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Article ; Online: Neurobiology: A pathogenic tug of war.

Cheng, Xiu-Tang / Sheng, Zu-Hang

2021 Volume 31, Issue 10, Page(s) R491–R493

Abstract: Pathogenic mutations in the kinase LRRK2 have been implicated in Parkinson's disease. A new study shows that hyperactivation of this kinase reduces the processivity of autophagosomal retrograde transport in axons through an unproductive 'tug-of-war' ... ...

Abstract	Pathogenic mutations in the kinase LRRK2 have been implicated in Parkinson's disease. A new study shows that hyperactivation of this kinase reduces the processivity of autophagosomal retrograde transport in axons through an unproductive 'tug-of-war' between anterograde and retrograde motors, thus contributing to autophagy dysfunction and axonal degeneration.
MeSH term(s)	Autophagy ; Axons ; Humans ; Mutation ; Neurobiology ; Parkinson Disease/genetics
Language	English
Publishing date	2021-06-23
Publishing country	England
Document type	Journal Article ; Comment
ZDB-ID	1071731-6
ISSN	1879-0445 ; 0960-9822
ISSN (online)	1879-0445
ISSN	0960-9822
DOI	10.1016/j.cub.2021.03.071
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Article ; Online: Programming axonal mitochondrial maintenance and bioenergetics in neurodegeneration and regeneration.

Cheng, Xiu-Tang / Huang, Ning / Sheng, Zu-Hang

Neuron

2022 Volume 110, Issue 12, Page(s) 1899–1923

Abstract: Mitochondria generate ATP essential for neuronal growth, function, and regeneration. Due to their polarized structures, neurons face exceptional challenges to deliver mitochondria to and maintain energy homeostasis throughout long axons and terminal ... ...

Abstract	Mitochondria generate ATP essential for neuronal growth, function, and regeneration. Due to their polarized structures, neurons face exceptional challenges to deliver mitochondria to and maintain energy homeostasis throughout long axons and terminal branches where energy is in high demand. Chronic mitochondrial dysfunction accompanied by bioenergetic failure is a pathological hallmark of major neurodegenerative diseases. Brain injury triggers acute mitochondrial damage and a local energy crisis that accelerates neuron death. Thus, mitochondrial maintenance defects and axonal energy deficits emerge as central problems in neurodegenerative disorders and brain injury. Recent studies have started to uncover the intrinsic mechanisms that neurons adopt to maintain (or reprogram) axonal mitochondrial density and integrity, and their bioenergetic capacity, upon sensing energy stress. In this review, we discuss recent advances in how neurons maintain a healthy pool of axonal mitochondria, as well as potential therapeutic strategies that target bioenergetic restoration to power neuronal survival, function, and regeneration.
MeSH term(s)	Axons/metabolism ; Brain Injuries/metabolism ; Energy Metabolism ; Humans ; Mitochondria/metabolism ; Neurodegenerative Diseases/metabolism ; Regeneration
Language	English
Publishing date	2022-04-16
Publishing country	United States
Document type	Journal Article ; Review ; Research Support, N.I.H., Intramural
ZDB-ID	808167-0
ISSN	1097-4199 ; 0896-6273
ISSN (online)	1097-4199
ISSN	0896-6273
DOI	10.1016/j.neuron.2022.03.015
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Zs.A 2496: Show issues			Location: Je nach Verfügbarkeit (siehe Angabe bei Bestand) bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular Jg. 1995 - 2021: Lesesall (2.OG) ab Jg. 2022: Lesesaal (EG)
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Article ; Online: Neuronal endolysosomal transport and lysosomal functionality in maintaining axonostasis.

Roney, Joseph C / Cheng, Xiu-Tang / Sheng, Zu-Hang

The Journal of cell biology

2022 Volume 221, Issue 3

Abstract: Lysosomes serve as degradation hubs for the turnover of endocytic and autophagic cargos, which is essential for neuron function and survival. Deficits in lysosome function result in progressive neurodegeneration in most lysosomal storage disorders and ... ...

Abstract	Lysosomes serve as degradation hubs for the turnover of endocytic and autophagic cargos, which is essential for neuron function and survival. Deficits in lysosome function result in progressive neurodegeneration in most lysosomal storage disorders and contribute to the pathogenesis of aging-related neurodegenerative diseases. Given their size and highly polarized morphology, neurons face exceptional challenges in maintaining cellular homeostasis in regions far removed from the cell body where mature lysosomes are enriched. Neurons therefore require coordinated bidirectional intracellular transport to sustain efficient clearance capacity in distal axonal regions. Emerging lines of evidence have started to uncover mechanisms and signaling pathways regulating endolysosome transport and maturation to maintain axonal homeostasis, or "axonostasis," that is relevant to a range of neurologic disorders. In this review, we discuss recent advances in how axonal endolysosomal trafficking, distribution, and lysosomal functionality support neuronal health and become disrupted in several neurodegenerative diseases.
MeSH term(s)	Animals ; Autophagy ; Axons/metabolism ; Biological Transport ; Endosomes/metabolism ; Humans ; Lysosomes/metabolism ; Neurodegenerative Diseases/metabolism ; Neurodegenerative Diseases/pathology
Language	English
Publishing date	2022-02-10
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Intramural ; Review
ZDB-ID	218154-x
ISSN	1540-8140 ; 0021-9525
ISSN (online)	1540-8140
ISSN	0021-9525
DOI	10.1083/jcb.202111077
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Article ; Online: Developmental regulation of microtubule-based trafficking and anchoring of axonal mitochondria in health and diseases.

Cheng, Xiu-Tang / Sheng, Zu-Hang

Developmental neurobiology

2020 Volume 81, Issue 3, Page(s) 284–299

Abstract: Mitochondria are cellular power plants that supply most of the ATP required in the brain to power neuronal growth, function, and regeneration. Given their extremely polarized structures and extended long axons, neurons face an exceptional challenge to ... ...

Abstract	Mitochondria are cellular power plants that supply most of the ATP required in the brain to power neuronal growth, function, and regeneration. Given their extremely polarized structures and extended long axons, neurons face an exceptional challenge to maintain energy homeostasis in distal axons, synapses, and growth cones. Anchored mitochondria serve as local energy sources; therefore, the regulation of mitochondrial trafficking and anchoring ensures that these metabolically active areas are adequately supplied with ATP. Chronic mitochondrial dysfunction is a hallmark feature of major aging-related neurodegenerative diseases, and thus, anchored mitochondria in aging neurons need to be removed when they become dysfunctional. Investigations into the regulation of microtubule (MT)-based trafficking and anchoring of axonal mitochondria under physiological and pathological circumstances represent an important emerging area. In this short review article, we provide an updated overview of recent in vitro and in vivo studies showing (1) how mitochondria are transported and positioned in axons and synapses during neuronal developmental and maturation stages, and (2) how altered mitochondrial motility and axonal energy deficits in aging nervous systems link to neurodegeneration and regeneration in a disease or injury setting. We also highlight a major role of syntaphilin as a key MT-based regulator of axonal mitochondrial trafficking and anchoring in mature neurons.
MeSH term(s)	Axons/metabolism ; Microtubules ; Mitochondria/pathology ; Neurons/metabolism ; Synapses/metabolism
Language	English
Publishing date	2020-05-02
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Intramural ; Review
ZDB-ID	2256184-5
ISSN	1932-846X ; 1097-4695 ; 1932-8451 ; 0022-3034
ISSN (online)	1932-846X ; 1097-4695
ISSN	1932-8451 ; 0022-3034
DOI	10.1002/dneu.22748
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Zs.A 853: Show issues

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Article ; Online: Mul1 restrains Parkin-mediated mitophagy in mature neurons by maintaining ER-mitochondrial contacts.

Puri, Rajat / Cheng, Xiu-Tang / Lin, Mei-Yao / Huang, Ning / Sheng, Zu-Hang

Nature communications

2019 Volume 10, Issue 1, Page(s) 3645

Abstract: Chronic mitochondrial stress associates with major neurodegenerative diseases. Recovering stressed mitochondria constitutes a critical step of mitochondrial quality control and thus energy maintenance in early stages of neurodegeneration. Here, we reveal ...

Abstract	Chronic mitochondrial stress associates with major neurodegenerative diseases. Recovering stressed mitochondria constitutes a critical step of mitochondrial quality control and thus energy maintenance in early stages of neurodegeneration. Here, we reveal Mul1-Mfn2 pathway that maintains neuronal mitochondrial integrity under stress conditions. Mul1 deficiency increases Mfn2 activity that triggers the first phasic mitochondrial hyperfusion and also acts as an ER-Mito tethering antagonist. Reduced ER-Mito coupling leads to increased cytoplasmic Ca
MeSH term(s)	Animals ; Calcium/metabolism ; Endoplasmic Reticulum/genetics ; Endoplasmic Reticulum/metabolism ; GTP Phosphohydrolases/genetics ; GTP Phosphohydrolases/metabolism ; Humans ; Mitochondria/genetics ; Mitochondria/metabolism ; Mitochondrial Proteins/genetics ; Mitochondrial Proteins/metabolism ; Mitophagy ; Neurons/cytology ; Neurons/metabolism ; Ubiquitin-Protein Ligases/genetics ; Ubiquitin-Protein Ligases/metabolism
Chemical Substances	Mitochondrial Proteins ; MUL1 protein, mouse (EC 2.3.2.27) ; Ubiquitin-Protein Ligases (EC 2.3.2.27) ; parkin protein (EC 2.3.2.27) ; GTP Phosphohydrolases (EC 3.6.1.-) ; Mfn2 protein, mouse (EC 3.6.1.-) ; Calcium (SY7Q814VUP)
Language	English
Publishing date	2019-08-13
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Intramural
ZDB-ID	2553671-0
ISSN	2041-1723 ; 2041-1723
ISSN (online)	2041-1723
ISSN	2041-1723
DOI	10.1038/s41467-019-11636-5
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Article ; Online: Defending stressed mitochondria: uncovering the role of MUL1 in suppressing neuronal mitophagy.

Puri, Rajat / Cheng, Xiu-Tang / Lin, Mei-Yao / Huang, Ning / Sheng, Zu-Hang

Autophagy

2019 Volume 16, Issue 1, Page(s) 176–178

Abstract: Chronic mitochondrial stress is associated with major neurodegenerative diseases; and thus, the recovery of those mitochondria constitutes a critical step of energy maintenance in early stages of neurodegeneration. Our recent study provides the first ... ...

Abstract	Chronic mitochondrial stress is associated with major neurodegenerative diseases; and thus, the recovery of those mitochondria constitutes a critical step of energy maintenance in early stages of neurodegeneration. Our recent study provides the first lines of evidence showing that the MUL1-MFN2 pathway acts as an early checkpoint to maintain mitochondrial integrity by regulating mitochondrial morphology and interplay with the endoplasmic reticulum (ER). This mechanism ensures that degradation through mitophagy is restrained in neurons under early stress conditions. MUL1 deficiency increases MFN2 activity, triggering the first phase of mitochondrial hyperfusion and acting as an antagonist of ER-mitochondria (ER-Mito) tethering. Reduced ER-Mito interplay enhances the cytoplasmic Ca
MeSH term(s)	Animals ; Autophagy/physiology ; Endoplasmic Reticulum/metabolism ; Humans ; Mitochondria/metabolism ; Mitochondrial Dynamics/physiology ; Mitochondrial Proteins/metabolism ; Mitophagy/physiology
Chemical Substances	Mitochondrial Proteins
Language	English
Publishing date	2019-11-07
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, N.I.H., Intramural ; Review
ZDB-ID	2454135-7
ISSN	1554-8635 ; 1554-8627
ISSN (online)	1554-8635
ISSN	1554-8627
DOI	10.1080/15548627.2019.1687216
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Zs.A 6741: Show issues

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Article ; Online: Ligand-free mitochondria-localized mutant AR-induced cytotoxicity in spinal bulbar muscular atrophy.

Feng, Xia / Cheng, Xiu-Tang / Zheng, Pengli / Li, Yan / Hakim, Jill / Zhang, Shirley Q / Anderson, Stacie M / Linask, Kaari / Prestil, Ryan / Zou, Jizhong / Sheng, Zu-Hang / Blackstone, Craig

Brain : a journal of neurology

2022 Volume 146, Issue 1, Page(s) 278–294

Abstract: Spinal bulbar muscular atrophy (SBMA), the first identified CAG-repeat expansion disorder, is an X-linked neuromuscular disorder involving CAG-repeat-expansion mutations in the androgen receptor (AR) gene. We utilized CRISPR-Cas9 gene editing to engineer ...

Abstract	Spinal bulbar muscular atrophy (SBMA), the first identified CAG-repeat expansion disorder, is an X-linked neuromuscular disorder involving CAG-repeat-expansion mutations in the androgen receptor (AR) gene. We utilized CRISPR-Cas9 gene editing to engineer novel isogenic human induced pluripotent stem cell (hiPSC) models, consisting of isogenic AR knockout, control and disease lines expressing mutant AR with distinct repeat lengths, as well as control and disease lines expressing FLAG-tagged wild-type and mutant AR, respectively. Adapting a small-molecule cocktail-directed approach, we differentiate the isogenic hiPSC models into motor neuron-like cells with a highly enriched population to uncover cell-type-specific mechanisms underlying SBMA and to distinguish gain- from loss-of-function properties of mutant AR in disease motor neurons. We demonstrate that ligand-free mutant AR causes drastic mitochondrial dysfunction in neurites of differentiated disease motor neurons due to gain-of-function mechanisms and such cytotoxicity can be amplified upon ligand (androgens) treatment. We further show that aberrant interaction between ligand-free, mitochondria-localized mutant AR and F-ATP synthase is associated with compromised mitochondrial respiration and multiple other mitochondrial impairments. These findings counter the established notion that androgens are requisite for mutant AR-induced cytotoxicity in SBMA, reveal a compelling mechanistic link between ligand-free mutant AR, F-ATP synthase and mitochondrial dysfunction, and provide innovative insights into motor neuron-specific therapeutic interventions for SBMA.
MeSH term(s)	Humans ; Receptors, Androgen/genetics ; Receptors, Androgen/metabolism ; Induced Pluripotent Stem Cells/metabolism ; Muscular Atrophy, Spinal/genetics ; Muscular Atrophy, Spinal/metabolism ; Muscular Atrophy ; Mitochondria/metabolism ; Adenosine Triphosphate/metabolism
Chemical Substances	Receptors, Androgen ; Adenosine Triphosphate (8L70Q75FXE)
Language	English
Publishing date	2022-07-21
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, N.I.H., Intramural ; Research Support, Non-U.S. Gov't
ZDB-ID	80072-7
ISSN	1460-2156 ; 0006-8950
ISSN (online)	1460-2156
ISSN	0006-8950
DOI	10.1093/brain/awac269
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Article ; Online: Defects in syntabulin-mediated synaptic cargo transport associate with autism-like synaptic dysfunction and social behavioral traits.

Xiong, Gui-Jing / Cheng, Xiu-Tang / Sun, Tao / Xie, Yuxiang / Huang, Ning / Li, Sunan / Lin, Mei-Yao / Sheng, Zu-Hang

Molecular psychiatry

2020 Volume 26, Issue 5, Page(s) 1472–1490

Abstract: The formation and maintenance of synapses require long-distance delivery of newly synthesized synaptic proteins from the soma to distal synapses, raising the fundamental question of whether impaired transport is associated with neurodevelopmental ... ...

Abstract	The formation and maintenance of synapses require long-distance delivery of newly synthesized synaptic proteins from the soma to distal synapses, raising the fundamental question of whether impaired transport is associated with neurodevelopmental disorders such as autism. We previously revealed that syntabulin acts as a motor adapter linking kinesin-1 motor and presynaptic cargos. Here, we report that defects in syntabulin-mediated transport and thus reduced formation and maturation of synapses are one of core synaptic mechanisms underlying autism-like synaptic dysfunction and social behavioral abnormalities. Syntabulin expression in the mouse brain peaks during the first 2 weeks of postnatal development and progressively declines during brain maturation. Neurons from conditional syntabulin
MeSH term(s)	Animals ; Autistic Disorder/genetics ; Cells, Cultured ; Humans ; Mice ; Neurons ; Synapses ; Synaptic Transmission
Language	English
Publishing date	2020-04-24
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Intramural
ZDB-ID	1330655-8
ISSN	1476-5578 ; 1359-4184
ISSN (online)	1476-5578
ISSN	1359-4184
DOI	10.1038/s41380-020-0713-9
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Zs.A 4812: Show issues

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Article ; Online: Neuronal Soma-Derived Degradative Lysosomes Are Continuously Delivered to Distal Axons to Maintain Local Degradation Capacity.

Farfel-Becker, Tamar / Roney, Joseph C / Cheng, Xiu-Tang / Li, Sunan / Cuddy, Sean R / Sheng, Zu-Hang

Cell reports

2019 Volume 28, Issue 1, Page(s) 51–64.e4

Abstract: Neurons face the challenge of maintaining cellular homeostasis through lysosomal degradation. While enzymatically active degradative lysosomes are enriched in the soma, their axonal trafficking and positioning and impact on axonal physiology remain ... ...

Abstract	Neurons face the challenge of maintaining cellular homeostasis through lysosomal degradation. While enzymatically active degradative lysosomes are enriched in the soma, their axonal trafficking and positioning and impact on axonal physiology remain elusive. Here, we characterized axon-targeted delivery of degradative lysosomes by applying fluorescent probes that selectively label active forms of lysosomal cathepsins D, B, L, and GCase. By time-lapse imaging of cortical neurons in microfluidic devices and standard dishes, we reveal that soma-derived degradative lysosomes rapidly influx into distal axons and target to autophagosomes and Parkinson disease-related α-synuclein cargos for local degradation. Impairing lysosome axonal delivery induces an aberrant accumulation of autophagosomes and α-synuclein cargos in distal axons. Our study demonstrates that the axon is an active compartment for local degradation and reveals fundamental aspects of axonal lysosomal delivery and maintenance. Our work establishes a foundation for investigations into axonal lysosome trafficking and functionality in neurodegenerative diseases.
MeSH term(s)	ADP-Ribosylation Factors/genetics ; ADP-Ribosylation Factors/metabolism ; Animals ; Autophagosomes/enzymology ; Autophagosomes/metabolism ; Autophagy/genetics ; Autophagy/physiology ; Axonal Transport/genetics ; Axonal Transport/physiology ; Axons/enzymology ; Axons/metabolism ; Cathepsins/antagonists & inhibitors ; Cathepsins/metabolism ; Female ; Ganglia, Spinal/enzymology ; Ganglia, Spinal/metabolism ; Glucosylceramidase/antagonists & inhibitors ; Glucosylceramidase/metabolism ; HEK293 Cells ; Homeostasis/genetics ; Homeostasis/physiology ; Humans ; Lysosomes/enzymology ; Lysosomes/metabolism ; Male ; Mice ; Mice, Inbred BALB C ; Mice, Inbred C57BL ; Neurons/enzymology ; Neurons/metabolism ; Protein Transport/genetics ; Protein Transport/physiology ; alpha-Synuclein/metabolism
Chemical Substances	Arl8B protein, mouse ; alpha-Synuclein ; Glucosylceramidase (EC 3.2.1.45) ; Cathepsins (EC 3.4.-) ; ARL5B protein, human (EC 3.6.1.2) ; ADP-Ribosylation Factors (EC 3.6.5.2)
Language	English
Publishing date	2019-07-03
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, N.I.H., Intramural
ZDB-ID	2649101-1
ISSN	2211-1247 ; 2211-1247
ISSN (online)	2211-1247
ISSN	2211-1247
DOI	10.1016/j.celrep.2019.06.013
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Article ; Online: The secret life of degradative lysosomes in axons: delivery from the soma, enzymatic activity, and local autophagic clearance.

Farfel-Becker, Tamar / Roney, Joseph C / Cheng, Xiu-Tang / Li, Sunan / Cuddy, Sean R / Sheng, Zu-Hang

Autophagy

2019 Volume 16, Issue 1, Page(s) 167–168

Abstract: Lysosomal degradation of protein aggregates and damaged organelles is essential for maintaining cellular homeostasis. This process in neurons is challenging due to their highly polarized architecture. While enzymatically active degradative lysosomes are ... ...

Abstract	Lysosomal degradation of protein aggregates and damaged organelles is essential for maintaining cellular homeostasis. This process in neurons is challenging due to their highly polarized architecture. While enzymatically active degradative lysosomes are enriched in the cell body, their trafficking and degradation capacity in axons remain elusive. We recently characterized the axonal delivery of degradative lysosomes by applying a set of fluorescent probes that selectively label active forms of lysosomal hydrolases on cortical neurons in microfluidic devices. We revealed that soma-derived degradative lysosomes rapidly influx into distal axons and target to autophagosomes and Parkinson disease-related SNCA/α-synuclein cargos for local degradation. Disrupting axon-targeted delivery of degradative lysosomes induces axonal autophagic stress. We demonstrate that the axon is an active compartment for local degradation, establishing a foundation for future investigations into axonal lysosome trafficking and functionality in neurodegenerative diseases and lysosomal storage disorders associated with axonal pathology and macroautophagy/autophagy stress.
MeSH term(s)	Animals ; Autophagy/physiology ; Axons/metabolism ; Cell Body/metabolism ; Homeostasis/physiology ; Humans ; Lysosomes/metabolism ; Neurons/metabolism
Language	English
Publishing date	2019-09-23
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, N.I.H., Intramural ; Review
ZDB-ID	2454135-7
ISSN	1554-8635 ; 1554-8627
ISSN (online)	1554-8635
ISSN	1554-8627
DOI	10.1080/15548627.2019.1669869
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