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In Silico Cross-Analyses with Postsynaptic Proteins and Neuropsychiatric Disorder Susceptibility Genes

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In Silico Cross-Analyses with Postsynaptic Proteins and Neuropsychiatric Disorder Susceptibility Genes bioRxiv preprint doi: https://doi.org/10.1101/801563; this version posted October 11, 2019. The copyright holder for this preprint (which was not certified by peer review) is the author/funder, who has granted bioRxiv a license to display the preprint in perpetuity. It is made available under aCC-BY-NC-ND 4.0 International license. Exploring the Pannexin 1 interactome: In silico cross-analyses with postsynaptic proteins and neuropsychiatric disorder susceptibility genes Simona D Frederiksen1, Leigh E Wicki-Stordeur1, Juan C Sanchez-Arias1, and Leigh Anne Swayne1 1Division of Medical Sciences, University of Victoria, Victoria, BC Canada The Pannexin 1 (Panx1) channel-forming protein is enriched in body, Panx1 is enriched in the central nervous system (CNS; the central nervous system, and has been associated with sev- reviewed by Boyce et al. (2018)). Within the mouse cortex, eral critical neurodevelopmental and plasticity functions; these it is highly expressed in neurons and oligodendrocytes (Ray include dendritic spine formation, neuronal network develop- et al., 2005; Vogt et al., 2005; Zhang et al., 2014; Zoidl et al., ment, synaptic plasticity, and pathological brain states such as 2007)[see brainrnaseq.org]. Consistent with its reported role ischemia, epilepsy, and neurodegeneration. Despite major ad- in regulating developmental cellular behaviours like prolif- vances in understanding the properties and activation modes eration and differentiation in a number of different cells and of Panx1, the Panx1 interactome remains largely uncharac- terized. Considering that Panx1 has been implicated in crit- tissues from other groups, work in our lab has uncovered a ical neurodevelopmental and neurodegenerative processes and role for Panx1 in regulating several aspects of neuronal de- diseases, we investigated the Panx1 interactome (482 Panx1- velopment. interacting proteins) identified from mouse N2a cells. These Our early work revealed that Panx1 promotes neural pre- proteins were cross-analyzed with the postsynaptic proteome cursor cell maintenance in vitro (Wicki-Stordeur et al., of the adult mouse brain previously identified by mass spec- 2012) and in vivo (Wicki-Stordeur et al., 2016). Con- trometry (LC-MS/MS), and neurodegenerative disease and neu- rodevelopmental disorder susceptibility genes previously iden- versely, we found that Panx1 inhibits neurite development tified by genome-wide association studies (GWAS); and then in Neuro2a (N2a) and neural precursor cells (Wicki-Stordeur further investigated using various bioinformatics tools (PAN- and Swayne, 2013). Similarly, cortical neurons from Panx1 THER, GO, KEGG and STRING databases). A total of 104 of knockout mice demonstrated an increased density of den- the Panx1-interacting proteins were located at the postsynapse, dritic spines, as well as larger groups of co-activated neu- and 99 of these formed a 16-cluster protein-protein interaction rons, also known as network ensembles (Sanchez-Arias et (PPI) network (hub proteins: Eef2, Rab6A, Ddx39b, Mapk1, al., 2019). This regulation of neurites and dendritic spines Fh1, Ndufv1 et cetera). The cross-analysis led to the discov- connects nicely with our earlier discovery of Panx1 protein- ery of proteins and candidate genes involved in synaptic func- protein interactions (PPIs) with dendritic spine regulating tion and homeostasis. Of particular note, our analyses also re- proteins, such as the actin-related protein (Arp) 2/3 com- vealed that certain Panx1-interacting proteins are implicated in plex components (Wicki-Stordeur and Swayne, 2013), and Parkinson disease, Alzheimer disease, Huntington disease, amy- otrophic lateral sclerosis, schizophrenia, autism spectrum disor- the microtubule-interacting protein collapsin-response medi- der and epilepsy. Altogether, our work revealed important clues ator protein 2 (Crmp2) (Xu et al., 2018). A role for Panx1 in to the role of Panx1 in neuronal function in health and disease by regulating neuronal development and connectivity is further expanding our knowledge of the PPI network of Panx1, and un- supported by work revealing its role in hippocampal synaptic veiling previously unidentified Panx1-interacting proteins and plasticity under naïve conditions (Ardiles et al., 2014; Ga- networks involved in biological processes and disease. jardo et al., 2018; Prochnow et al., 2012), as well as re- cently reported connections to intellectual disability (Shao Panx1 | PPIs | pathway analysis | neurodegenerative diseases | neurodevel- opmental disorders | Parkinson disease | Alzheimer disease | chaperones | et al., 2016) and autism spectrum disorder (ASD) (Davis et vesicle-mediated transport al., 2012). Moreover, Panx1 has been implicated in synap- Correspondence: Dr. Leigh Anne Swayne. Division of Medical Sciences, Uni- tic dysfunction in ischemia (MacVicar and Thompson, 2010; versity of Victoria, 3800 Finnerty Rd, Victoria BC V8P 5C2, Canada. Phone: +1 250-853-3723. E-mail: [email protected]. Twitter: @dr_swayne Weilinger et al., 2016; Weilinger et al., 2013) and has been suggested to be involved in CNS dysfunction associated with Alzheimer disease (Orellana et al., 2011b) and Parkinson dis- Introduction ease (Diaz et al., 2019). Pannexin 1 (Panx1) is a channel-forming protein that is most Given the newly-discovered role in regulating development commonly known for its role in mediating ATP release (Dahl, of dendritic spines and neuronal networks, our goal in this 2015; Lohman and Isakson, 2014) with context-specific (tis- study was to further expand our analysis of the Panx1 inter- sue and cell type expression, developmental stage and dis- actome, that we previously reported on – partially in Wicki- ease state) properties and regulation (reviewed by Chiu et Stordeur and Swayne (2013) and Wicki-Stordeur (2015), us- al. (2018)). Although ubiquitously expressed throughout the ing in silico tools (Fig. 1). Firstly, we performed over- Frederiksen et al. | bioRχiv | October 10, 2019 | 1–29 bioRxiv preprint doi: https://doi.org/10.1101/801563; this version posted October 11, 2019. The copyright holder for this preprint (which was not certified by peer review) is the author/funder, who has granted bioRxiv a license to display the preprint in perpetuity. It is made available under aCC-BY-NC-ND 4.0 International license. Fig. 1. Work flow for the current study from materials and methods to results. In this study, five subanalyses were conducted (further described in Fig. S1), which explored the: (1) Panx1 interactome in mouse N2a cells, (2) postsynaptic proteome in the adult mouse brain associated with the Panx1 interactome, and (3) neurodegenerative disease and neurodevelopmental disorder susceptibility genes associated with the Panx1 interactome. The data was obtained from three sources: Swayne lab [our lab], the genome-wide association study (GWAS) catalog (Buniello et al., 2019) and the original research article, Roy et al. (2018). The data were analyzed using the statistical computing environment R and the following databases: PANTHER [Protein ANalysis THrough Evolutionary Relationships] (Mi et al., 2019a; Mi et al., 2019b), KEGG [Kyoto Encyclopedia of Genes and Genomes] (Kanehisa et al., 2017; Kanehisa and Goto, 2000) and STRING [Search Tool for the Retrieval of Interacting Genes/Proteins] (Szklarczyk et al., 2019). In addition to the subanalyses, the findings across analyses were combined to provide a comprehensive overview for each neurodegenerative diseases and neurodevelopment disorders in relation to the Panx1 interactome. representation analyses of the entire Panx1 interactome to comparisons, the R statistical computing environment v3.6.0 get a better sense of its putative cellular and pathophysio- was applied. logical roles. Overrepresentation analyses determine if the Panx1-interacting proteins are present more than would be Identification of the Panx1 interactome in mouse N2a expected within the protein classes, cellular components and cells. We previously identified the putative Panx1 interac- biological pathways under investigation. Next, to gain fur- tome from mouse N2a neuroblastoma-derived cells (Wicki- ther insight into how Panx1 regulates dendritic spines, we Stordeur and Swayne, 2013), using methods that were com- performed a cross-analysis with the mouse brain postsynaptic prehensively described in that work as well as in Wicki- proteome, and identified links to existing PPI networks. To Stordeur (2015). Briefly, proteins co-precipitating with further examine the link between Panx1 and neurodegener- Panx1-EGFP [enhanced green fluorescent protein] or EGFP ative diseases and neurodevelopmental disorders associated from N2a cells, were identified by the UVIC-Genome with abnormalities of dendritic spines (recipients of excita- BC Proteomics Centre using high performance liquid tory inputs) (Forrest et al., 2018; Maiti et al., 2015; Pen- chromatography-tandem mass spectrometry (LC-MS/MS) zes et al., 2011), we also cross-analyzed the Panx1 interac- followed by analysis with Proteome Discoverer v1.3.0.339 tome with suggestive candidate genes identified by genome- (Thermo Scientific) and Mascot v2.2 (Perkins et al., 1999) wide association studies (GWAS). Here, we focused specifi- [percolator settings: Max delta Cn 0.05, Target false discov- cally on Parkinson disease, Alzheimer disease, amyotrophic ery rate (FDR) strict 0.01, Target FDR relaxed 0.05 with val- lateral sclerosis (ALS), Huntington disease, schizophrenia, idation based on q-value]. The q-value refers to the minimal ASD and epilepsy.
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