SMN requirement for synaptic vesicle, active zone and microtubule postnatal organization in motor nerve terminals
Low levels of the Survival Motor Neuron (SMN) protein produce Spinal Muscular Atrophy (SMA), a severe monogenetic disease in infants characterized by muscle weakness and impaired synaptic transmission. We report here severe structural and functional alterations in the organization of the organelles...
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| Veröffentlicht in: | PloS one 2011-10, Vol.6 (10), p.e26164-e26164 |
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| creator | Torres-Benito, Laura Neher, Margret Feodora Cano, Raquel Ruiz, Rocio Tabares, Lucia |
| description | Low levels of the Survival Motor Neuron (SMN) protein produce Spinal Muscular Atrophy (SMA), a severe monogenetic disease in infants characterized by muscle weakness and impaired synaptic transmission. We report here severe structural and functional alterations in the organization of the organelles and the cytoskeleton of motor nerve terminals in a mouse model of SMA. The decrease in SMN levels resulted in the clustering of synaptic vesicles (SVs) and Active Zones (AZs), reduction in the size of the readily releasable pool (RRP), and the recycling pool (RP) of synaptic vesicles, a decrease in active mitochondria and limiting of neurofilament and microtubule maturation. We propose that SMN is essential for the normal postnatal maturation of motor nerve terminals and that SMN deficiency disrupts the presynaptic organization leading to neurodegeneration. |
| doi_str_mv | 10.1371/journal.pone.0026164 |
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We report here severe structural and functional alterations in the organization of the organelles and the cytoskeleton of motor nerve terminals in a mouse model of SMA. The decrease in SMN levels resulted in the clustering of synaptic vesicles (SVs) and Active Zones (AZs), reduction in the size of the readily releasable pool (RRP), and the recycling pool (RP) of synaptic vesicles, a decrease in active mitochondria and limiting of neurofilament and microtubule maturation. We propose that SMN is essential for the normal postnatal maturation of motor nerve terminals and that SMN deficiency disrupts the presynaptic organization leading to neurodegeneration.</description><identifier>ISSN: 1932-6203</identifier><identifier>EISSN: 1932-6203</identifier><identifier>DOI: 10.1371/journal.pone.0026164</identifier><identifier>PMID: 22022549</identifier><language>eng</language><publisher>United States: Public Library of Science</publisher><subject>Actins - metabolism ; Analysis ; Animals ; Animals, Newborn ; Atrophy ; Bassoon music ; Biology ; Biophysics ; Cell survival ; Cluster Analysis ; Clustering ; Cytoskeleton ; Functional morphology ; Growth factors ; Hypotheses ; Infants ; Maturation ; Medicine ; Mice ; Microtubules - metabolism ; Microtubules - pathology ; Mitochondria ; Mitochondria - metabolism ; Motility ; Motor Neurons - metabolism ; Motor Neurons - pathology ; Muscular Atrophy, Spinal - metabolism ; Nerve endings ; Nerve Endings - metabolism ; Nerve Endings - pathology ; Neurodegeneration ; Neuromuscular diseases ; Neurons ; Organelles ; Pediatric diseases ; Physiology ; Proteins ; Rodents ; SMN protein ; Spinal muscular atrophy ; Structure-function relationships ; Survival of Motor Neuron 1 Protein - metabolism ; Synaptic transmission ; Synaptic vesicles ; Synaptic Vesicles - metabolism ; Synaptic Vesicles - pathology ; Terminals ; Vesicles</subject><ispartof>PloS one, 2011-10, Vol.6 (10), p.e26164-e26164</ispartof><rights>COPYRIGHT 2011 Public Library of Science</rights><rights>2011 Torres-Benito et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License: https://creativecommons.org/licenses/by/4.0/ (the “License”), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.</rights><rights>Torres-Benito et al. 2011</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c691t-544d84f07d6831af0118347d102b22eec22425c95dc44fdb9dfb7e524a34e0f53</citedby><cites>FETCH-LOGICAL-c691t-544d84f07d6831af0118347d102b22eec22425c95dc44fdb9dfb7e524a34e0f53</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC3192162/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC3192162/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,727,780,784,864,885,2100,2926,23864,27922,27923,53789,53791,79370,79371</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/22022549$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><contributor>Feany, Mel B.</contributor><creatorcontrib>Torres-Benito, Laura</creatorcontrib><creatorcontrib>Neher, Margret Feodora</creatorcontrib><creatorcontrib>Cano, Raquel</creatorcontrib><creatorcontrib>Ruiz, Rocio</creatorcontrib><creatorcontrib>Tabares, Lucia</creatorcontrib><title>SMN requirement for synaptic vesicle, active zone and microtubule postnatal organization in motor nerve terminals</title><title>PloS one</title><addtitle>PLoS One</addtitle><description>Low levels of the Survival Motor Neuron (SMN) protein produce Spinal Muscular Atrophy (SMA), a severe monogenetic disease in infants characterized by muscle weakness and impaired synaptic transmission. 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We propose that SMN is essential for the normal postnatal maturation of motor nerve terminals and that SMN deficiency disrupts the presynaptic organization leading to neurodegeneration.</description><subject>Actins - metabolism</subject><subject>Analysis</subject><subject>Animals</subject><subject>Animals, Newborn</subject><subject>Atrophy</subject><subject>Bassoon music</subject><subject>Biology</subject><subject>Biophysics</subject><subject>Cell survival</subject><subject>Cluster Analysis</subject><subject>Clustering</subject><subject>Cytoskeleton</subject><subject>Functional morphology</subject><subject>Growth factors</subject><subject>Hypotheses</subject><subject>Infants</subject><subject>Maturation</subject><subject>Medicine</subject><subject>Mice</subject><subject>Microtubules - metabolism</subject><subject>Microtubules - pathology</subject><subject>Mitochondria</subject><subject>Mitochondria - metabolism</subject><subject>Motility</subject><subject>Motor Neurons - metabolism</subject><subject>Motor Neurons - 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We report here severe structural and functional alterations in the organization of the organelles and the cytoskeleton of motor nerve terminals in a mouse model of SMA. The decrease in SMN levels resulted in the clustering of synaptic vesicles (SVs) and Active Zones (AZs), reduction in the size of the readily releasable pool (RRP), and the recycling pool (RP) of synaptic vesicles, a decrease in active mitochondria and limiting of neurofilament and microtubule maturation. We propose that SMN is essential for the normal postnatal maturation of motor nerve terminals and that SMN deficiency disrupts the presynaptic organization leading to neurodegeneration.</abstract><cop>United States</cop><pub>Public Library of Science</pub><pmid>22022549</pmid><doi>10.1371/journal.pone.0026164</doi><tpages>e26164</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | Actins - metabolism Analysis Animals Animals, Newborn Atrophy Bassoon music Biology Biophysics Cell survival Cluster Analysis Clustering Cytoskeleton Functional morphology Growth factors Hypotheses Infants Maturation Medicine Mice Microtubules - metabolism Microtubules - pathology Mitochondria Mitochondria - metabolism Motility Motor Neurons - metabolism Motor Neurons - pathology Muscular Atrophy, Spinal - metabolism Nerve endings Nerve Endings - metabolism Nerve Endings - pathology Neurodegeneration Neuromuscular diseases Neurons Organelles Pediatric diseases Physiology Proteins Rodents SMN protein Spinal muscular atrophy Structure-function relationships Survival of Motor Neuron 1 Protein - metabolism Synaptic transmission Synaptic vesicles Synaptic Vesicles - metabolism Synaptic Vesicles - pathology Terminals Vesicles |
| title | SMN requirement for synaptic vesicle, active zone and microtubule postnatal organization in motor nerve terminals |
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