Lysosomal Hydrolase Cathepsin D Non-proteolytically Modulates Dendritic Morphology in Drosophila
Autor: | Ting Zhang, Liya Zhu, Daxiao Cheng, Xingyue Wang, Qiang Ke, Cunjin Wu, Yi-Jun Liu, Shumin Duan, Huifang Lou, Xiao-Dong Wang |
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Rok vydání: | 2019 |
Předmět: |
0301 basic medicine
Nervous system Central Nervous System Physiology Cathepsin D 03 medical and health sciences 0302 clinical medicine Dendritic arborization medicine Animals Drosophila Proteins Tissue homeostasis Actin Gene knockdown Sensory neuron Cell growth Chemistry General Neuroscience General Medicine Dendrites Mushroom body Cell biology 030104 developmental biology medicine.anatomical_structure Mushroom bodies Drosophila Original Article Lysosomes 030217 neurology & neurosurgery |
Zdroj: | Neuroscience Bulletin |
ISSN: | 1995-8218 |
Popis: | The main lysosomal protease cathepsin D (cathD) is essential for maintaining tissue homeostasis via its degradative function, and its loss leads to ceroid accumulation in the mammalian nervous system, which results in progressive neurodegeneration. Increasing evidence implies non-proteolytic roles of cathD in regulating various biological processes such as apoptosis, cell proliferation, and migration. Along these lines, we here showed that cathD is required for modulating dendritic architecture in the nervous system independent of its traditional degradative function. Upon cathD depletion, class I and class III arborization (da) neurons in Drosophila larvae exhibited aberrant dendritic morphology, including over-branching, aberrant turning, and elongation defects. Re-introduction of wild-type cathD or its proteolytically-inactive mutant dramatically abolished these morphological defects. Moreover, cathD knockdown also led to dendritic defects in the adult mushroom bodies, suggesting that cathD-mediated processes are required in both the peripheral and central nervous systems. Taken together, our results demonstrate a critical role of cathD in shaping dendritic architecture independent of its proteolytic function. Electronic supplementary material The online version of this article (10.1007/s12264-020-00479-6) contains supplementary material, which is available to authorized users. |
Databáze: | OpenAIRE |
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