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4. Psychosis Risk Candidate ZNF804A Localizes to Synapses and Regulates Neurite Formation and Dendritic Spine Structure

Author

Deans, PJM, Raval, P, Sellers, KJ, Gatford, NG, Halai, S, Duarte, RRR, Shum, C, Warre-Cornish, K, Kaplun, VE, Cocks, G, Hill, M, Bray, NJ, Price, J, and Srivastava, DP

Subjects
GluN1, Bipolar disorder, Dendritic Spines, Kruppel-Like Transcription Factors, Action Potentials, autism spectrum disorder, neural progenitor cells, induced pluripotent stem cells (iPSC), Induced pluripotent stem cells (iPSCs), Polymorphism, Single Nucleotide, superresolution microscopy, Human neurons, synapse, Neurites, Animals, Humans, Genetic Predisposition to Disease, psychosis, Neural progenitor cells, Autism spectrum disorder, Super-resolution microscopy, RNA, Small Interfering, human neurons, PSD-95, Cells, Cultured, Biological Psychiatry, Neurons, dendritic spine, Psychosis, Synapse, R1, Rats, Archival Report, Psychotic Disorders, Dendritic spine, Synapses, Schizophrenia, Genome-Wide Association Study
Abstract

Background Variation in the gene encoding zinc finger binding protein 804A (ZNF804A) is associated with schizophrenia and bipolar disorder. Evidence suggests that ZNF804A is a regulator of gene transcription and is present in nuclear and extranuclear compartments. However, a detailed examination of ZNF804A distribution and its neuronal functions has yet to be performed. Methods The localization of ZNF804A protein was examined in neurons derived from human neural progenitor cells, human induced pluripotent stem cells, or in primary rat cortical neurons. In addition, small interfering RNA-mediated knockdown of ZNF804A was conducted to determine its role in neurite formation, maintenance of dendritic spine morphology, and responses to activity-dependent stimulations. Results Endogenous ZNF804A protein localized to somatodendritic compartments and colocalized with the putative synaptic markers in young neurons derived from human neural progenitor cells and human induced pluripotent stem cells. In mature rat neurons, Zfp804A, the homolog of ZNF804A, was present in a subset of dendritic spines and colocalized with synaptic proteins in specific nanodomains, as determined by super-resolution microscopy. Interestingly, knockdown of ZNF804A attenuated neurite outgrowth in young neurons, an effect potentially mediated by reduced neuroligin-4 expression. Furthermore, knockdown of ZNF804A in mature neurons resulted in the loss of dendritic spine density and impaired responses to activity-dependent stimulation. Conclusions These data reveal a novel subcellular distribution for ZNF804A within somatodendritic compartments and a nanoscopic organization at excitatory synapses. Moreover, our results suggest that ZNF804A plays an active role in neurite formation, maintenance of dendritic spines, and activity-dependent structural plasticity.

Published
2016
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5. Visual accessibility in graphic design: A client-designer communication failure

Author

Cornish, K, Goodman-Deane, J, Ruggeri, K, John Clarkson, P, Deane, Joy [0000-0001-8166-1705], Ruggeri, Kai [0000-0002-8470-101X], and Apollo - University of Cambridge Repository

Subjects
communication, user centred design, design processes, visual accessibility, graphic design
Abstract

It is essential that graphic design is visually clear and accessible. However, evidence suggests that a lack of consideration is given to visual accessibility in print-based graphic design. Furthermore, effective client-designer communication is a vital component in this. This paper investigates current graphic design practice, with regard to visual accessibility, specifically focussing on client-designer communication. A survey of 122 graphic designers and clients identified that these two groups may not be communicating with each other effectively with regard to visual accessibility, and that there is a need to develop inclusive design tools to assist them with this. This paper adds a novel contribution to our limited understanding of visual accessibility in the UK’s graphic design industry.

Published
2015

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