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Article: Specific depletion of the motor protein KIF5B leads to deficits in dendritic transport, synaptic plasticity and memory

TitleSpecific depletion of the motor protein KIF5B leads to deficits in dendritic transport, synaptic plasticity and memory
Authors
Keywordscell biology
mouse
neuroscience
rat
Issue Date2020
PublishereLife Sciences Publications Ltd. The Journal's web site is located at http://elifesciences.org/
Citation
eLife, 2020, v. 9, p. article no. e53456 How to Cite?
AbstractThe kinesin I family of motor proteins are crucial for axonal transport, but their roles in dendritic transport and postsynaptic function are not well-defined. Gene duplication and subsequent diversification give rise to three homologous kinesin I proteins (KIF5A, KIF5B and KIF5C) in vertebrates, but it is not clear whether and how they exhibit functional specificity. Here we show that knockdown of KIF5A or KIF5B differentially affects excitatory synapses and dendritic transport in hippocampal neurons. The functional specificities of the two kinesins are determined by their diverse carboxyl-termini, where arginine methylation occurs in KIF5B and regulates its function. KIF5B conditional knockout mice exhibit deficits in dendritic spine morphogenesis, synaptic plasticity and memory formation. Our findings provide insights into how expansion of the kinesin I family during evolution leads to diversification and specialization of motor proteins in regulating postsynaptic function.
Persistent Identifierhttp://hdl.handle.net/10722/280340
ISSN
2023 Impact Factor: 6.4
2023 SCImago Journal Rankings: 3.932
ISI Accession Number ID

 

DC FieldValueLanguage
dc.contributor.authorZHAO, J-
dc.contributor.authorFOK, AHK-
dc.contributor.authorFAN, R-
dc.contributor.authorKwan, PY-
dc.contributor.authorCHAN, HL-
dc.contributor.authorLO, LHY-
dc.contributor.authorChan, YS-
dc.contributor.authorYung, WH-
dc.contributor.authorHuang, J-
dc.contributor.authorLai, CSW-
dc.contributor.authorLai, K-O-
dc.date.accessioned2020-02-07T07:39:44Z-
dc.date.available2020-02-07T07:39:44Z-
dc.date.issued2020-
dc.identifier.citationeLife, 2020, v. 9, p. article no. e53456-
dc.identifier.issn2050-084X-
dc.identifier.urihttp://hdl.handle.net/10722/280340-
dc.description.abstractThe kinesin I family of motor proteins are crucial for axonal transport, but their roles in dendritic transport and postsynaptic function are not well-defined. Gene duplication and subsequent diversification give rise to three homologous kinesin I proteins (KIF5A, KIF5B and KIF5C) in vertebrates, but it is not clear whether and how they exhibit functional specificity. Here we show that knockdown of KIF5A or KIF5B differentially affects excitatory synapses and dendritic transport in hippocampal neurons. The functional specificities of the two kinesins are determined by their diverse carboxyl-termini, where arginine methylation occurs in KIF5B and regulates its function. KIF5B conditional knockout mice exhibit deficits in dendritic spine morphogenesis, synaptic plasticity and memory formation. Our findings provide insights into how expansion of the kinesin I family during evolution leads to diversification and specialization of motor proteins in regulating postsynaptic function.-
dc.languageeng-
dc.publishereLife Sciences Publications Ltd. The Journal's web site is located at http://elifesciences.org/-
dc.relation.ispartofeLife-
dc.rightsThis work is licensed under a Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International License.-
dc.subjectcell biology-
dc.subjectmouse-
dc.subjectneuroscience-
dc.subjectrat-
dc.titleSpecific depletion of the motor protein KIF5B leads to deficits in dendritic transport, synaptic plasticity and memory-
dc.typeArticle-
dc.identifier.emailKwan, PY: pykwanaa@hku.hk-
dc.identifier.emailChan, YS: yschan@hku.hk-
dc.identifier.emailHuang, J: jdhuang@hku.hk-
dc.identifier.emailLai, CSW: coraswl@hku.hk-
dc.identifier.emailLai, K-O: laiko@hku.hk-
dc.identifier.authorityChan, YS=rp00318-
dc.identifier.authorityHuang, J=rp00451-
dc.identifier.authorityLai, CSW=rp01895-
dc.identifier.authorityLai, K-O=rp01891-
dc.description.naturepublished_or_final_version-
dc.identifier.doi10.7554/eLife.53456-
dc.identifier.pmid31961321-
dc.identifier.scopuseid_2-s2.0-85079117411-
dc.identifier.hkuros309092-
dc.identifier.volume9-
dc.identifier.spagearticle no. e53456-
dc.identifier.epagearticle no. e53456-
dc.identifier.isiWOS:000516559200001-
dc.publisher.placeCambridge, UK-
dc.identifier.issnl2050-084X-

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