A mechanism for the segregation of age in mammalian neural stem cells
Throughout life, neural stem cells (NSCs) generate neurons in the mammalian brain. Using photobleaching experiments, we found that during cell division in vitro and within the developing mouse forebrain, NSCs generate a lateral diffusion barrier in the membrane of the endoplasmic reticulum, thereby...
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| Veröffentlicht in: | Science (American Association for the Advancement of Science) 2015-09, Vol.349 (6254), p.1334-1338 |
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| container_title | Science (American Association for the Advancement of Science) |
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| creator | Moore, D. L. Pilz, G. A. Araúzo-Bravo, M. J. Barral, Y. Jessberger, S. |
| description | Throughout life, neural stem cells (NSCs) generate neurons in the mammalian brain. Using photobleaching experiments, we found that during cell division in vitro and within the developing mouse forebrain, NSCs generate a lateral diffusion barrier in the membrane of the endoplasmic reticulum, thereby promoting asymmetric segregation of cellular components. The diffusion barrier weakens with age and in response to impairment of lamin-associated nuclear envelope constituents. Weakening of the diffusion barrier disrupts asymmetric segregation of damaged proteins, a product of aging. Damaged proteins are asymmetrically inherited by the nonstem daughter cell in embryonic and young adult NSC divisions, whereas in the older adult brain, damaged proteins are more symmetrically distributed between progeny. Thus, these data identify a mechanism of how damage that accumulates with age is asymmetrically distributed during somatic stem cell division. |
| doi_str_mv | 10.1126/science.aac9868 |
| format | Article |
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L. ; Pilz, G. A. ; Araúzo-Bravo, M. J. ; Barral, Y. ; Jessberger, S.</creator><creatorcontrib>Moore, D. L. ; Pilz, G. A. ; Araúzo-Bravo, M. J. ; Barral, Y. ; Jessberger, S.</creatorcontrib><description>Throughout life, neural stem cells (NSCs) generate neurons in the mammalian brain. Using photobleaching experiments, we found that during cell division in vitro and within the developing mouse forebrain, NSCs generate a lateral diffusion barrier in the membrane of the endoplasmic reticulum, thereby promoting asymmetric segregation of cellular components. The diffusion barrier weakens with age and in response to impairment of lamin-associated nuclear envelope constituents. Weakening of the diffusion barrier disrupts asymmetric segregation of damaged proteins, a product of aging. Damaged proteins are asymmetrically inherited by the nonstem daughter cell in embryonic and young adult NSC divisions, whereas in the older adult brain, damaged proteins are more symmetrically distributed between progeny. Thus, these data identify a mechanism of how damage that accumulates with age is asymmetrically distributed during somatic stem cell division.</description><identifier>ISSN: 0036-8075</identifier><identifier>EISSN: 1095-9203</identifier><identifier>DOI: 10.1126/science.aac9868</identifier><identifier>PMID: 26383951</identifier><identifier>CODEN: SCIEAS</identifier><language>eng</language><publisher>United States: American Association for the Advancement of Science</publisher><subject>Age ; Animals ; Asymmetry ; Cell Division ; Cellular Senescence ; Damage ; Diffusion ; Diffusion barriers ; Endoplasmic Reticulum - physiology ; Endoplasmic Reticulum - ultrastructure ; Intracellular Membranes - physiology ; Intracellular Membranes - ultrastructure ; Lamin Type A - metabolism ; Mammals ; Mice ; Neural Stem Cells - cytology ; Neural Stem Cells - metabolism ; Neurons ; Photobleaching ; Prosencephalon - cytology ; Prosencephalon - growth & development ; Prosencephalon - metabolism ; Protein Transport ; Proteins ; Rodents ; Segregations ; Stem cells</subject><ispartof>Science (American Association for the Advancement of Science), 2015-09, Vol.349 (6254), p.1334-1338</ispartof><rights>Copyright © 2015 American Association for the Advancement of Science</rights><rights>Copyright © 2015, American Association for the Advancement of Science.</rights><rights>Copyright © 2015, American Association for the Advancement of Science</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c479t-c84cebe76f30d57a02983eff1507717741a41c152339d84bbc6607fb92670e923</citedby><cites>FETCH-LOGICAL-c479t-c84cebe76f30d57a02983eff1507717741a41c152339d84bbc6607fb92670e923</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.jstor.org/stable/pdf/24749341$$EPDF$$P50$$Gjstor$$H</linktopdf><linktohtml>$$Uhttps://www.jstor.org/stable/24749341$$EHTML$$P50$$Gjstor$$H</linktohtml><link.rule.ids>314,780,784,803,2884,2885,27924,27925,58017,58250</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/26383951$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Moore, D. L.</creatorcontrib><creatorcontrib>Pilz, G. A.</creatorcontrib><creatorcontrib>Araúzo-Bravo, M. J.</creatorcontrib><creatorcontrib>Barral, Y.</creatorcontrib><creatorcontrib>Jessberger, S.</creatorcontrib><title>A mechanism for the segregation of age in mammalian neural stem cells</title><title>Science (American Association for the Advancement of Science)</title><addtitle>Science</addtitle><description>Throughout life, neural stem cells (NSCs) generate neurons in the mammalian brain. Using photobleaching experiments, we found that during cell division in vitro and within the developing mouse forebrain, NSCs generate a lateral diffusion barrier in the membrane of the endoplasmic reticulum, thereby promoting asymmetric segregation of cellular components. The diffusion barrier weakens with age and in response to impairment of lamin-associated nuclear envelope constituents. Weakening of the diffusion barrier disrupts asymmetric segregation of damaged proteins, a product of aging. Damaged proteins are asymmetrically inherited by the nonstem daughter cell in embryonic and young adult NSC divisions, whereas in the older adult brain, damaged proteins are more symmetrically distributed between progeny. Thus, these data identify a mechanism of how damage that accumulates with age is asymmetrically distributed during somatic stem cell division.</description><subject>Age</subject><subject>Animals</subject><subject>Asymmetry</subject><subject>Cell Division</subject><subject>Cellular Senescence</subject><subject>Damage</subject><subject>Diffusion</subject><subject>Diffusion barriers</subject><subject>Endoplasmic Reticulum - physiology</subject><subject>Endoplasmic Reticulum - ultrastructure</subject><subject>Intracellular Membranes - physiology</subject><subject>Intracellular Membranes - ultrastructure</subject><subject>Lamin Type A - metabolism</subject><subject>Mammals</subject><subject>Mice</subject><subject>Neural Stem Cells - cytology</subject><subject>Neural Stem Cells - metabolism</subject><subject>Neurons</subject><subject>Photobleaching</subject><subject>Prosencephalon - cytology</subject><subject>Prosencephalon - growth & development</subject><subject>Prosencephalon - metabolism</subject><subject>Protein Transport</subject><subject>Proteins</subject><subject>Rodents</subject><subject>Segregations</subject><subject>Stem cells</subject><issn>0036-8075</issn><issn>1095-9203</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2015</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqF0TtPxDAMB_AIgbjjMTOBIrGwFJwmzWNE6HhISCwwV2nOPXpq2iNpB749rVpAYmHy4F8sO39CzhhcM5bKm-gqbBxeW-uMlnqPLBmYLDEp8H2yBOAy0aCyBTmKcQsw9Aw_JItUcs1NxpZkdUs9unfbVNHTsg20e0cacRNwY7uqbWhbUrtBWjXUW-9tXdmGNtgHW9PYoacO6zqekIPS1hFP53pM3u5Xr3ePyfPLw9Pd7XPihDJd4rRwWKCSJYd1piykRnMsS5aBUkwpwaxgjmUp52atRVE4KUGVhUmlAjQpPyZX09xdaD96jF3uqzhuYBts-5gzAyLl0hj1P9Vs1ELA_1Sx4bNA63GByz902_ahGW6elOZa8kHdTMqFNsaAZb4LlbfhM2eQj7nlc275nNvw4mKe2xce1z_-O6gBnE9gG7s2_PaFEoYLxr8Azq2cFA</recordid><startdate>20150918</startdate><enddate>20150918</enddate><creator>Moore, D. 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| source | MEDLINE; JSTOR Archive Collection A-Z Listing; American Association for the Advancement of Science |
| subjects | Age Animals Asymmetry Cell Division Cellular Senescence Damage Diffusion Diffusion barriers Endoplasmic Reticulum - physiology Endoplasmic Reticulum - ultrastructure Intracellular Membranes - physiology Intracellular Membranes - ultrastructure Lamin Type A - metabolism Mammals Mice Neural Stem Cells - cytology Neural Stem Cells - metabolism Neurons Photobleaching Prosencephalon - cytology Prosencephalon - growth & development Prosencephalon - metabolism Protein Transport Proteins Rodents Segregations Stem cells |
| title | A mechanism for the segregation of age in mammalian neural stem cells |
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