Mechanisms of Cellular Protrusions Branch Out

Carlson, Benjamin R.; Soderling, Scott H.

doi:10.1016/j.devcel.2009.08.015

Cited by 14 publications

(15 citation statements)

References 10 publications

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“…Analyses of the F-BAR domain in proteins such as FBP17 and srGAP2 have shown that it can either produce invagination or evagination of membranes (Kamioka et al, 2004; Tsujita et al, 2006; Carlson and Soderling, 2009; Guerrier et al, 2009). This possibility for WRP was tested in cell-based assays for WRP.…”

Section: Resultsmentioning

confidence: 99%

“…Surprisingly, a recent study of srGAP2 showed that its F-BAR domain enhances outward membrane protrusions (Guerrier et al, 2009). Because the membrane topology facilitated by the F-BAR domain of srGAP2 is opposite of other F-BAR domains, it has been termed an inverse F-BAR or inverse F-BAR (IF-BAR) domain (Carlson and Soderling, 2009). Yet, how common the IF-BAR domain is or what the physiological functions of these domains are remains very unclear.…”

Section: Introductionmentioning

confidence: 99%

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WRP/srGAP3Facilitates the Initiation of Spine Development by an Inverse F-BAR Domain, and Its Loss Impairs Long-Term Memory

Carlson¹,

Lloyd²,

Kruszewski³

et al. 2011

J. Neurosci.

110

147

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The WAVE-associated Rac GAP, WRP, is thought to regulate key aspects of synapse development and function and may be linked to mental retardation in humans. WRP contains a newly described inverse F-BAR (IF-BAR) domain of unknown function. Our studies show that this domain senses/facilitates outward protrusions analogous to filopodia and that the molecular basis for this is likely explained by a convex lipid-binding surface on the WRP IF-BAR domain. In dendrites the IF-BAR domain of WRP forms a bud on the shaft from which precursors to spines emerge. Loss of WRP in vivo and in vitro results in reduced density of spines. In vivo this is primarily a loss of mushroom-shaped spines. Developmentally, WRP function is critical at the onset of spinogenesis, when dendritic filopodia are prevalent. Finally, because WRP is implicated in mental retardation, behaviors of WRP heterozygous and null mice have been evaluated. Results from these studies confirm that loss of WRP is linked to impaired learning and memory.

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Section: Resultsmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

WRP/srGAP3Facilitates the Initiation of Spine Development by an Inverse F-BAR Domain, and Its Loss Impairs Long-Term Memory

Carlson¹,

Lloyd²,

Kruszewski³

et al. 2011

J. Neurosci.

110

147

View full text Add to dashboard Cite

show abstract

“…This force may be mediated by the BAR-domain superfamily of proteins, a group of molecules that control curvature of the plasma membrane ( Fig. 2B; Guerrier et al, 2009;Carlson & Soderling, 2009). The balance of expansion and contraction may give rise to rapid fluctuation, or morphing, of spines within 1 min (Matus, 2000).…”

Section: Molecular Bases Of Spine Persistence and 'Intrinsic Fluctuatmentioning

confidence: 99%

Learning rules and persistence of dendritic spines

Kasai

Hayama

Ishikawa

et al. 2010

Eur J of Neuroscience

111

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Structural plasticity of dendritic spines underlies learning, memory and cognition in the cerebral cortex. We here summarize fifteen rules of spine structural plasticity, or 'spine learning rules.' Together, they suggest how the spontaneous generation, selection and strengthening (SGSS) of spines represents the physical basis for learning and memory. This SGSS mechanism is consistent with Hebb's learning rule but suggests new relations between synaptic plasticity and memory. We describe the cellular and molecular bases of the spine learning rules, such as the persistence of spine structures and the fundamental role of actin, which polymerizes to form a 'memory gel' required for the selection and strengthening of spine synapses. We also discuss the possible link between transcriptional and translational regulation of structural plasticity. The SGSS mechanism and spine learning rules elucidate the integral nature of synaptic plasticity in neuronal network operations within the actual brain tissue.

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“…Surprisingly, a recent study of the related srGAP2 showed that its F-BAR domain enhances outward membrane protrusions that appear similar to that of filopodia (Guerrier et al, 2009). Because the membrane topology facilitated by the F-BAR domain of srGAP2 is opposite of other F-BAR domains it has been termed an Inverse F-BAR or IF-BAR domain (Carlson and Soderling, 2009). Yet what the physiological function of this domain is remains very unclear.…”

Section: Regulation Of Spine Formation and Function By The Candidate mentioning

confidence: 99%

Regulation of the Postsynaptic Cytoskeleton: Roles in Development, Plasticity, and Disorders

Svitkina¹,

Lin²,

Webb³

et al. 2010

J. Neurosci.

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The small size of dendritic spines belies the elaborate role they play in excitatory synaptic transmission and ultimately complex behaviors. The cytoskeletal architecture of the spine is predominately composed of actin filaments. These filaments, which at first glance might appear simple, are also surprisingly complex. They dynamically assemble into different structures and serve as a platform for orchestrating the elaborate responses of the spine during experience-dependent plasticity. This mini-symposium review will feature ongoing research into how spines are regulated by actin-signaling pathways during development and plasticity. It will also highlight evolving studies into how disruptions to these pathways might be functionally coupled to congenital disorders such as mental retardation.

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Mechanisms of Cellular Protrusions Branch Out

Cited by 14 publications

References 10 publications

WRP/srGAP3Facilitates the Initiation of Spine Development by an Inverse F-BAR Domain, and Its Loss Impairs Long-Term Memory

WRP/srGAP3Facilitates the Initiation of Spine Development by an Inverse F-BAR Domain, and Its Loss Impairs Long-Term Memory

Learning rules and persistence of dendritic spines

Regulation of the Postsynaptic Cytoskeleton: Roles in Development, Plasticity, and Disorders

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