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Article ; Online: Striatal Induction and Spread of the Huntington's Disease Protein: A Novel Rhes Route.

Subramaniam, Srinivasa

2022 Volume 11, Issue 3, Page(s) 281–290

Abstract: The CAG/CAA expansion encoding polyQ huntingtin (mutant huntingtin [mHTT]) causes Huntington's disease (HD), which is characterized by atrophy and loss of striatal medium spiny neurons (MSNs), which are preceded by neuropathological alterations in the ... ...

Abstract	The CAG/CAA expansion encoding polyQ huntingtin (mutant huntingtin [mHTT]) causes Huntington's disease (HD), which is characterized by atrophy and loss of striatal medium spiny neurons (MSNs), which are preceded by neuropathological alterations in the cortex. Previous studies have shown that mHTT can spread in the brain, but the mechanisms involved in the stereotyped degeneration and dysfunction of the neurons from the striatum to the cortex remain unclear. In this study, we found that the mHTT expression initially restricted in the striatum later spread to the cortical regions in mouse brains. Such transmission was diminished in mice that lacked the striatal-enriched protein Ras-homolog enriched in the striatum (Rhes). Rhes restricted to MSNs was also found in the cortical layers of the brain, indicating a new transmission route for the Rhes protein to the brain. Mechanistically, Rhes promotes such transmission via a direct cell-to-cell contact mediated by tunneling nanotubes (TNTs), the membranous protrusions that enable the transfer of mHTT, Rhes, and other vesicular cargoes. These transmission patterns suggest that Rhes and mHTT are likely co-transported in the brain using TNT-like cell-to-cell contacts. On the basis of these new results, a perspective is presented in this review: Rhes may ignite the mHTT transmission from the striatum that may coincide with HD onset and disease progression through an anatomically connected striato-cortical retrograde route.
MeSH term(s)	Animals ; Corpus Striatum/metabolism ; Disease Models, Animal ; GTP-Binding Proteins/metabolism ; Huntingtin Protein/genetics ; Huntingtin Protein/metabolism ; Huntington Disease/metabolism ; Mice ; Neostriatum/metabolism ; Neurons/metabolism
Chemical Substances	Huntingtin Protein ; GTP-Binding Proteins (EC 3.6.1.-)
Language	English
Publishing date	2022-06-30
Publishing country	Netherlands
Document type	Journal Article ; Review ; Research Support, Non-U.S. Gov't ; Research Support, N.I.H., Extramural
ZDB-ID	2673033-9
ISSN	1879-6400 ; 1879-6397
ISSN (online)	1879-6400
ISSN	1879-6397
DOI	10.3233/JHD-220548
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Article ; Online: Ribosome traffic jam in neurodegeneration: decoding hurdles in Huntington disease.

Subramaniam, Srinivasa

Cell stress

2021 Volume 5, Issue 6, Page(s) 86–88

Abstract: A ribosome typically moves at a particular rate on a given mRNA transcript to decode the nucleic acid information required to synthesize proteins. The speed and directionality of the ribosome movements during mRNA translation are determined by the mRNA ... ...

Abstract	A ribosome typically moves at a particular rate on a given mRNA transcript to decode the nucleic acid information required to synthesize proteins. The speed and directionality of the ribosome movements during mRNA translation are determined by the mRNA sequence and structure and by various decoding factors. However, the molecular mechanisms of this remarkable movement during protein synthesis, or its relevance in brain disorders, remain unknown. Recent studies have indicated that defects in protein synthesis occur in various neurodegenerative diseases, but the mechanistic details are unclear. This is a major problem because identifying the factors that determine protein synthesis defects may offer new avenues for developing therapeutic remedies for currently incurable diseases like neurodegenerative disorders. Based on our recent study (Eshraghi
Language	English
Publishing date	2021-05-03
Publishing country	Austria
Document type	Journal Article ; Comment
ISSN	2523-0204
ISSN (online)	2523-0204
DOI	10.15698/cst2021.06.251
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Article ; Online: Exaggerated mitophagy: a weapon of striatal destruction in the brain?

Subramaniam, Srinivasa

Biochemical Society transactions

2020 Volume 48, Issue 2, Page(s) 709–717

Abstract: Mechanisms responsible for neuronal vulnerability in the brain remain unclear. Striatal neurons are preferentially damaged by 3-nitropropionic acid (3-NP), a mitochondrial complex-II inhibitor, causing striatal damage reminiscent of Huntington's disease ( ...

Abstract	Mechanisms responsible for neuronal vulnerability in the brain remain unclear. Striatal neurons are preferentially damaged by 3-nitropropionic acid (3-NP), a mitochondrial complex-II inhibitor, causing striatal damage reminiscent of Huntington's disease (HD), but the mechanisms of the selectivity are not as well understood. We have discovered that Rhes, a protein enriched in the striatum, removes mitochondria via the mitophagy process. The process becomes intensified in the presence of 3-NP, thereby eliminating most of the mitochondria from the striatum. We put forward the hypothesis that Rhes acts as a 'mitophagy ligand' in the brain and promotes mitophagy via NIX, a mitophagy receptor. Since Rhes interacts and promotes toxicity in association with mutant huntingtin (mHTT), the genetic cause of HD, it is tempting to speculate on whether the exaggerated mitophagy may be a contributing factor to the striatal lesion found in HD. Thus, Rhes-mediated exaggerated mitophagy may act as a weapon of striatal destruction in the brain.
MeSH term(s)	Animals ; Brain/drug effects ; Brain/pathology ; Corpus Striatum/metabolism ; Drug Development ; Hippocampus/metabolism ; Humans ; Huntingtin Protein/genetics ; Huntington Disease/drug therapy ; Lysosomes/metabolism ; Membrane Proteins/metabolism ; Mitochondria/metabolism ; Mitophagy ; Neurons/metabolism ; Nitro Compounds/adverse effects ; Propionates/adverse effects ; Protein Domains ; Proto-Oncogene Proteins/metabolism
Chemical Substances	BNIP3 protein, human ; HTT protein, human ; Huntingtin Protein ; Membrane Proteins ; Nitro Compounds ; Propionates ; Proto-Oncogene Proteins ; 3-nitropropionic acid (QY4L0FOX0D)
Language	English
Publishing date	2020-01-15
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	184237-7
ISSN	1470-8752 ; 0300-5127
ISSN (online)	1470-8752
ISSN	0300-5127
DOI	10.1042/BST20191283
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Article ; Online: Rhes Tunnels: A Radical New Way of Communication in the Brain's Striatum?

Subramaniam, Srinivasa

BioEssays : news and reviews in molecular, cellular and developmental biology

2020 Volume 42, Issue 6, Page(s) e1900231

Abstract: Ras homolog enriched in the striatum (Rhes) is a striatal enriched protein that promotes the formation of thin membranous tubes resembling tunneling nanotubes (TNT)-"Rhes tunnels"-that connect neighboring cell and transport cargoes: vesicles and proteins ...

Abstract	Ras homolog enriched in the striatum (Rhes) is a striatal enriched protein that promotes the formation of thin membranous tubes resembling tunneling nanotubes (TNT)-"Rhes tunnels"-that connect neighboring cell and transport cargoes: vesicles and proteins between the neuronal cells. Here the literature on TNT-like structures is reviewed, and the implications of Rhes-mediated TNT, the mechanisms of its formation, and its potential in novel cell-to-cell communication in regulating striatal biology and disease are emphasized. Thought-provoking ideas regarding how Rhes-mediated TNT, if it exists, in vivo, would radically change the way neurons communicate in the brain are discussed.
MeSH term(s)	Brain/metabolism ; Communication ; Corpus Striatum/metabolism ; GTP-Binding Proteins ; Humans ; Neurons/metabolism
Chemical Substances	GTP-Binding Proteins (EC 3.6.1.-)
Language	English
Publishing date	2020-04-01
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	50140-2
ISSN	1521-1878 ; 0265-9247
ISSN (online)	1521-1878
ISSN	0265-9247
DOI	10.1002/bies.201900231
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Article: Tunneling Nanotube: An Enticing Cell-Cell Communication in the Nervous System.

Dagar, Sunayana / Subramaniam, Srinivasa

Biology

2023 Volume 12, Issue 10

Abstract: The field of neuroscience is rapidly progressing, continuously uncovering new insights and discoveries. Among the areas that have shown immense potential in research, tunneling nanotubes (TNTs) have emerged as a promising subject of study. These minute ... ...

Abstract	The field of neuroscience is rapidly progressing, continuously uncovering new insights and discoveries. Among the areas that have shown immense potential in research, tunneling nanotubes (TNTs) have emerged as a promising subject of study. These minute structures act as conduits for the transfer of cellular materials between cells, representing a mechanism of communication that holds great significance. In particular, the interplay facilitated by TNTs among various cell types within the brain, including neurons, astrocytes, oligodendrocytes, glial cells, and microglia, can be essential for the normal development and optimal functioning of this complex organ. The involvement of TNTs in neurodegenerative disorders, such as Alzheimer's disease, Huntington's disease, and Parkinson's disease, has attracted significant attention. These disorders are characterized by the progressive degeneration of neurons and the subsequent decline in brain function. Studies have predicted that TNTs likely play critical roles in the propagation and spread of pathological factors, contributing to the advancement of these diseases. Thus, there is a growing interest in understanding the precise functions and mechanisms of TNTs within the nervous system. This review article, based on our recent work on Rhes-mediated TNTs, aims to explore the functions of TNTs within the brain and investigate their implications for neurodegenerative diseases. Using the knowledge gained from studying TNTs could offer novel opportunities for designing targeted treatments that can stop the progression of neurodegenerative disorders.
Language	English
Publishing date	2023-09-27
Publishing country	Switzerland
Document type	Journal Article ; Review
ZDB-ID	2661517-4
ISSN	2079-7737
ISSN	2079-7737
DOI	10.3390/biology12101288
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Article ; Online: Curbing Rhes Actions: Mechanism-based Molecular Target for Huntington's Disease and Tauopathies.

Subramaniam, Srinivasa / Boregowda, Siddaraju

CNS & neurological disorders drug targets

2023 Volume 23, Issue 1, Page(s) 21–29

Abstract: A highly interconnected network of diverse brain regions is necessary for the precise execution of human behaviors, including cognitive, psychiatric, and motor functions. Unfortunately, degeneration of specific brain regions causes several ... ...

Abstract	A highly interconnected network of diverse brain regions is necessary for the precise execution of human behaviors, including cognitive, psychiatric, and motor functions. Unfortunately, degeneration of specific brain regions causes several neurodegenerative disorders, but the mechanisms that elicit selective neuronal vulnerability remain unclear. This knowledge gap greatly hinders the development of effective mechanism-based therapies, despite the desperate need for new treatments. Here, we emphasize the importance of the Rhes (Ras homolog-enriched in the striatum) protein as an emerging therapeutic target. Rhes, an atypical small GTPase with a SUMO (small ubiquitin-like modifier) E3-ligase activity, modulates biological processes such as dopaminergic transmission, alters gene expression, and acts as an inhibitor of motor stimuli in the brain striatum. Mutations in the Rhes gene have also been identified in selected patients with autism and schizophrenia. Moreover, Rhes SUMOylates pathogenic form of mutant huntingtin (mHTT) and tau, enhancing their solubility and cell toxicity in Huntington's disease and tauopathy models. Notably, Rhes uses membrane projections resembling tunneling nanotubes to transport mHTT between cells and Rhes deletion diminishes mHTT spread in the brain. Thus, we predict that effective strategies aimed at diminishing brain Rhes levels will prevent or minimize the abnormalities that occur in HD and tauopathies and potentially in other brain disorders. We review the emerging technologies that enable specific targeting of Rhes in the brain to develop effective disease-modifying therapeutics.
Language	English
Publishing date	2023-03-24
Publishing country	United Arab Emirates
Document type	Journal Article
ZDB-ID	2228394-8
ISSN	1996-3181 ; 1871-5273
ISSN (online)	1996-3181
ISSN	1871-5273
DOI	10.2174/1871527322666230320103518
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Article ; Online: Selective Neuronal Death in Neurodegenerative Diseases: The Ongoing Mystery.

Subramaniam, Srinivasa

The Yale journal of biology and medicine

2019 Volume 92, Issue 4, Page(s) 695–705

Abstract: A major unresolved problem in neurodegenerative disease is why and how a specific set of neurons in the brain are highly vulnerable to neuronal death. Multiple pathways and mechanisms have been proposed to play a role in Alzheimer disease (AD), Parkinson ...

Abstract	A major unresolved problem in neurodegenerative disease is why and how a specific set of neurons in the brain are highly vulnerable to neuronal death. Multiple pathways and mechanisms have been proposed to play a role in Alzheimer disease (AD), Parkinson disease (PD), amyotrophic lateral sclerosis (ALS), and Huntington disease (HD), yet how they contribute to neuronal vulnerability remains far from clear. In this review, various mechanisms ascribed in AD, PD, ALS, and HD will be briefly summarized. Particular focus will be placed on Rhes-mediated intercellular transport of the HD protein and its role in mitophagy, in which I will discuss some intriguing observations that I apply to model striatal vulnerability in HD. I may have unintentionally missed referring some studies in this review, and I extend my apologies to the authors in those circumstances.
MeSH term(s)	Animals ; Apoptosis ; GTP-Binding Proteins/metabolism ; Humans ; Neurodegenerative Diseases/pathology ; Neurons/pathology
Chemical Substances	GTP-Binding Proteins (EC 3.6.1.-)
Language	English
Publishing date	2019-12-20
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	200515-3
ISSN	1551-4056 ; 0044-0086
ISSN (online)	1551-4056
ISSN	0044-0086
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Article: Rhes Tunnels: A Radical New Way of Communication in the Brain's Striatum?

Subramaniam, Srinivasa

BioEssays. 2020 June, v. 42, no. 6

2020

Abstract: Ras homolog enriched in the striatum (Rhes) is a striatal enriched protein that promotes the formation of thin membranous tubes resembling tunneling nanotubes (TNT)—“Rhes tunnels”—that connect neighboring cell and transport cargoes: vesicles and proteins ...

Abstract	Ras homolog enriched in the striatum (Rhes) is a striatal enriched protein that promotes the formation of thin membranous tubes resembling tunneling nanotubes (TNT)—“Rhes tunnels”—that connect neighboring cell and transport cargoes: vesicles and proteins between the neuronal cells. Here the literature on TNT‐like structures is reviewed, and the implications of Rhes‐mediated TNT, the mechanisms of its formation, and its potential in novel cell‐to‐cell communication in regulating striatal biology and disease are emphasized. Thought‐provoking ideas regarding how Rhes‐mediated TNT, if it exists, in vivo, would radically change the way neurons communicate in the brain are discussed.
Keywords	brain ; cell communication ; nanotubes ; neurons
Language	English
Dates of publication	2020-06
Publishing place	John Wiley & Sons, Ltd
Document type	Article
Note	NAL-AP-2-clean ; JOURNAL ARTICLE
ZDB-ID	50140-2
ISSN	1521-1878 ; 0265-9247
ISSN (online)	1521-1878
ISSN	0265-9247
DOI	10.1002/bies.201900231
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Article ; Online: Rhes travels from cell to cell and transports Huntington disease protein via TNT-like protrusion.

Sharma, Manish / Subramaniam, Srinivasa

The Journal of cell biology

2019 Volume 218, Issue 6, Page(s) 1972–1993

Abstract: Tunneling nanotubes (TNT) are thin, membranous, tunnel-like cell-to-cell connections, but the mechanisms underlying their biogenesis or functional role remains obscure. Here, we report, Rhes, a brain-enriched GTPase/SUMO E3-like protein, induces the ... ...

Abstract	Tunneling nanotubes (TNT) are thin, membranous, tunnel-like cell-to-cell connections, but the mechanisms underlying their biogenesis or functional role remains obscure. Here, we report, Rhes, a brain-enriched GTPase/SUMO E3-like protein, induces the biogenesis of TNT-like cellular protrusions, "Rhes tunnels," through which Rhes moves from cell to cell and transports Huntington disease (HD) protein, the poly-Q expanded mutant Huntingtin (mHTT). The formation of TNT-like Rhes tunnels requires the Rhes's serine 33, C-terminal CAAX, and a SUMO E3-like domain. Electron microscopy analysis revealed that TNT-like Rhes tunnels appear continuous, cell-cell connections, and <200 nm in diameter. Live-cell imaging shows that Rhes tunnels establish contact with the neighboring cell and deliver Rhes-positive cargoes, which travel across the plasma membrane of the neighboring cell before entering it. The Rhes tunnels carry Rab5a/Lyso 20-positive vesicles and transport mHTT, but not normal HTT, mTOR, or wtTau proteins. SUMOylation-defective mHTT, Rhes C263S (cannot SUMOylate mHTT), or CRISPR/Cas9-mediated depletion of three isoforms of SUMO diminishes Rhes-mediated mHTT transport. Thus, Rhes promotes the biogenesis of TNT-like cellular protrusions and facilitates the cell-cell transport of mHTT involving SUMO-mediated mechanisms.
MeSH term(s)	Actin Cytoskeleton/metabolism ; Animals ; Cell Communication ; Cell Surface Extensions/metabolism ; GTP-Binding Proteins/metabolism ; Huntingtin Protein/metabolism ; Huntington Disease ; Mice ; Mice, Inbred C57BL ; Nanotubes/chemistry ; Neurons/metabolism ; Protein Transport
Chemical Substances	Htt protein, mouse ; Huntingtin Protein ; GTP-Binding Proteins (EC 3.6.1.-) ; Rasd2 protein, mouse (EC 3.6.1.-)
Language	English
Publishing date	2019-05-10
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	218154-x
ISSN	1540-8140 ; 0021-9525
ISSN (online)	1540-8140
ISSN	0021-9525
DOI	10.1083/jcb.201807068
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Article ; Online: Ribosome Profiling and Mass Spectrometry Reveal Widespread Mitochondrial Translation Defects in a Striatal Cell Model of Huntington Disease.

Dagar, Sunayana / Sharma, Manish / Tsaprailis, George / Tapia, Catherina Scharager / Crynen, Gogce / Joshi, Preksha Sandipkumar / Shahani, Neelam / Subramaniam, Srinivasa

Molecular & cellular proteomics : MCP

2024 Volume 23, Issue 4, Page(s) 100746

Abstract: Huntington disease (HD) is caused by an expanded polyglutamine mutation in huntingtin (mHTT) that promotes prominent atrophy in the striatum and subsequent psychiatric, cognitive deficits, and choreiform movements. Multiple lines of evidence point to an ... ...

Abstract	Huntington disease (HD) is caused by an expanded polyglutamine mutation in huntingtin (mHTT) that promotes prominent atrophy in the striatum and subsequent psychiatric, cognitive deficits, and choreiform movements. Multiple lines of evidence point to an association between HD and aberrant striatal mitochondrial functions; however, the present knowledge about whether (or how) mitochondrial mRNA translation is differentially regulated in HD remains unclear. We found that protein synthesis is diminished in HD mitochondria compared to healthy control striatal cell models. We utilized ribosome profiling (Ribo-Seq) to analyze detailed snapshots of ribosome occupancy of the mitochondrial mRNA transcripts in control and HD striatal cell models. The Ribo-Seq data revealed almost unaltered ribosome occupancy on the nuclear-encoded mitochondrial transcripts involved in oxidative phosphorylation (SDHA, Ndufv1, Timm23, Tomm5, Mrps22) in HD cells. By contrast, ribosome occupancy was dramatically increased for mitochondrially encoded oxidative phosphorylation mRNAs (mt-Nd1, mt-Nd2, mt-Nd4, mt-Nd4l, mt-Nd5, mt-Nd6, mt-Co1, mt-Cytb, and mt-ATP8). We also applied tandem mass tag-based mass spectrometry identification of mitochondrial proteins to derive correlations between ribosome occupancy and actual mature mitochondrial protein products. We found many mitochondrial transcripts with comparable or higher ribosome occupancy, but diminished mitochondrial protein products, in HD. Thus, our study provides the first evidence of a widespread dichotomous effect on ribosome occupancy and protein abundance of mitochondria-related genes in HD.
MeSH term(s)	Huntington Disease/metabolism ; Huntington Disease/genetics ; Huntington Disease/pathology ; Mitochondria/metabolism ; Humans ; Protein Biosynthesis ; Ribosomes/metabolism ; RNA, Messenger/metabolism ; RNA, Messenger/genetics ; Oxidative Phosphorylation ; Corpus Striatum/metabolism ; Corpus Striatum/pathology ; Mitochondrial Proteins/metabolism ; Mitochondrial Proteins/genetics ; Cell Line ; RNA, Mitochondrial/metabolism ; RNA, Mitochondrial/genetics ; Mass Spectrometry ; Ribosome Profiling
Chemical Substances	RNA, Messenger ; Mitochondrial Proteins ; RNA, Mitochondrial
Language	English
Publishing date	2024-03-05
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Research Support, N.I.H., Extramural
ZDB-ID	2075924-1
ISSN	1535-9484 ; 1535-9476
ISSN (online)	1535-9484
ISSN	1535-9476
DOI	10.1016/j.mcpro.2024.100746
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