Cellular and subcellular localization of paralemmin-1, a protein involved in cell shape control, in the rat brain, adrenal gland and kidney

Kutzleb, Christian; Petrasch‐Parwez, Elisabeth; Kilimann, Manfred W.

doi:10.1007/s00418-006-0209-y

Cited by 17 publications

(17 citation statements)

References 16 publications

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“…Alternatively, altered membrane dynamics may indirectly regulate recruitment of actin-bundling proteins and GTPases that regulate protrusion formation. It is also possible that palmitoylation-dependent targeting of paralemmin-1 and other palmitoylated proteins to lipid rafts affects signaling molecules that reside in these lipid microdomains, resulting in the activation of molecules directly involved in protrusion expansion (Anderson and Jacobson, 2002;Gauthier-Campbell et al, 2004;Kutzleb et al, 2007). Alterations in cholesterol/sphingolipid-enriched lipid raft microdomains in neurons influence protein trafficking, formation of signaling complexes, and regulation of the actin cytoskeleton (Hering et al, 2003).…”

Section: Discussionmentioning

confidence: 99%

Paralemmin-1, a Modulator of Filopodia Induction Is Required for Spine Maturation

Arstikaitis

Gauthier-Campbell

Herrera

et al. 2008

MBoC

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Dendritic filopodia are thought to participate in neuronal contact formation and development of dendritic spines; however, molecules that regulate filopodia extension and their maturation to spines remain largely unknown. Here we identify paralemmin-1 as a regulator of filopodia induction and spine maturation. Paralemmin-1 localizes to dendritic membranes, and its ability to induce filopodia and recruit synaptic elements to contact sites requires protein acylation. Effects of paralemmin-1 on synapse maturation are modulated by alternative splicing that regulates spine formation and recruitment of AMPA-type glutamate receptors. Paralemmin-1 enrichment at the plasma membrane is subject to rapid changes in neuronal excitability, and this process controls neuronal activity-driven effects on protrusion expansion. Knockdown of paralemmin-1 in developing neurons reduces the number of filopodia and spines formed and diminishes the effects of Shank1b on the transformation of existing filopodia into spines. Our study identifies a key role for paralemmin-1 in spine maturation through modulation of filopodia induction. INTRODUCTIONDuring CNS excitatory synapse development, the formation of spines, bulbous protrusions enriched with F-actin, is essential for proper synaptic transmission and neuronal function (Hall and Nobes, 2000;Yuste and Bonhoeffer, 2004;Halpain et al., 2005;Matus, 2005;. Spines contain a plethora of proteins including neurotransmitter receptors, cytoskeleton-associated proteins, and cell adhesion molecules. Spines are pleomorphic protrusions that can be modified by changes in neuronal activity, which regulate actin-based motility (Fischer et al., 1998;Portera-Cailliau et al., 2003;Matus, 2005). Defects in spine maturation and function have been associated with several forms of mental retardation including Down, Rett, Fragile X, and fetal alcohol syndromes. Some of these disorders exhibit a reduction in spine size and density and the formation of long, thin filopodia-like structures (Hering and Sheng, 2001;Zoghbi, 2003).Although our knowledge of molecules that control the morphology and functional properties of dendritic spines has expanded, information about the structures from which spines emerge is lacking. Dendritic filopodia, thin protrusions ranging in length from 2 to 35 m, are thought to participate in synaptogenesis, dendritic branching and the development of spines. During synaptogenesis, filopodia decorate the dendrites of neurons. Studies show that dendritic filopodia exhibit highly dynamic protrusive motility during periods of active synaptogenesis (Dailey and Smith, 1996;Ziv and Smith, 1996;Marrs et al., 2001). Thus, filopodia are thought to function by extending and probing the environment for appropriate presynaptic partners, thereby aiding in synapse formation. These results are further supported by electron microscopy studies which show that synapses can be formed at the tip and base of dendritic filopodia (Fiala et al., 1998;Kirov et al., 2004). As synapses form, the number of filopodia d...

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Section: Discussionmentioning

confidence: 99%

Paralemmin-1, a Modulator of Filopodia Induction Is Required for Spine Maturation

Arstikaitis

Gauthier-Campbell

Herrera

et al. 2008

MBoC

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“…Other highly downregulated genes include ABCA2 (FC of 16), which was also significantly downregulated at 3 dpi, and the lipidanchored membrane paralemmin (PALM, FC of 8), which regulates neuron cell shape and motility (80). Some of the most downregulated DEGs that mapped to these GO terms were also detected at 3 dpi, notably GFAP, MAG, MOBP, and CLDN11.…”

Section: Fig 7 Immunohistochemistry Gene Validation Ihc Staining Andmentioning

confidence: 99%

Acute Simian Varicella Virus Infection Causes Robust and Sustained Changes in Gene Expression in the Sensory Ganglia

Arnold

Girke

Sureshchandra

et al. 2016

J Virol

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Primary infection with varicella-zoster virus (VZV), a neurotropic alphaherpesvirus, results in varicella. VZV establishes latency in the sensory ganglia and can reactivate later in life to cause herpes zoster. The relationship between VZV and its host during acute infection in the sensory ganglia is not well understood due to limited access to clinical specimens. Intrabronchial inoculation of rhesus macaques with simian varicella virus (SVV) recapitulates the hallmarks of VZV infection in humans. We leveraged this animal model to characterize the host-pathogen interactions in the ganglia during both acute and latent infection by measuring both viral and host transcriptomes on days postinfection (dpi) 3, 7, 10, 14, and 100. SVV DNA and transcripts were detected in sensory ganglia 3 dpi, before the appearance of rash. CD4 and CD8 T cells were also detected in the sensory ganglia 3 dpi. Moreover, lung-resident T cells isolated from the same animals 3 dpi also harbored SVV DNA and transcripts, suggesting that T cells may be responsible for trafficking SVV to the ganglia. Transcriptome sequencing (RNA-Seq) analysis showed that cessation of viral transcription 7 dpi coincides with a robust antiviral innate immune response in the ganglia. Interestingly, a significant number of genes that play a critical role in nervous system development and function remained downregulated into latency. These studies provide novel insights into host-pathogen interactions in the sensory ganglia during acute varicella and demonstrate that SVV infection results in profound and sustained changes in neuronal gene expression. IMPORTANCEMany aspects of VZV infection of sensory ganglia remain poorly understood, due to limited access to human specimens and the fact that VZV is strictly a human virus. Infection of rhesus macaques with simian varicella virus (SVV), a homolog of VZV, provides a robust model of the human disease. Using this model, we show that SVV reaches the ganglia early after infection, most likely by T cells, and that the induction of a robust innate immune response correlates with cessation of virus transcription. We also report significant changes in the expression of genes that play an important role in neuronal function. Importantly, these changes persist long after viral replication ceases. Given the homology between SVV and VZV, and the genetic and physiological similarities between rhesus macaques and humans, our results provide novel insight into the interactions between VZV and its human host and explain some of the neurological consequences of VZV infection. V aricella-zoster virus (VZV) is a neurotropic alphaherpesvirus and the causative agent of varicella (chickenpox) (1). VZV establishes latency in the sensory ganglia and can reactivate later in life to cause herpes zoster (shingles), a painful disease that affects almost 1 million individuals in the United States alone (2). VZV is transmitted through the inhalation of virus-laden saliva droplets or by direct contact with the infectious fluid from vesicles...

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“…3A, B). These receptor-like molecules have also been reported to be located within membrane microdomains [18]. Thus, we investigated the localization of caveolin as an indicator of the locations of membrane microdomains, and thereby determined the locations of the receptor-like molecules.…”

Section: Resultsmentioning

confidence: 99%

Receptor-like Molecules on Human Intestinal Epithelial Cells Interact with an Adhesion Factor from <i>Lactobacillus reuteri</i>

Matsuo

Miyoshi²,

Okada³

et al. 2012

Bioscience of Microbiota, Food and Health

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A surface protein of Lactobacillus reuteri, mucus adhesion-promoting protein (MapA), is considered to be an adhesion factor. MapA is expressed in L. reuteri strains and adheres to piglet gastric mucus, collagen type I, and human intestinal epithelial cells such as Caco-2. The aim of this study was to identify molecules that mediate the attachment of MapA from L. reuteri to the intestinal epithelial cell surface by investigating the adhesion of MapA to receptor-like molecules on Caco-2 cells. MapA-binding receptor-like molecules were detected in Caco-2 cell lysates by 2D-PAGE. Two proteins, annexin A13 (ANXA13) and paralemmin (PALM), were identified by MALDI TOF-MS. The results of a pull-down assay showed that MapA bound directly to ANXA13 and PALM. Fluorescence microscopy studies confirmed that MapA binding to ANXA13 and PALM was colocalized on the Caco-2 cell membrane. To evaluate whether ANXA13 and PALM are important for MapA adhesion, ANXA13 and PALM knockdown cell lines were established. The adhesion of MapA to the abovementioned cell lines was reduced compared with that to wild-type Caco-2 cells. These knockdown experiments established the importance of these receptor-like molecules in MapA adhesion.

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Cellular and subcellular localization of paralemmin-1, a protein involved in cell shape control, in the rat brain, adrenal gland and kidney

Cited by 17 publications

References 16 publications

Paralemmin-1, a Modulator of Filopodia Induction Is Required for Spine Maturation

Paralemmin-1, a Modulator of Filopodia Induction Is Required for Spine Maturation

Acute Simian Varicella Virus Infection Causes Robust and Sustained Changes in Gene Expression in the Sensory Ganglia

Receptor-like Molecules on Human Intestinal Epithelial Cells Interact with an Adhesion Factor from <i>Lactobacillus reuteri</i>

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