Unlabelled: Class IV ddaC neurons specifically prune larval dendrites without affecting axons during metamorphosis. ddaCs distribute the minus ends of microtubules (MTs) to dendrites but the plus ends to axons. However, a requirement of MT minus-end-binding proteins in dendrite-specific pruning remains completely unknown. Here, we identified Patronin, a minus-end-binding protein, for its crucial and dose-sensitive role in ddaC dendrite pruning. The CKK domain is important for Patronin's function in dendrite pruning. Moreover, we show that both knockdown and overexpression resulted in a drastic decrease of MT minus ends and a concomitant increase of plus-end-out MTs in ddaC dendrites, suggesting that Patronin stabilizes dendritic minus-end-out MTs. Consistently, attenuation of Klp10A MT depolymerase in mutant neurons significantly restored minus-end-out MTs in dendrites and thereby rescued dendrite-pruning defects. Thus, our study demonstrates that Patronin orients minus-end-out MT arrays in dendrites to promote dendrite-specific pruning mainly through antagonizing Klp10A activity.
Editorial Note: This article has been through an editorial process in which the authors decide how to respond to the issues raised during peer review. The Reviewing Editor's assessment is that minor issues remain unresolved (see decision letter).
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http://dx.doi.org/10.7554/eLife.39964 | DOI Listing |
Trends Biochem Sci
January 2025
Research Group Neuroplasticity, Leibniz Institute for Neurobiology, Magdeburg, Germany; Leibniz Group 'Dendritic Organelles and Synaptic Function', Center for Molecular Neurobiology, ZMNH, University Medical Center Hamburg-Eppendorf, Hamburg, Germany; Center for Behavioral Brain Sciences, Otto von Guericke University, Magdeburg, Germany; German Center for Neurodegenerative Diseases (DZNE), Magdeburg, Germany. Electronic address:
The brain is an exceptionally lipid-rich organ with a very complex lipid composition. Lipids are central in several neuronal processes, including membrane formation and fusion, myelin packing, and lipid-mediated signal transmission. Lipid diversity is associated with the evolution of higher cognitive abilities in primates, is affected by neuronal activity, and is instrumental for synaptic plasticity, illustrating that lipids are not static components of synaptic membranes.
View Article and Find Full Text PDFeNeuro
January 2025
University of Rochester Medical Center, Department of Neuroscience,
A unique pool of immature glutamatergic neurons in the primate amygdala, known as the paralaminar nucleus (PL), are maturing between infancy and adolescence. The PL is a potential substrate for the steep growth curve of amygdala volume during this developmental period. A microglial component is also embedded among the PL neurons, and likely supports local neuronal maturation and emerging synaptogenesis.
View Article and Find Full Text PDFJ Neurosci
January 2025
Institute of Neuroimmunology, Slovak Academy of Science, 84510 Bratislava, Slovakia.
Extracellular matrix (ECM) is a network of macromolecules which has two forms - perineuronal nets (PNNs) and a diffuse ECM (dECM) - both influence brain development, synapse formation, neuroplasticity, CNS injury and progression of neurodegenerative diseases. ECM remodeling can influence extrasynaptic transmission, mediated by diffusion of neuroactive substances in the extracellular space (ECS). In this study we analyzed how disrupted PNNs and dECM influence brain diffusibility.
View Article and Find Full Text PDFSci Adv
January 2025
Laboratory of Neurobiology of Emotions, Nencki-EMBL Partnership for Neural Plasticity and Brain Disorders-BRAINCITY, Nencki Institute of Experimental Biology of Polish Academy of Sciences, Warsaw, Poland.
Being part of a social structure offers chances for social learning vital for survival and reproduction. Nevertheless, studying the neural mechanisms of social learning under laboratory conditions remains challenging. To investigate the impact of socially transmitted information about rewards on individual behavior, we used Eco-HAB, an automated system monitoring the voluntary behavior of group-housed mice under seminaturalistic conditions.
View Article and Find Full Text PDFAlzheimers Dement
December 2024
Affiliated Drum Tower Hospital of Nanjing University Medical School, Nanjing, China.
Background: Compelling evidence has shown that long non-coding RNAs (lncRNAs) contribute to Alzheimer's disease (AD) pathogenesis including β-amyloid plaque deposition (Aβ) and intracellular neurofibrillary tangles. In this study, we aimed to investigate the critical role of lncRNA Gm20063 in AD.
Method: Six-month-old male APP/PS1 transgenic mice and wild type (WT) C57BL/6 (B6) littermates were obtained from the Nanjing University Animal Model Research Center.
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