Caldendrin and myosin V regulate synaptic spine apparatus localization via ER stabilization in dendritic spines
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Caldendrin and myosin V regulate synaptic spine apparatus localization via ER stabilization in dendritic spines. / Konietzny, Anja; Grendel, Jasper; Kadek, Alan; Bucher, Michael; Han, Yuhao; Hertrich, Nathalie; Dekkers, Dick H W; Demmers, Jeroen A A; Grünewald, Kay; Uetrecht, Charlotte; Mikhaylova, Marina.
in: EMBO J, Jahrgang 41, Nr. 4, e106523, 15.02.2022.Publikationen: SCORING: Beitrag in Fachzeitschrift/Zeitung › SCORING: Zeitschriftenaufsatz › Forschung › Begutachtung
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TY - JOUR
T1 - Caldendrin and myosin V regulate synaptic spine apparatus localization via ER stabilization in dendritic spines
AU - Konietzny, Anja
AU - Grendel, Jasper
AU - Kadek, Alan
AU - Bucher, Michael
AU - Han, Yuhao
AU - Hertrich, Nathalie
AU - Dekkers, Dick H W
AU - Demmers, Jeroen A A
AU - Grünewald, Kay
AU - Uetrecht, Charlotte
AU - Mikhaylova, Marina
N1 - © 2021 The Authors. Published under the terms of the CC BY NC ND 4.0 license.
PY - 2022/2/15
Y1 - 2022/2/15
N2 - Excitatory synapses of principal hippocampal neurons are frequently located on dendritic spines. The dynamic strengthening or weakening of individual inputs results in structural and molecular diversity of dendritic spines. Active spines with large calcium ion (Ca2+ ) transients are frequently invaded by a single protrusion from the endoplasmic reticulum (ER), which is dynamically transported into spines via the actin-based motor myosin V. An increase in synaptic strength correlates with stable anchoring of the ER, followed by the formation of an organelle referred to as the spine apparatus. Here, we show that myosin V binds the Ca2+ sensor caldendrin, a brain-specific homolog of the well-known myosin V interactor calmodulin. While calmodulin is an essential activator of myosin V motor function, we found that caldendrin acts as an inhibitor of processive myosin V movement. In mouse and rat hippocampal neurons, caldendrin regulates spine apparatus localization to a subset of dendritic spines through a myosin V-dependent pathway. We propose that caldendrin transforms myosin into a stationary F-actin tether that enables the localization of ER tubules and formation of the spine apparatus in dendritic spines.
AB - Excitatory synapses of principal hippocampal neurons are frequently located on dendritic spines. The dynamic strengthening or weakening of individual inputs results in structural and molecular diversity of dendritic spines. Active spines with large calcium ion (Ca2+ ) transients are frequently invaded by a single protrusion from the endoplasmic reticulum (ER), which is dynamically transported into spines via the actin-based motor myosin V. An increase in synaptic strength correlates with stable anchoring of the ER, followed by the formation of an organelle referred to as the spine apparatus. Here, we show that myosin V binds the Ca2+ sensor caldendrin, a brain-specific homolog of the well-known myosin V interactor calmodulin. While calmodulin is an essential activator of myosin V motor function, we found that caldendrin acts as an inhibitor of processive myosin V movement. In mouse and rat hippocampal neurons, caldendrin regulates spine apparatus localization to a subset of dendritic spines through a myosin V-dependent pathway. We propose that caldendrin transforms myosin into a stationary F-actin tether that enables the localization of ER tubules and formation of the spine apparatus in dendritic spines.
U2 - 10.15252/embj.2020106523
DO - 10.15252/embj.2020106523
M3 - SCORING: Journal article
C2 - 34935159
VL - 41
JO - EMBO J
JF - EMBO J
SN - 0261-4189
IS - 4
M1 - e106523
ER -
