Annotated protein:LIM domain kinase 1 (LIMK-1) (EC 2.7.11.1). Gene symbol: LIMK1. Taxonomy: Rattus norvegicus (Rat). Uniprot ID: P53669
antibody wiki:
SynGO gene info:SynGO data @ LIMK1
Ontology domain:Biological Process
SynGO term:regulation of modification of postsynaptic actin cytoskeleton (GO:1905274)
Synapse type(s):hippocampus, glutamatergic
Annotated paper:George J, et al. "Palmitoylation of LIM Kinase-1 ensures spine-specific actin polymerization and morphological plasticity" Elife. 2015 Apr 17;4:e06327 PMID:25884247
Figure(s):Figure 4, 5, 6
Annotation description:Figure 4: Acute loss of palmitoyl-LIMK1 impairs Fluorescence Recovery After Photobleaching (FRAP) of GFP-actin in dendritic spines.

"Taken together, these data suggest that the predominant effect of loss of palmitoyl-LIMK1 on GFP-actin turnover is to reduce the pool of mobile actin in spines. This deficit is initially surprising, because LIMK1 is best known as a negative regulator of cofilin, and increased cofilin activity in the absence of palmitoyl-LIMK1 might be expected to increase actin turnover. We consider possible molecular explanations for this finding in the 'Discussion', but taken together, these results suggest that palmitoyl-LIMK1 is essential for normal actin turnover in spines."

Figure 5: Palmitoyl-LIMK1 is required for spine-specific activity-dependent morphological plasticity.

Figure 6: Prolonged loss of palmitoyl-LIMK1 reduces dendritic spine and synapse number.
Evidence tracking, Biological System:Cultured neurons
Evidence tracking, Protein Targeting:RNAi / shRNA
Evidence tracking, Experiment Assay:Confocal
Annotator(s):Frank Koopmans (ORCID:0000-0002-4973-5732)
Guus Smit (ORCID:0000-0002-2286-1587)
Matthijs Verhage (ORCID:0000-0002-2514-0216)
Lab:Department of Functional Genomics, Department of Molecular and Cellular Neurobiology, Center for Neurogenomics and Cognitive Research, Vrije Universiteit Amsterdam, 1081 HV Amsterdam, The Netherlands
Additional literature:"Using LIMK-1 knockout mice, we demonstrate a significant role for LIMK-1 in vivo in regulating cofilin and the actin cytoskeleton. Furthermore, we show that the knockout mice exhibited significant abnormalities in spine morphology and in synaptic function, including enhanced hippocampal long-term potentiation." @ PMID:12123613

" Here, we studied the effects of high-level NRG1 on dendritic spine development and function. We showed that spine density in the prefrontal cortex and hippocampus was reduced in mice (ctoNrg1) that overexpressed NRG1 in neurons. The frequency of miniature excitatory postsynaptic currents (mEPSCs) was reduced in both brain regions of ctoNrg1 mice. High expression of NRG1 activated LIMK1 and increased cofilin phosphorylation in postsynaptic densities. Spine reduction was attenuated by inhibiting LIMK1 or blocking the NRG1-LIMK1 interaction, or by restoring NRG1 protein level." @ PMID:33854034
SynGO annotation ID:5267
Dataset release (version):20231201
View annotation as GO-CAM model:Gene Ontology