Single‐neuron analysis of aging‐associated changes in learning reveals impairments in transcriptional plasticity
The molecular mechanisms underlying age‐related declines in learning and long‐term memory are still not fully understood. To address this gap, our study focused on investigating the transcriptional landscape of a singularly identified motor neuron L7 in Aplysia, which is pivotal in a specific type o...
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creator | Badal, Kerriann K. Sadhu, Abhishek Raveendra, Bindu L. McCracken, Carrie Lozano‐Villada, Sebastian Shetty, Amol C. Gillette, Phillip Zhao, Yibo Stommes, Dustin Fieber, Lynne A. Schmale, Michael C. Mahurkar, Anup Hawkins, Robert D. Puthanveettil, Sathyanarayanan V. |
description | The molecular mechanisms underlying age‐related declines in learning and long‐term memory are still not fully understood. To address this gap, our study focused on investigating the transcriptional landscape of a singularly identified motor neuron L7 in Aplysia, which is pivotal in a specific type of nonassociative learning known as sensitization of the siphon‐withdraw reflex. Employing total RNAseq analysis on a single isolated L7 motor neuron after short‐term or long‐term sensitization (LTS) training of Aplysia at 8, 10, and 12 months (representing mature, late mature, and senescent stages), we uncovered aberrant changes in transcriptional plasticity during the aging process. Our findings specifically highlight changes in the expression of messenger RNAs (mRNAs) that encode transcription factors, translation regulators, RNA methylation participants, and contributors to cytoskeletal rearrangements during learning and long noncoding RNAs (lncRNAs). Furthermore, our comparative gene expression analysis identified distinct transcriptional alterations in two other neurons, namely the motor neuron L11 and the giant cholinergic neuron R2, whose roles in LTS are not yet fully elucidated. Taken together, our analyses underscore cell type‐specific impairments in the expression of key components related to learning and memory within the transcriptome as organisms age, shedding light on the complex molecular mechanisms driving cognitive decline during aging.
The image illustrates a single‐neuron total RNA sequencing approach designed to uncover molecular insights into age‐related learning impairments. We studied short‐term and long‐term sensitization, a type of nonassociative learning, in the sea slug Aplysia californica at three distinct ages. Our molecular analyses identified mRNAs and lncRNAs that were differentially expressed during sensitization. These results indicate that transcriptional plasticity associated with learning is compromised with aging. |
doi_str_mv | 10.1111/acel.14228 |
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The image illustrates a single‐neuron total RNA sequencing approach designed to uncover molecular insights into age‐related learning impairments. We studied short‐term and long‐term sensitization, a type of nonassociative learning, in the sea slug Aplysia californica at three distinct ages. Our molecular analyses identified mRNAs and lncRNAs that were differentially expressed during sensitization. These results indicate that transcriptional plasticity associated with learning is compromised with aging.</description><identifier>ISSN: 1474-9718</identifier><identifier>ISSN: 1474-9726</identifier><identifier>EISSN: 1474-9726</identifier><identifier>DOI: 10.1111/acel.14228</identifier><identifier>PMID: 38924663</identifier><language>eng</language><publisher>England: John Wiley & Sons, Inc</publisher><subject>Age groups ; Aging ; Aging - genetics ; Animals ; Aplysia ; Aplysia - genetics ; Cholinergic nerves ; Cognitive ability ; Cytoskeleton ; DNA methylation ; Gene expression ; Kinases ; Learning - physiology ; Memory ; molecular biology of aging ; Molecular modelling ; Motor Neurons - metabolism ; Motor skill learning ; Nervous system ; Neuronal Plasticity - genetics ; Neurons ; neuroscience ; Phosphatase ; Plasticity ; Proteins ; senescence ; Single-Cell Analysis ; Transcription factors ; Transcription, Genetic ; Transcriptomes</subject><ispartof>Aging cell, 2024-09, Vol.23 (9), p.e14228-n/a</ispartof><rights>2024 The Author(s). published by Anatomical Society and John Wiley & Sons Ltd.</rights><rights>2024 The Author(s). Aging Cell published by Anatomical Society and John Wiley & Sons Ltd.</rights><rights>2024. This work is published under http://creativecommons.org/licenses/by/4.0/ (the "License"). Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><cites>FETCH-LOGICAL-c3388-4abe6ef9548450a99093ba8f16be09fcb619c1f526d97566dc1814ba8f8447303</cites><orcidid>0000-0002-1302-6766</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC11488329/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC11488329/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,315,728,781,785,865,886,1418,11567,27929,27930,45579,45580,46057,46481,53796,53798</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/38924663$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Badal, Kerriann K.</creatorcontrib><creatorcontrib>Sadhu, Abhishek</creatorcontrib><creatorcontrib>Raveendra, Bindu L.</creatorcontrib><creatorcontrib>McCracken, Carrie</creatorcontrib><creatorcontrib>Lozano‐Villada, Sebastian</creatorcontrib><creatorcontrib>Shetty, Amol C.</creatorcontrib><creatorcontrib>Gillette, Phillip</creatorcontrib><creatorcontrib>Zhao, Yibo</creatorcontrib><creatorcontrib>Stommes, Dustin</creatorcontrib><creatorcontrib>Fieber, Lynne A.</creatorcontrib><creatorcontrib>Schmale, Michael C.</creatorcontrib><creatorcontrib>Mahurkar, Anup</creatorcontrib><creatorcontrib>Hawkins, Robert D.</creatorcontrib><creatorcontrib>Puthanveettil, Sathyanarayanan V.</creatorcontrib><title>Single‐neuron analysis of aging‐associated changes in learning reveals impairments in transcriptional plasticity</title><title>Aging cell</title><addtitle>Aging Cell</addtitle><description>The molecular mechanisms underlying age‐related declines in learning and long‐term memory are still not fully understood. To address this gap, our study focused on investigating the transcriptional landscape of a singularly identified motor neuron L7 in Aplysia, which is pivotal in a specific type of nonassociative learning known as sensitization of the siphon‐withdraw reflex. Employing total RNAseq analysis on a single isolated L7 motor neuron after short‐term or long‐term sensitization (LTS) training of Aplysia at 8, 10, and 12 months (representing mature, late mature, and senescent stages), we uncovered aberrant changes in transcriptional plasticity during the aging process. Our findings specifically highlight changes in the expression of messenger RNAs (mRNAs) that encode transcription factors, translation regulators, RNA methylation participants, and contributors to cytoskeletal rearrangements during learning and long noncoding RNAs (lncRNAs). Furthermore, our comparative gene expression analysis identified distinct transcriptional alterations in two other neurons, namely the motor neuron L11 and the giant cholinergic neuron R2, whose roles in LTS are not yet fully elucidated. Taken together, our analyses underscore cell type‐specific impairments in the expression of key components related to learning and memory within the transcriptome as organisms age, shedding light on the complex molecular mechanisms driving cognitive decline during aging.
The image illustrates a single‐neuron total RNA sequencing approach designed to uncover molecular insights into age‐related learning impairments. We studied short‐term and long‐term sensitization, a type of nonassociative learning, in the sea slug Aplysia californica at three distinct ages. Our molecular analyses identified mRNAs and lncRNAs that were differentially expressed during sensitization. These results indicate that transcriptional plasticity associated with learning is compromised with aging.</description><subject>Age groups</subject><subject>Aging</subject><subject>Aging - genetics</subject><subject>Animals</subject><subject>Aplysia</subject><subject>Aplysia - genetics</subject><subject>Cholinergic nerves</subject><subject>Cognitive ability</subject><subject>Cytoskeleton</subject><subject>DNA methylation</subject><subject>Gene expression</subject><subject>Kinases</subject><subject>Learning - physiology</subject><subject>Memory</subject><subject>molecular biology of aging</subject><subject>Molecular modelling</subject><subject>Motor Neurons - metabolism</subject><subject>Motor skill learning</subject><subject>Nervous system</subject><subject>Neuronal Plasticity - genetics</subject><subject>Neurons</subject><subject>neuroscience</subject><subject>Phosphatase</subject><subject>Plasticity</subject><subject>Proteins</subject><subject>senescence</subject><subject>Single-Cell Analysis</subject><subject>Transcription factors</subject><subject>Transcription, Genetic</subject><subject>Transcriptomes</subject><issn>1474-9718</issn><issn>1474-9726</issn><issn>1474-9726</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2024</creationdate><recordtype>article</recordtype><sourceid>24P</sourceid><sourceid>WIN</sourceid><sourceid>EIF</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>AZQEC</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><sourceid>DWQXO</sourceid><sourceid>GNUQQ</sourceid><recordid>eNp9kc1u1DAUhS1ERUthwwOgSGwQ0hQ7dhx7hapR-ZFG6qKwtm48ztSVYwc7aTU7HoFn5Em40ymjwgJvbPl8Pjq-h5BXjJ4xXO_BunDGRF2rJ-SEiVYsdFvLp4czU8fkeSk3lLJWU_6MHHOlayElPyHTlY-b4H79-BndnFOsIELYFl-q1FewQRElKCVZD5NbV_Ya4saVyscqOMgRgSq7WwcB74YRfB5cnO71KUMsNvtx8glNqzFAmbz10_YFOerxgXv5sJ-Sbx8vvi4_L1aXn74sz1cLy7lSCwGdk67XjVCioaA11bwD1TPZOap720mmLeubWq5120i5tkwxsSOUEC2n_JR82PuOcze4tcVkGYIZsx8gb00Cb_5Wor82m3RrGBNK8Vqjw9sHh5y-z65MZvAFxx0gujQXw2lbt1ozxRF98w96k-aMH0eK4eDRTjdIvdtTNqdSsusPaRg1uzbNrk1z3ybCrx_nP6B_6kOA7YE7H9z2P1bmfHmx2pv-BlGJrxI</recordid><startdate>202409</startdate><enddate>202409</enddate><creator>Badal, Kerriann K.</creator><creator>Sadhu, Abhishek</creator><creator>Raveendra, Bindu L.</creator><creator>McCracken, Carrie</creator><creator>Lozano‐Villada, Sebastian</creator><creator>Shetty, Amol C.</creator><creator>Gillette, Phillip</creator><creator>Zhao, Yibo</creator><creator>Stommes, Dustin</creator><creator>Fieber, Lynne A.</creator><creator>Schmale, Michael C.</creator><creator>Mahurkar, Anup</creator><creator>Hawkins, Robert D.</creator><creator>Puthanveettil, Sathyanarayanan V.</creator><general>John Wiley & Sons, Inc</general><general>John Wiley and Sons Inc</general><scope>24P</scope><scope>WIN</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>7TK</scope><scope>8FE</scope><scope>8FH</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BHPHI</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>GNUQQ</scope><scope>HCIFZ</scope><scope>LK8</scope><scope>M7P</scope><scope>PIMPY</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>7X8</scope><scope>5PM</scope><orcidid>https://orcid.org/0000-0002-1302-6766</orcidid></search><sort><creationdate>202409</creationdate><title>Single‐neuron analysis of aging‐associated changes in learning reveals impairments in transcriptional plasticity</title><author>Badal, Kerriann K. ; Sadhu, Abhishek ; Raveendra, Bindu L. ; McCracken, Carrie ; Lozano‐Villada, Sebastian ; Shetty, Amol C. ; Gillette, Phillip ; Zhao, Yibo ; Stommes, Dustin ; Fieber, Lynne A. ; Schmale, Michael C. ; Mahurkar, Anup ; Hawkins, Robert D. ; Puthanveettil, Sathyanarayanan V.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c3388-4abe6ef9548450a99093ba8f16be09fcb619c1f526d97566dc1814ba8f8447303</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2024</creationdate><topic>Age groups</topic><topic>Aging</topic><topic>Aging - genetics</topic><topic>Animals</topic><topic>Aplysia</topic><topic>Aplysia - genetics</topic><topic>Cholinergic nerves</topic><topic>Cognitive ability</topic><topic>Cytoskeleton</topic><topic>DNA methylation</topic><topic>Gene expression</topic><topic>Kinases</topic><topic>Learning - physiology</topic><topic>Memory</topic><topic>molecular biology of aging</topic><topic>Molecular modelling</topic><topic>Motor Neurons - metabolism</topic><topic>Motor skill learning</topic><topic>Nervous system</topic><topic>Neuronal Plasticity - genetics</topic><topic>Neurons</topic><topic>neuroscience</topic><topic>Phosphatase</topic><topic>Plasticity</topic><topic>Proteins</topic><topic>senescence</topic><topic>Single-Cell Analysis</topic><topic>Transcription factors</topic><topic>Transcription, Genetic</topic><topic>Transcriptomes</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Badal, Kerriann K.</creatorcontrib><creatorcontrib>Sadhu, Abhishek</creatorcontrib><creatorcontrib>Raveendra, Bindu L.</creatorcontrib><creatorcontrib>McCracken, Carrie</creatorcontrib><creatorcontrib>Lozano‐Villada, Sebastian</creatorcontrib><creatorcontrib>Shetty, Amol C.</creatorcontrib><creatorcontrib>Gillette, Phillip</creatorcontrib><creatorcontrib>Zhao, Yibo</creatorcontrib><creatorcontrib>Stommes, Dustin</creatorcontrib><creatorcontrib>Fieber, Lynne A.</creatorcontrib><creatorcontrib>Schmale, Michael C.</creatorcontrib><creatorcontrib>Mahurkar, Anup</creatorcontrib><creatorcontrib>Hawkins, Robert D.</creatorcontrib><creatorcontrib>Puthanveettil, Sathyanarayanan V.</creatorcontrib><collection>Wiley-Blackwell Open Access Collection</collection><collection>Wiley Free Archive</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>Neurosciences Abstracts</collection><collection>ProQuest SciTech Collection</collection><collection>ProQuest Natural Science Collection</collection><collection>ProQuest Central (Alumni)</collection><collection>ProQuest Central UK/Ireland</collection><collection>ProQuest Central Essentials</collection><collection>Biological Science Collection</collection><collection>ProQuest Central</collection><collection>ProQuest Natural Science Collection</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central</collection><collection>ProQuest Central Student</collection><collection>SciTech Premium Collection (Proquest) (PQ_SDU_P3)</collection><collection>ProQuest Biological Science Collection</collection><collection>Biological Science Database</collection><collection>Publicly Available Content Database (Proquest) (PQ_SDU_P3)</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>ProQuest Central China</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Aging cell</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Badal, Kerriann K.</au><au>Sadhu, Abhishek</au><au>Raveendra, Bindu L.</au><au>McCracken, Carrie</au><au>Lozano‐Villada, Sebastian</au><au>Shetty, Amol C.</au><au>Gillette, Phillip</au><au>Zhao, Yibo</au><au>Stommes, Dustin</au><au>Fieber, Lynne A.</au><au>Schmale, Michael C.</au><au>Mahurkar, Anup</au><au>Hawkins, Robert D.</au><au>Puthanveettil, Sathyanarayanan V.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Single‐neuron analysis of aging‐associated changes in learning reveals impairments in transcriptional plasticity</atitle><jtitle>Aging cell</jtitle><addtitle>Aging Cell</addtitle><date>2024-09</date><risdate>2024</risdate><volume>23</volume><issue>9</issue><spage>e14228</spage><epage>n/a</epage><pages>e14228-n/a</pages><issn>1474-9718</issn><issn>1474-9726</issn><eissn>1474-9726</eissn><abstract>The molecular mechanisms underlying age‐related declines in learning and long‐term memory are still not fully understood. To address this gap, our study focused on investigating the transcriptional landscape of a singularly identified motor neuron L7 in Aplysia, which is pivotal in a specific type of nonassociative learning known as sensitization of the siphon‐withdraw reflex. Employing total RNAseq analysis on a single isolated L7 motor neuron after short‐term or long‐term sensitization (LTS) training of Aplysia at 8, 10, and 12 months (representing mature, late mature, and senescent stages), we uncovered aberrant changes in transcriptional plasticity during the aging process. Our findings specifically highlight changes in the expression of messenger RNAs (mRNAs) that encode transcription factors, translation regulators, RNA methylation participants, and contributors to cytoskeletal rearrangements during learning and long noncoding RNAs (lncRNAs). Furthermore, our comparative gene expression analysis identified distinct transcriptional alterations in two other neurons, namely the motor neuron L11 and the giant cholinergic neuron R2, whose roles in LTS are not yet fully elucidated. Taken together, our analyses underscore cell type‐specific impairments in the expression of key components related to learning and memory within the transcriptome as organisms age, shedding light on the complex molecular mechanisms driving cognitive decline during aging.
The image illustrates a single‐neuron total RNA sequencing approach designed to uncover molecular insights into age‐related learning impairments. We studied short‐term and long‐term sensitization, a type of nonassociative learning, in the sea slug Aplysia californica at three distinct ages. Our molecular analyses identified mRNAs and lncRNAs that were differentially expressed during sensitization. These results indicate that transcriptional plasticity associated with learning is compromised with aging.</abstract><cop>England</cop><pub>John Wiley & Sons, Inc</pub><pmid>38924663</pmid><doi>10.1111/acel.14228</doi><tpages>18</tpages><orcidid>https://orcid.org/0000-0002-1302-6766</orcidid><oa>free_for_read</oa></addata></record> |
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subjects | Age groups Aging Aging - genetics Animals Aplysia Aplysia - genetics Cholinergic nerves Cognitive ability Cytoskeleton DNA methylation Gene expression Kinases Learning - physiology Memory molecular biology of aging Molecular modelling Motor Neurons - metabolism Motor skill learning Nervous system Neuronal Plasticity - genetics Neurons neuroscience Phosphatase Plasticity Proteins senescence Single-Cell Analysis Transcription factors Transcription, Genetic Transcriptomes |
title | Single‐neuron analysis of aging‐associated changes in learning reveals impairments in transcriptional plasticity |
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