Axonal transport is crucial for neuronal homeostasis, survival, and development. Indeed, axonal transport needs to be precisely regulated for developing axons to swiftly and accurately respond to their complex and evolving environment in space and time. A growing number of studies have started to unravel the diversity of regulatory and adaptor proteins required to orchestrate the axonal transport machinery. Despite some discrepancies between in vitro and in vivo axonal transport studies, most analyses aiming at deciphering these regulatory complexes, as well as their mode of action, were carried out in vitro in primary cultures of neurons, and mainly focused on their impact on axon specification and elongation, but rarely on axon navigation per se. Given the clear influence of the in vivo environment on axonal transport, including chemical and physical interactions with neighboring cells, it is essential to develop in vivo models to identify and characterize the molecular complexes involved in this key process. Here, we describe an experimental system to monitor axonal transport in vivo in developing axons of live zebrafish embryos with high spatial and temporal resolution. Due to its optical transparency and easy genetic manipulation, the zebrafish embryo is ideally suited to study such cellular dynamics at a single axon scale. Using this approach, we were able to unravel the key role of Fidgetin-like 1 in the regulation of bidirectional axonal transport required for motor axon targeting. Moreover, this protocol can be easily adapted to characterize a wide range of axonal transport regulators and components in physiological conditions and may additionally be used to screen new therapeutic compounds based on their ability to recue axonal transport defects in pathological conditions.
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http://dx.doi.org/10.1007/978-1-0716-1990-2_17 | DOI Listing |
Neuroscience
January 2025
Departamento de Genómica, Instituto de Investigaciones Biológicas Clemente Estable, MEC, Av. Italia 3318, Montevideo, CP 11600, Uruguay; Departamento de Biología Celular y Molecular, Facultad de Ciencias, Universidad de la República, Iguá, Montevideo, 4225, CP 11400, Uruguay. Electronic address:
Local protein synthesis (LPS) in axons is now recognized as a physiological process, participating both in the maintenance of axonal function and diverse plastic phenomena. In the last decades of the 20th century, the existence and function of axonal LPS were topics of significant debate. Very early, axonal LPS was thought not to occur at all and was later accepted to play roles only during development or in response to specific conditions.
View Article and Find Full Text PDFInt J Biol Sci
January 2025
Department of Ophthalmology, The Second Hospital of Jilin University, Jilin University, Changchun 130000, Jilin, China.
Glaucoma is a neurodegenerative disorder marked by the loss of retinal ganglion cells (RGCs) and axonal degeneration, resulting in irreversible vision impairment. While intraocular pressure (IOP) is presently acknowledged as the sole modifiable risk factor, the sensitivity of RGCs to IOP varies among individuals. Consequently, progressive vision loss may ensue even when IOP is effectively managed.
View Article and Find Full Text PDFAlzheimers Dement
December 2024
Genetics and Aging Research Unit, MassGeneral Institute for Neurodegenerative Disease, Henry and Allison McCance Center for Brain Health, Department of Neurology, Massachusetts General Hospital, Harvard Medical School, Charlestown, Massachusetts, USA.
Introduction: We previously demonstrated that regulating mitochondria-associated endoplasmic reticulum (ER) membranes (MAMs) affects axonal Aβ generation in a well-characterized three-dimensional (3D) neural Alzheimer's disease (AD) model. MAMs vary in thickness and length, impacting their functions. Here, we examined the effect of MAM thickness on Aβ in our 3D neural model of AD.
View Article and Find Full Text PDFFront Cell Neurosci
December 2024
Lab for Enteric NeuroScience (LENS), TARGID, KU Leuven, Leuven, Belgium.
Due to their large scale and uniquely branched architecture, neurons critically rely on active transport of mitochondria in order to match energy production and calcium buffering to local demand. Consequently, defective mitochondrial trafficking is implicated in various neurological and neurodegenerative diseases. A key signal regulating mitochondrial transport is intracellular calcium.
View Article and Find Full Text PDFNeuromuscul Disord
November 2024
Department of Neurology, Yale University School of Medicine, New Haven, CT, USA.
Axonal Charcot-Marie-Tooth disease (CMT2) and distal hereditary motor neuropathy (dHMN) are associated with a heterogeneous group of genes encoding proteins that are involved in axonal transport, control of RNA metabolism, mitochondrial dynamics and DNA repair. VRK1 (vaccinia-related kinase 1) is a serine/threonine kinase which is widely expressed in human tissue and plays a role in RNA maturation and processing and in DNA damage response. Variants of VRK1 have been associated with neurodevelopmental and neuromuscular disorders including pontocerebellar hypoplasia, motor neuron disorders and distal hereditary motor neuropathy.
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