Alterations in gene expression in the spinal cord of mice lacking Nfix
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Alterations in gene expression in the spinal cord of mice lacking Nfix Elise Matuzelski1, Alexandra Essebier2, Lachlan Harris1, Richard M. Gronostajski3, Tracey J. Harvey1 and Michael Piper1,4*
Abstract Objective: Nuclear Factor One X (NFIX) is a transcription factor expressed by neural stem cells within the developing mouse brain and spinal cord. In order to characterise the pathways by which NFIX may regulate neural stem cell biology within the developing mouse spinal cord, we performed an microarray-based transcriptomic analysis of the spinal cord of embryonic day (E)14.5 Nfix−/− mice in comparison to wild-type controls. Data description: Using microarray and differential gene expression analyses, we were able to identify differentially expressed genes in the spinal cords of E14.5 Nfix−/− mice compared to wild-type controls. We performed microarraybased sequencing on spinal cords from n = 3 E14.5 Nfix−/− mice and n = 3 E14.5 Nfix+/+ mice. Differential gene expression analysis, using a false discovery rate (FDR) p-value of p ± 1.5, revealed 1351 differentially regulated genes in the spinal cord of Nfix−/− mice. Of these, 828 were upregulated, and 523 were downregulated. This resource provides a tool to interrogate the role of this transcription factor in spinal cord development. Keywords: Nuclear Factor One, NFIX, Spinal cord, Microarray Objective Transcription factors play a central role in promoting stem cell biology within the developing embryo. For example, the Nuclear Factor One (NFI) transcription factors regulate fetal muscle gene expression [1], retinal development [2], and dorsal telencephalic formation [3, 4]. NFIX specifically promotes neural stem cell differentiation within the developing neocortex, hippocampus and cerebellum [5–8], as well as within the adult forebrain neurogenic niches [9, 10]. Mechanistically, NFIs have been shown to drive differentiation within the nervous system via the activation of lineage-specific gene expression patterns, as well as via the repression of stem cell self-renewal genes [11, 12]. *Correspondence: [email protected] 1 School of Biomedical Sciences, The Faculty of Medicine, The University of Queensland, Brisbane, QLD 4072, Australia Full list of author information is available at the end of the article
NFIs also contribute to mouse spinal cord development. Mice lacking either Nfia or Nfib exhibit reduced expression of the astrocyte marker GFAP at E18.5 [13]. Moreover, NFIA has been proposed to mediate the switch in neural progenitor cell activity, promoting progression down a glial lineage, rather than the neural lineage [13]. NFIA has more recently been shown to interact with SOX9 in order to promote the expression of astrocytic genes, including Apcdd1 and Mmd2 [14]. We have also recently shown that Nfix-deficient mice also exhibit delayed astrocytic differentiation within the mouse spinal cord, with Nfix expression reliant, at least in part, on the activity of NFIB [15]. However, although we analysed the expression
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