Important roles of Vilse in dendritic architecture and synaptic plasticity

Lee, Jin-Yu; Lee, Li-Jen; Fan, Chih-Chen; Chang, Ho-Ching; Shih, Hsin-An; Min, Ming‐Yuan; Chang, Mau-Sun

doi:10.1038/srep45646

Cited by 15 publications

(15 citation statements)

References 31 publications

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“…Furthermore, other studies have revealed that changes in dendritic complexity impaired LMC (Freymuth & Fitzsimons, 2017;Lee et al, 2017). Both the microinjection of dme-miR-92b antagomirs and overexpression of crebA in D. melanogaster did result in significant increase of LMC (Bi et al, 2019), further supporting a miRNA-target pathway that regulates the change of LMC in Drosophila induced by Wolbachia infection.…”

Section: Effect Of Wolbachia On Learning and Memory Capacity (Lmc) Inmentioning

confidence: 71%

The effect of the endosymbiont Wolbachia on the behavior of insect hosts

Wang

2019

Insect Science

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As one of the most successful intracellular symbiotic bacteria, Wolbachia can infect many arthropods and nematodes. Wolbachia infection usually affects the reproduction of their hosts to promote their own proliferation and transmission. Currently, most of the studies focus on the mechanisms of Wolbachia interactions with host reproduction. However, in addition to distribution in the reproductive tissues, Wolbachia also infect various somatic tissues of their hosts, including the brain. This raises the potential that Wolbachia may influence some somatic processes, such as behaviors in their hosts. So far, information about the effects of Wolbachia infection on host behavior is still very limited. The present review presents the current literature on different aspects of the influence of Wolbachia on various behaviors, including sleep, learning and memory, mating, feeding and aggression in their insect hosts. We then highlight ongoing scientific efforts in the field that need addressing to advance this field, which can have significant implications for further developing Wolbachia as environmentally friendly biocontrol agents to control insect‐borne diseases and agricultural pests.

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Section: Effect Of Wolbachia On Learning and Memory Capacity (Lmc) Inmentioning

confidence: 71%

The effect of the endosymbiont Wolbachia on the behavior of insect hosts

Wang

2019

Insect Science

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“…It is plausible that CNK2 serves this purpose for a diverse set of signalling complexes. In this context, the fact that CNK2 also interacts with Vilse/ARHGAP39 (see Supplemental Table 1 and Lim et al 5 ), which has been shown to influence dendritic architecture 42 (see also Nowak et al 43 , for review), may be of relevance. As is the case for TNIK, the interaction with Vilse/ARHGAP39 relies on residues of CNK2 that are present in the C-terminal half of the molecule.…”

Section: Discussionmentioning

confidence: 99%

Disease-associated synaptic scaffold protein CNK2 modulates PSD size and influences localisation of the regulatory kinase TNIK

Zieger

Kunde

Rademacher

et al. 2020

Sci Rep

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Scaffold proteins are responsible for structural organisation within cells; they form complexes with other proteins to facilitate signalling pathways and catalytic reactions. The scaffold protein connector enhancer of kinase suppressor of Ras 2 (CNK2) is predominantly expressed in neural tissues and was recently implicated in X-linked intellectual disability (ID). We have investigated the role of CNK2 in neurons in order to contribute to our understanding of how CNK2 alterations might cause developmental defects, and we have elucidated a functional role for CNK2 in the molecular processes that govern morphology of the postsynaptic density (PSD). We have also identified novel CNK2 interaction partners and explored their functional interdependency with CNK2. We focussed on the novel interaction partner TRAF2-and NCK-interacting kinase TNIK, which is also associated with ID. Both CNK2 and TNIK are expressed in neuronal dendrites and concentrated in dendritic spines, and staining with synaptic markers indicates a clear postsynaptic localisation. Importantly, our data highlight that CNK2 plays a role in directing TNIK subcellular localisation, and in neurons, CNK2 participates in ensuring that this multifunctional kinase is present in the correct place at desirable levels. In summary, our data indicate that CNK2 expression is critical for modulating PSD morphology; moreover, our study highlights that CNK2 functions as a scaffold with the potential to direct the localisation of regulatory proteins within the cell. Importantly, we describe a novel link between CNK2 and the regulatory kinase TNIK, and provide evidence supporting the idea that alterations in CNK2 localisation and expression have the potential to influence the behaviour of TNIK and other important regulatory molecules in neurons. Scaffold proteins are multi-domain proteins that typically lack enzymatic activity. However, they are crucial in regulating signal transduction cascades: through multiple protein-protein interactions, they organise protein complex formation and ensure spatiotemporal organisation of signalling processes and signal propagation. The scaffold protein connector enhancer of kinase suppressor of Ras (CNK/CNKSR) was first discovered in Drosophila, where it was shown to regulate Ras/MAPK signalling by binding to the Ras effector RAF and thereby play an essential role in eye and wing development 1,2. Subsequent studies on CNKs in various organisms showed that CNK homologues are present across species, ranging e.g. from C. elegans 3 to humans 1 , and that they likewise influence signalling by acting as scaffolds downstream of Ras 1. CNKs possess multiple protein interaction domains, including e.g. a sterile alpha motif (SAM), a conserved region in CNK (CRIC), a PSD-95/DLG-1/ZO-1 (PDZ) domain, and a pleckstrin homology (PH) domain, and the domain architecture is essentially conserved throughout the CNK family proteins and also across species. Since the original discovery of the D-CNK protein in Drosophila, it has become clear that CNK family ...

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“…Arhgap39/Porf-2 has been shown to function through regulation of two Rho GTPases, Rac1 and Cdc42. Several investigators have shown that Arhgap39/Porf-2 is a regulator of Rho GTPases and as such plays a role in endothelial cell migration ( Kaur et al, 2008 ), ganglion and axon tracking ( Lundström et al, 2004 ; Hu et al, 2005 ), neural stem cell fate ( Ma and Nowak, 2011 ; Huang et al, 2016 ), and dendritic spine formation ( Lim et al, 2014 ; Lee et al, 2017 ). These studies further link Arhgap39/Porf-2 to angiogenesis, tracheal innervation, and CNS development.…”

Section: Functional Roles and Downstream Effectors ( Table mentioning

confidence: 99%

“…This may reflect variation in expression of mRNA variants 1 and 2, an interesting observation, since they both encode the same protein isoform, but differ in the 5′ UTR. Quite recently, Lee et al (2017) described the effects in hippocampus of a widespread Arhgap39/Porf-2 knockout in mouse forebrain under the direction of the CamKII promoter. These mice show behavioral deficits in learning and memory as measured by Morris water maze and Y-maze performance.…”

Section: Functional Roles and Downstream Effectors ( Table mentioning

confidence: 99%

Porf-2 = Arhgap39 = Vilse: A Pivotal Role in Neurodevelopment, Learning and Memory

Nowak

2018

eNeuro

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Small GTP-converting enzymes, GTPases, are essential for the efficient completion of many physiological and developmental processes. They are regulated by GTPase activating proteins (GAPs) and guanine nucleotide exchange factors (GEFs). Arhgap39, also known as preoptic regulatory factor-2 (Porf-2) or Vilse, a member of the Rho GAP group, was first identified in 1990 in the rat CNS. It has since been shown to regulate apoptosis, cell migration, neurogenesis, and cerebral and hippocampal dendritic spine morphology. It plays a pivotal role in neurodevelopment and learning and memory. Homologous or orthologous genes are found in more than 280 vertebrate and invertebrate species, suggesting preservation through evolution. Not surprisingly, loss of the Arhgap39/Porf-2 gene in mice manifests as an embryonic lethal condition. Although Arhgap39/Porf-2 is highly expressed in the brain, it is also widely distributed throughout the body, with potential additional roles in oncogenesis and morphogenesis. This review summarizes, for the first time, the known information about this gene under its various names, in addition to considering its transcripts and proteins. The majority of findings described have been made in rats, mice, humans, and fruit flies. This work surveys the known functions, functional mediators, variables modifying expression and upstream regulators of expression, and potential physiological and pathological roles of Arhgap39/Porf-2 in health and disease.

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Important roles of Vilse in dendritic architecture and synaptic plasticity

Cited by 15 publications

References 31 publications

The effect of the endosymbiont Wolbachia on the behavior of insect hosts

The effect of the endosymbiont Wolbachia on the behavior of insect hosts

Disease-associated synaptic scaffold protein CNK2 modulates PSD size and influences localisation of the regulatory kinase TNIK

Porf-2 = Arhgap39 = Vilse: A Pivotal Role in Neurodevelopment, Learning and Memory

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