Scopus İndeksli Yayınlar Koleksiyonu / Scopus Indexed Publications Collection

Permanent URI for this collectionhttps://hdl.handle.net/11147/7148

Browse

Search Results

Now showing 1 - 2 of 2
  • Article
    Citation - WoS: 1
    Citation - Scopus: 1
    The Role of Trna Fragments on Neurogenesis Alteration by H2o2-Induced Oxidative Stress
    (Springernature, 2025) Karacicek, Bilge; Katkat, Esra; Binokay, Leman; Ozhan, Gunes; Karakulah, Goekhan; Genc, Sermin
    Transfer RNAs (tRNAs) are small non-coding RNA molecules transcribed from tRNA genes. tRNAs cleaved into a diverse population tRNA fragments (tRFs) ranging in length from 18 to 40 nucleotides, they interact with RNA binding proteins and influence the stability and translation. Stress is one of the reasons for tRFs cleavage. In our study, we modeled oxidative stress conditions with hydrogen peroxide (H2O2) exposure and dealt with one of the frequently expressed tRF in the hippocampus region of the brain, which is tRF-Glu-CTC. For this purpose, neural stem cells (NSCs) were exposed to H2O2, and tRF-Glu-CTC levels were increased in various H(2)O(2 )concentrations. A decrease was seen in microtubule-associated protein 2 (MAP2) marker expression. To understand the H(2)O(2)oxidative stress condition on the expression of tRNA fragments, 72 hpf zebrafish embryos exposed to different H(2)O(2 )concentrations, an increase in the level of tRF-Glu-CTC was observed in all concentrations of H(2)O(2 )compared to control. Subsequently, neurogenesis markers were figured out via Calb2a (calbindin 2a) in situ hybridization (ISH) and HuC/D immunofluorescence staining (IF) staining experiments. Under H(2)O(2 )exposure, a decline was observed in Calb2a and HuC/D markers. To understand the inhibitory role of tRF-Glu-CTC on neurogenesis, NSCs were transfected via tRF-Glu-CTC inhibitor, and neurogenesis markers (ss III-tubulin, MAP2, and GFAP) were determined with qRT-PCR and IF staining. tRF-Glu-CTC inhibitor reversed the diminished neuronal markers expression under the exposure of H2O2. Gene Ontology (GO) enrichment analysis showed us that targets of tRF-Glu-CTC are generally related to neuronal function and synaptic processes.
  • Article
    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.