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Notum1a Inhibition Promotes Neurogenesis in the Adult Zebrafish Brain
(Nature Portfolio, 2025) Kocagoz, Yigit; Erdogan, Nuray Sogunmez; Ozdinc, Sevval; Ipekgil, Dogac; Katkat, Esra; Ozhan, Gunes
Notum is a carboxylesterase enzyme that modulates extracellular signaling by hydrolyzing palmitoleoyl residues from proteins, thereby influencing key pathways involved in cell differentiation, survival, and proliferation. While notum1 expression has been identified in the brain, its role in adult neurogenesis remains poorly understood. Using the adult zebrafish brain as a model system, we demonstrate that the notum1a homolog is broadly expressed across various brain cell types but is absent in undifferentiated radial glial cells. Pharmacological inhibition of Notum activity with the small molecule inhibitor ABC99 stimulates activation of radial glial cells, leading to increased neurogenesis. A BrdU pulse-chase assay confirms that ABC99-induced proliferation enhances the production of mature neurons. Despite Notum's established role in Wnt signaling, transcriptional analysis following ABC99 treatment reveals no sustained impact on Wnt pathway targets, suggesting that Notum may regulate neurogenesis through alternative mechanisms. Our findings highlight notum1a as a potential modulator of neural progenitor cell dynamics in the adult brain and suggest that targeting Notum could represent a novel therapeutic strategy for neurodegenerative conditions characterized by impaired neurogenesis.
Nanoencapsulation of Hydroxytyrosol Extract of Fermented Olive Leaf Brine Using Proniosomes
(Wiley, 2025) Kadiroglu, Pinar; Kilincli, Betul; Ilgaz, Ceren; Bayindir, Zerrin Sezgin; Kelebek, Hasim; Helvacioglu, Selin; Ozhan, Gunes
BACKGROUND: Olive leaves are rich in bioactive compounds with potential health benefits; however, their limited bioavailability and stability hinder their effective utilization. Emerging technologies, nanocarrier-based delivery systems, have shown promise in enhancing these properties. RESULTS: The optimal conditions for proniosome formulation were 50 rpm rotational speed and 35 degrees C, achieving 81.20 +/- 0.80% encapsulation efficiency. Particle sizes ranged from 188.6 to 248.9 nm, with a zeta potential of similar to-30 mV, indicating high stability and resistance to aggregation. Advanced instrumental analysis confirmed interactions between the extract and proniosome components. After 30 days at 4 degrees C, extract-loaded proniosomes maintained better homogeneity and lower polydispersity index. Cytotoxicity studies showed that both the extract and its proniosomal form were nontoxic to HEK293T cells up to 200 mu g mL(-1). In zebrafish assays, minimal larval mortality was observed up to 3200 mu g mL(-1) for the extract, while no mortality occurred up to 1600 mu g mL(-1) for the proniosomal extract, highlighting its improved safety profile. CONCLUSION: The findings from this research could contribute to the advancement of sustainable and health-promoting food innovations by integrating cutting-edge nanotechnology-driven encapsulation strategies into plant-based food formulations. (c) 2025 Society of Chemical Industry.
Citation - WoS: 1
Citation - Scopus: 2
<i>tubg1</I> Somatic Mutants Show Tubulinopathy-Associated Neurodevelopmental Phenotypes in a Zebrafish Model
(Springer, 2024) Cark, Ozge; Katkat, Esra; Aydogdu, Ipek; Iscan, Evin; Oktay, Yavuz; Ozhan, Gunes
Development of the multilayered cerebral cortex relies on precise orchestration of neurogenesis, neuronal migration, and differentiation, processes tightly regulated by microtubule dynamics. Mutations in tubulin superfamily genes have been associated with tubulinopathies, encompassing a spectrum of cortical malformations including microcephaly and lissencephaly. Here, we focus on gamma-tubulin, a pivotal regulator of microtubule nucleation encoded by TUBG1. We investigate its role in brain development using a zebrafish model with somatic tubg1 mutation, recapitulating features of TUBG1-associated tubulinopathies in patients and mouse disease models. We demonstrate that gamma-tubulin deficiency disrupts neurogenesis and brain development, mirroring microcephaly phenotypes. Furthermore, we uncover a novel potential regulatory link between gamma-tubulin and canonical Wnt/beta-catenin signaling, with gamma-tubulin deficiency impairing Wnt activity. Our findings provide insights into the pathogenesis of cortical defects and suggest that gamma-tubulin could be a potential target for further research in neurodevelopmental disorders, although challenges such as mode of action, specificity, and potential side effects must be addressed.

Scopus İndeksli Yayınlar Koleksiyonu / Scopus Indexed Publications Collection

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