Articles by Cagri Yalgin in JoVE
Immunohistological Märkning av mikrotubuli i sensoriska neuron dendriter, Tracheae och muskler i Drosophila Larva Body Wall Cagri Yalgin1,2, M. Rezaul Karim1,2, Adrian W. Moore1 1Disease Mechanism Research Core, RIKEN Brain Science Institute, 2Graduate School of Science and Engineering, Saitama University För att förstå hur komplexa cell former som neuronala dendriter, uppnås under utveckling är det viktigt att kunna korrekt analys mikrotubuli organisation. Här beskriver vi ett robust immunohistological märkning metod för att undersöka mikrotubuli organisation av dendritiska sensoriska arborization neuron dendriter, luftstrupe, muskler och andra
Other articles by Cagri Yalgin on PubMed
Selection of Behaviors and Segmental Coordination During Larval Locomotion is Disrupted by Nuclear Polyglutamine Inclusions in a New Drosophila Huntington's Disease-like Model Journal of Neurogenetics. Dec, 2010 | Pubmed ID: 21087194 Huntington's disease is an autosomal dominant neurodegenerative disorder that is caused by abnormal expansion of a polyglutamine tract in the huntingtin protein, resulting in intracellular aggregate formation and neurodegeneration. How neuronal cells are affected by such a polyglutamine tract expansion remains obscure. To dissect the ways in which polyglutamine expansion can cause neural dysfunction, the authors generated Drosophila transgenic strains expressing either a nuclear targeted or cytoplasmic form of pathogenic (NHtt-152Q(NLS), NHtt-152Q), or nonpathogenic (NHtt-18Q(NLS), NHtt-18Q) N-terminal human huntingtin. These proteins were expressed in the dendritic arborization neurons of the larval peripheral nervous system and their effects on neuronal survival, morphology, and larval locomotion were examined. The authors found that NHtt-152Q(NLS) larvae had altered dendrite morphology and larval locomotion, whereas NHtt-152Q, NHtt-18Q(NLS), and NHtt-18Q larvae did not. Furthermore, the authors examined the physiological defect underlying this disrupted larval locomotion in detail by recording spontaneous ongoing segmental nerve activity. NHtt-152Q(NLS) larvae displayed uncoordinated activity between anterior and posterior segments. Moreover, anterior segments had shorter bursts and longer interburst intervals in NHtt-152Q(NLS) larvae than in NHtt-18Q(NLS) larvae, whereas posterior segments had longer bursts and shorter interburst intervals. These results suggest that the pathogenic protein disrupts neuron function without inducing cell death, and describe how this dysfunction leads to a locomotor defect. These results also suggest that sensory inputs are necessary for the coordination of anterior and posterior body parts during locomotion. From these analyses the authors show that examination of motor behaviors in the Drosophila larvae is a powerful new model to dissect non-cell-lethal mechanisms of mutant Htt toxicity.