Spartin Regulates Synaptic Growth and Neuronal Survival by Inhibiting BMP-Mediated Microtubule Stabilization
Troyer syndrome is a hereditary spastic paraplegia caused by human spartin (SPG20) gene mutations. We have generated a Drosophila disease model showing that Spartin functions presynaptically with endocytic adaptor Eps15 to regulate synaptic growth and function. Spartin inhibits bone morphogenetic pr...
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| Veröffentlicht in: | Neuron (Cambridge, Mass.) Mass.), 2013-02, Vol.77 (4), p.680-695 |
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| creator | Nahm, Minyeop Lee, Min-Jung Parkinson, William Lee, Mihye Kim, Haeran Kim, Yoon-Jung Kim, Sungdae Cho, Yi Sul Min, Byung-Moo Bae, Yong Chul Broadie, Kendal Lee, Seungbok |
| description | Troyer syndrome is a hereditary spastic paraplegia caused by human spartin (SPG20) gene mutations. We have generated a Drosophila disease model showing that Spartin functions presynaptically with endocytic adaptor Eps15 to regulate synaptic growth and function. Spartin inhibits bone morphogenetic protein (BMP) signaling by promoting endocytic degradation of BMP receptor wishful thinking (Wit). Drosophila fragile X mental retardation protein (dFMRP) and Futsch/MAP1B are downstream effectors of Spartin and BMP signaling in regulating microtubule stability and synaptic growth. Loss of Spartin or elevation of BMP signaling induces age-dependent progressive defects resembling hereditary spastic paraplegias, including motor dysfunction and brain neurodegeneration. Null spartin phenotypes are prevented by administration of the microtubule-destabilizing drug vinblastine. Together, these results demonstrate that Spartin regulates both synaptic development and neuronal survival by controlling microtubule stability via the BMP-dFMRP-Futsch pathway, suggesting that impaired regulation of microtubule stability is a core pathogenic component in Troyer syndrome.
► HSP gene spartin mutations cause synapse overgrowth and brain neurodegeneration ► Spartin inhibits BMP signaling by endocytic degradation of the BMP receptor Wit ► FMRP and Futsch/MAP1B are downstream effectors of Spartin and BMP signaling ► Restoration of microtubule stability rescues spartin-induced neuronal phenotypes
Troyer syndrome hereditary spastic paraplegia is caused by human spartin gene mutations. Nahm et al. develop a Drosophila disease model to show that Spartin regulates both synaptic development and neuronal survival by controlling microtubule stability via the BMP-FMRP-Futsch pathway. |
| doi_str_mv | 10.1016/j.neuron.2012.12.015 |
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► HSP gene spartin mutations cause synapse overgrowth and brain neurodegeneration ► Spartin inhibits BMP signaling by endocytic degradation of the BMP receptor Wit ► FMRP and Futsch/MAP1B are downstream effectors of Spartin and BMP signaling ► Restoration of microtubule stability rescues spartin-induced neuronal phenotypes
Troyer syndrome hereditary spastic paraplegia is caused by human spartin gene mutations. Nahm et al. develop a Drosophila disease model to show that Spartin regulates both synaptic development and neuronal survival by controlling microtubule stability via the BMP-FMRP-Futsch pathway.</description><identifier>ISSN: 0896-6273</identifier><identifier>EISSN: 1097-4199</identifier><identifier>DOI: 10.1016/j.neuron.2012.12.015</identifier><identifier>PMID: 23439121</identifier><language>eng</language><publisher>United States: Elsevier Inc</publisher><subject>Animals ; Base Sequence - genetics ; Bone Morphogenetic Protein Receptors - genetics ; Bone Morphogenetic Protein Receptors - metabolism ; Bone Morphogenetic Proteins - genetics ; Cell division ; Cell Survival ; Drosophila ; Drosophila - genetics ; Genomes ; Humans ; Insects ; Microtubule-Associated Proteins - metabolism ; Microtubules - genetics ; Microtubules - metabolism ; Mutation ; Neurodegeneration ; Neurons - cytology ; Neurons - metabolism ; Protein Binding - physiology ; Proteins ; Signal Transduction - genetics ; Spastic Paraplegia, Hereditary - genetics ; Spastic Paraplegia, Hereditary - metabolism ; Synapses - metabolism</subject><ispartof>Neuron (Cambridge, Mass.), 2013-02, Vol.77 (4), p.680-695</ispartof><rights>2013 Elsevier Inc.</rights><rights>Copyright © 2013 Elsevier Inc. All rights reserved.</rights><rights>Copyright Elsevier Limited Feb 20, 2013</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c590t-9ed4ce7715488f93e23b3c8b90c0b8149176e3af1237aba9d07206a14c3c518f3</citedby><cites>FETCH-LOGICAL-c590t-9ed4ce7715488f93e23b3c8b90c0b8149176e3af1237aba9d07206a14c3c518f3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://www.sciencedirect.com/science/article/pii/S0896627312011257$$EHTML$$P50$$Gelsevier$$Hfree_for_read</linktohtml><link.rule.ids>230,314,776,780,881,3537,27901,27902,65306</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/23439121$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Nahm, Minyeop</creatorcontrib><creatorcontrib>Lee, Min-Jung</creatorcontrib><creatorcontrib>Parkinson, William</creatorcontrib><creatorcontrib>Lee, Mihye</creatorcontrib><creatorcontrib>Kim, Haeran</creatorcontrib><creatorcontrib>Kim, Yoon-Jung</creatorcontrib><creatorcontrib>Kim, Sungdae</creatorcontrib><creatorcontrib>Cho, Yi Sul</creatorcontrib><creatorcontrib>Min, Byung-Moo</creatorcontrib><creatorcontrib>Bae, Yong Chul</creatorcontrib><creatorcontrib>Broadie, Kendal</creatorcontrib><creatorcontrib>Lee, Seungbok</creatorcontrib><title>Spartin Regulates Synaptic Growth and Neuronal Survival by Inhibiting BMP-Mediated Microtubule Stabilization</title><title>Neuron (Cambridge, Mass.)</title><addtitle>Neuron</addtitle><description>Troyer syndrome is a hereditary spastic paraplegia caused by human spartin (SPG20) gene mutations. We have generated a Drosophila disease model showing that Spartin functions presynaptically with endocytic adaptor Eps15 to regulate synaptic growth and function. Spartin inhibits bone morphogenetic protein (BMP) signaling by promoting endocytic degradation of BMP receptor wishful thinking (Wit). Drosophila fragile X mental retardation protein (dFMRP) and Futsch/MAP1B are downstream effectors of Spartin and BMP signaling in regulating microtubule stability and synaptic growth. Loss of Spartin or elevation of BMP signaling induces age-dependent progressive defects resembling hereditary spastic paraplegias, including motor dysfunction and brain neurodegeneration. Null spartin phenotypes are prevented by administration of the microtubule-destabilizing drug vinblastine. Together, these results demonstrate that Spartin regulates both synaptic development and neuronal survival by controlling microtubule stability via the BMP-dFMRP-Futsch pathway, suggesting that impaired regulation of microtubule stability is a core pathogenic component in Troyer syndrome.
► HSP gene spartin mutations cause synapse overgrowth and brain neurodegeneration ► Spartin inhibits BMP signaling by endocytic degradation of the BMP receptor Wit ► FMRP and Futsch/MAP1B are downstream effectors of Spartin and BMP signaling ► Restoration of microtubule stability rescues spartin-induced neuronal phenotypes
Troyer syndrome hereditary spastic paraplegia is caused by human spartin gene mutations. Nahm et al. develop a Drosophila disease model to show that Spartin regulates both synaptic development and neuronal survival by controlling microtubule stability via the BMP-FMRP-Futsch pathway.</description><subject>Animals</subject><subject>Base Sequence - genetics</subject><subject>Bone Morphogenetic Protein Receptors - genetics</subject><subject>Bone Morphogenetic Protein Receptors - metabolism</subject><subject>Bone Morphogenetic Proteins - genetics</subject><subject>Cell division</subject><subject>Cell Survival</subject><subject>Drosophila</subject><subject>Drosophila - genetics</subject><subject>Genomes</subject><subject>Humans</subject><subject>Insects</subject><subject>Microtubule-Associated Proteins - metabolism</subject><subject>Microtubules - genetics</subject><subject>Microtubules - metabolism</subject><subject>Mutation</subject><subject>Neurodegeneration</subject><subject>Neurons - cytology</subject><subject>Neurons - metabolism</subject><subject>Protein Binding - physiology</subject><subject>Proteins</subject><subject>Signal Transduction - genetics</subject><subject>Spastic Paraplegia, Hereditary - genetics</subject><subject>Spastic Paraplegia, Hereditary - metabolism</subject><subject>Synapses - metabolism</subject><issn>0896-6273</issn><issn>1097-4199</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2013</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqNkV2LEzEUhoMobl39ByIBb7yZmq-ZSW4EXXRd2KpYvQ6ZzJk2ZZrUJFOpv97UruvHhQgHEshz3nPyvgg9pmROCW2eb-Yephj8nBHK5qUIre-gGSWqrQRV6i6aEamaqmEtP0MPUtoQQkWt6H10xrjgijI6Q-NyZ2J2Hn-E1TSaDAkvD97ssrP4MoaveY2N7_G7H6PMiJdT3Lt9uXQHfOXXrnOleYVfLT5UC-hdEejxwtkY8tRNI-BlNp0b3TeTXfAP0b3BjAke3Zzn6POb158u3lbX7y-vLl5eV7ZWJFcKemGhbWktpBwUB8Y7bmWniCWdpELRtgFuBsp4azqjetIy0hgqLLc1lQM_Ry9Ourup20JvwedoRr2LbmviQQfj9J8v3q31Kuw1l2UmU0Xg2Y1ADF8mSFlvXbIwjsZDmJKmnHFJBGvJf6CUSVFYUdCnf6GbMMXiaqEaUfOaS3mkxIkqJqYUYbjdmxJ9TF5v9Cl5fUxelyrJl7Ynv__5tuln1L9MgeL83kHUyTrwtqQWwWbdB_fvCd8BpJDCUA</recordid><startdate>20130220</startdate><enddate>20130220</enddate><creator>Nahm, Minyeop</creator><creator>Lee, Min-Jung</creator><creator>Parkinson, William</creator><creator>Lee, Mihye</creator><creator>Kim, Haeran</creator><creator>Kim, Yoon-Jung</creator><creator>Kim, Sungdae</creator><creator>Cho, Yi Sul</creator><creator>Min, Byung-Moo</creator><creator>Bae, Yong Chul</creator><creator>Broadie, Kendal</creator><creator>Lee, Seungbok</creator><general>Elsevier Inc</general><general>Elsevier Limited</general><scope>6I.</scope><scope>AAFTH</scope><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7QP</scope><scope>7QR</scope><scope>7TK</scope><scope>8FD</scope><scope>FR3</scope><scope>K9.</scope><scope>NAPCQ</scope><scope>P64</scope><scope>RC3</scope><scope>7X8</scope><scope>7SS</scope><scope>5PM</scope></search><sort><creationdate>20130220</creationdate><title>Spartin Regulates Synaptic Growth and Neuronal Survival by Inhibiting BMP-Mediated Microtubule Stabilization</title><author>Nahm, Minyeop ; Lee, Min-Jung ; Parkinson, William ; Lee, Mihye ; Kim, Haeran ; Kim, Yoon-Jung ; Kim, Sungdae ; Cho, Yi Sul ; Min, Byung-Moo ; Bae, Yong Chul ; Broadie, Kendal ; Lee, Seungbok</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c590t-9ed4ce7715488f93e23b3c8b90c0b8149176e3af1237aba9d07206a14c3c518f3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2013</creationdate><topic>Animals</topic><topic>Base Sequence - genetics</topic><topic>Bone Morphogenetic Protein Receptors - genetics</topic><topic>Bone Morphogenetic Protein Receptors - metabolism</topic><topic>Bone Morphogenetic Proteins - genetics</topic><topic>Cell division</topic><topic>Cell Survival</topic><topic>Drosophila</topic><topic>Drosophila - genetics</topic><topic>Genomes</topic><topic>Humans</topic><topic>Insects</topic><topic>Microtubule-Associated Proteins - metabolism</topic><topic>Microtubules - genetics</topic><topic>Microtubules - metabolism</topic><topic>Mutation</topic><topic>Neurodegeneration</topic><topic>Neurons - cytology</topic><topic>Neurons - metabolism</topic><topic>Protein Binding - physiology</topic><topic>Proteins</topic><topic>Signal Transduction - genetics</topic><topic>Spastic Paraplegia, Hereditary - genetics</topic><topic>Spastic Paraplegia, Hereditary - metabolism</topic><topic>Synapses - metabolism</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Nahm, Minyeop</creatorcontrib><creatorcontrib>Lee, Min-Jung</creatorcontrib><creatorcontrib>Parkinson, William</creatorcontrib><creatorcontrib>Lee, Mihye</creatorcontrib><creatorcontrib>Kim, Haeran</creatorcontrib><creatorcontrib>Kim, Yoon-Jung</creatorcontrib><creatorcontrib>Kim, Sungdae</creatorcontrib><creatorcontrib>Cho, Yi Sul</creatorcontrib><creatorcontrib>Min, Byung-Moo</creatorcontrib><creatorcontrib>Bae, Yong Chul</creatorcontrib><creatorcontrib>Broadie, Kendal</creatorcontrib><creatorcontrib>Lee, Seungbok</creatorcontrib><collection>ScienceDirect Open Access Titles</collection><collection>Elsevier:ScienceDirect:Open Access</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Calcium & Calcified Tissue Abstracts</collection><collection>Chemoreception Abstracts</collection><collection>Neurosciences Abstracts</collection><collection>Technology Research Database</collection><collection>Engineering Research Database</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Nursing & Allied Health Premium</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>Genetics Abstracts</collection><collection>MEDLINE - Academic</collection><collection>Entomology Abstracts (Full archive)</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Neuron (Cambridge, Mass.)</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Nahm, Minyeop</au><au>Lee, Min-Jung</au><au>Parkinson, William</au><au>Lee, Mihye</au><au>Kim, Haeran</au><au>Kim, Yoon-Jung</au><au>Kim, Sungdae</au><au>Cho, Yi Sul</au><au>Min, Byung-Moo</au><au>Bae, Yong Chul</au><au>Broadie, Kendal</au><au>Lee, Seungbok</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Spartin Regulates Synaptic Growth and Neuronal Survival by Inhibiting BMP-Mediated Microtubule Stabilization</atitle><jtitle>Neuron (Cambridge, Mass.)</jtitle><addtitle>Neuron</addtitle><date>2013-02-20</date><risdate>2013</risdate><volume>77</volume><issue>4</issue><spage>680</spage><epage>695</epage><pages>680-695</pages><issn>0896-6273</issn><eissn>1097-4199</eissn><abstract>Troyer syndrome is a hereditary spastic paraplegia caused by human spartin (SPG20) gene mutations. We have generated a Drosophila disease model showing that Spartin functions presynaptically with endocytic adaptor Eps15 to regulate synaptic growth and function. Spartin inhibits bone morphogenetic protein (BMP) signaling by promoting endocytic degradation of BMP receptor wishful thinking (Wit). Drosophila fragile X mental retardation protein (dFMRP) and Futsch/MAP1B are downstream effectors of Spartin and BMP signaling in regulating microtubule stability and synaptic growth. Loss of Spartin or elevation of BMP signaling induces age-dependent progressive defects resembling hereditary spastic paraplegias, including motor dysfunction and brain neurodegeneration. Null spartin phenotypes are prevented by administration of the microtubule-destabilizing drug vinblastine. Together, these results demonstrate that Spartin regulates both synaptic development and neuronal survival by controlling microtubule stability via the BMP-dFMRP-Futsch pathway, suggesting that impaired regulation of microtubule stability is a core pathogenic component in Troyer syndrome.
► HSP gene spartin mutations cause synapse overgrowth and brain neurodegeneration ► Spartin inhibits BMP signaling by endocytic degradation of the BMP receptor Wit ► FMRP and Futsch/MAP1B are downstream effectors of Spartin and BMP signaling ► Restoration of microtubule stability rescues spartin-induced neuronal phenotypes
Troyer syndrome hereditary spastic paraplegia is caused by human spartin gene mutations. Nahm et al. develop a Drosophila disease model to show that Spartin regulates both synaptic development and neuronal survival by controlling microtubule stability via the BMP-FMRP-Futsch pathway.</abstract><cop>United States</cop><pub>Elsevier Inc</pub><pmid>23439121</pmid><doi>10.1016/j.neuron.2012.12.015</doi><tpages>16</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | Animals Base Sequence - genetics Bone Morphogenetic Protein Receptors - genetics Bone Morphogenetic Protein Receptors - metabolism Bone Morphogenetic Proteins - genetics Cell division Cell Survival Drosophila Drosophila - genetics Genomes Humans Insects Microtubule-Associated Proteins - metabolism Microtubules - genetics Microtubules - metabolism Mutation Neurodegeneration Neurons - cytology Neurons - metabolism Protein Binding - physiology Proteins Signal Transduction - genetics Spastic Paraplegia, Hereditary - genetics Spastic Paraplegia, Hereditary - metabolism Synapses - metabolism |
| title | Spartin Regulates Synaptic Growth and Neuronal Survival by Inhibiting BMP-Mediated Microtubule Stabilization |
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