microbial communities. This thesis investigates the host mechanisms that control bacterial colonization in the early-diverging sea anemone Nematostella vectensis, uncovering how innate immune structures, metabolic cues, and transcriptional regulators orchestrate microbial regulation in the absence of adaptive immunity. In the first chapter, I demonstrate that host nutritional status profoundly influences microbial community structure. Starvation leads to a significant reduction in microbial diversity and the selection for stress-tolerant bacterial taxa, whereas continuous feeding promotes microbial proliferation and compositional flexibility. Notably, feeding with germfree Artemia larvae resulted in a strong increase in bacterial abundance, suggesting that Nematostella actively stimulates microbial proliferation through host-mediated environmental changes rather than passive microbial introduction. In the second chapter, I identify nematosomes—motile multicellular structures in the gastric cavity—as key players in bacterial degradation. Nematosomes selectively phagocytose foreign bacteria while sparing native colonizers, revealing an unexpected level of innate immune specificity. The transcription factor cJUN emerges as a critical regulator of nematosome proliferation and function. CRISPR/Cas9-mediated knockout of cJUN impaired lysosomal activation during phagocytosis and led to dysbiosis, with altered microbial community composition dominated by non-native strains. These findings highlight cJUN as a central node linking immune recognition, phagocytosis, and microbial homeostasis. In the third chapter, I show that nematosomes exhibit memory-like immune behavior after microbial exposure. Nematosomes previously colonized by specific bacterial strains displayed reduced phagocytic and lysosomal responses upon re-encounter with the same strain but maintained full responsiveness to heterologous strains. This strain-specific modulation, abolished in cJUN-deficient polyps, resembles trained immunity—a phenomenon where innate immune cells adapt functionally based on prior microbial encounters. These results suggest that mechanisms of immune training and tolerance are deeply rooted in early metazoan evolution. Together, this work establishes Nematostella vectensis as a powerful model for studying the evolution of innate immune plasticity and host-microbe regulation. It reveals that even basal animals employ complex immune strategies to sculpt their microbial communities—strategies that integrate environmental sensing, selective phagocytosis, and transcriptional memory. By uncovering ancient immune mechanisms of bacterial control, this thesis reframes innate immunity not as a static, nonspecific defense, but as a dynamic, adaptive interface between host and microbiota, honed by millions of years of co-evolution. | |||||||
Lizenz: | ![]() Dieses Werk ist lizenziert unter einer Creative Commons Namensnennung 4.0 International Lizenz | |||||||
Fachbereich / Einrichtung: | Mathematisch- Naturwissenschaftliche Fakultät | |||||||
Dokument erstellt am: | 04.09.2025 | |||||||
Dateien geändert am: | 04.09.2025 | |||||||
Promotionsantrag am: | 08.05.2025 | |||||||
Datum der Promotion: | 23.07.2025 |