Nuclear factor I gene expression in the developing forebrain

Plachez, Céline; Lindwall, Charlotta; Sunn, Nana; Piper, Michael; Moldrich, Randal X.; Campbell, Christine; Osinski, Jason M.; Gronostajski, Richard M.; Richards, Linda J.

doi:10.1002/cne.21722

Cited by 20 publications

(53 citation statements)

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“…NFIA is a transcription factor expressed in both neurons and glia cells. A lack of development of the corpus callosum due to malformation of the midline glial structures was observed in NFIA KO mice (das Neves et al, 1999; Shu et al, 2003; Plachez et al, 2008), suggesting a role for this transcription factor in normal brain development. Hence, we analyzed the expression of NFIA in the cerebral cortex of CD and WT mice by real-time PCR.…”

Section: Resultsmentioning

confidence: 96%

Aspartoacylase deficiency affects early postnatal development of oligodendrocytes and myelination

Mattan

Ghiani

Lloyd

et al. 2010

Neurobiology of Disease

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Canavan disease (CD) is a neurodegenerative disease, caused by a deficiency in the enzyme aspartoacylase (ASPA). This enzyme has been localized to oligodendrocytes; however, it is still undefined how ASPA deficiency affects oligodendrocyte development. In normal mice the pattern of ASPA expression coincides with oligodendrocyte maturation. Therefore, postnatal oligodendrocyte maturation was analyzed in ASPA-deficient mice (CD mice). Early in development, CD mice brains showed decreased expression of neural cell markers that was later compensated. In addition, the levels of myelin proteins were decreased along with abnormal myelination in CD mice compared to wild-type (WT). These defects were associated with increased global levels of acetylated histone H3, decreased chromatin compaction and increased GFAP protein, a marker for astrogliosis. Together, these findings strongly suggest that, early in postnatal development, ASPA deficiency affects oligodendrocyte maturation and myelination.

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Section: Resultsmentioning

confidence: 96%

Aspartoacylase deficiency affects early postnatal development of oligodendrocytes and myelination

Mattan

Ghiani

Lloyd

et al. 2010

Neurobiology of Disease

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“…NFIA does not just affect glial populations, however, as it appears to play a role in neuronal development as well (Plachez et al, ). NFIA is expressed by cerebellar granule cells and is involved in their migration, dendritic arborization, and axon guidance (Wang et al, ).…”

Section: Discussionmentioning

confidence: 99%

DNER and NFIA are expressed by developing and mature AII amacrine cells in the mouse retina

Keeley

Reese

2017

J of Comparative Neurology

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The present study has taken advantage of publicly available cell type specific mRNA expression databases in order to identify potential genes participating in the development of retinal AII amacrine cells. We profile two such genes, Delta/Notch-like EGF repeat containing (Dner) and nuclear factor I/A (Nfia), that are each heavily expressed in AII amacrine cells in the mature mouse retina, and which conjointly identify this retinal cell population in its entirety when using antibodies to DNER and NFIA. DNER is present on the plasma membrane, while NFIA is confined to the nucleus, consistent with known functions of each of these two proteins. DNER also identifies some other subsets of retinal ganglion and amacrine cell types, along with horizontal cells, while NFIA identifies a subset of bipolar cells as well as Muller glia and astrocytes. During early postnatal development, NFIA labels astrocytes on the day of birth, AII amacrine cells at postnatal (P) day 5, and Muller glia by P10, when horizontal cells also transiently exhibit NFIA immunofluorescence. DNER, by contrast, is present in ganglion and amacrine cells on P1, also labeling the horizontal cells by P10. Developing AII amacrine cells exhibit accumulating DNER labeling at the dendritic stalk, labeling that becomes progressively conspicuous by P10, as it is in maturity. This developmental time course is consistent with a prospective role for each gene in the differentiation of AII amacrine cells.

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“…We identified a set of candidate factors that may interact with SOX2-BRN2 that included RFX and NF-I family members. NF-I factors are expressed in NPCs in vivo and their loss in development leads to defects in central nervous system formation and specifically NPC dysfunction [97], [121]–[124]. RFX family members also play essential roles in proper brain development [99], [125].…”

Section: Discussionmentioning

confidence: 99%

SOX2 Co-Occupies Distal Enhancer Elements with Distinct POU Factors in ESCs and NPCs to Specify Cell State

et al. 2013

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SOX2 is a master regulator of both pluripotent embryonic stem cells (ESCs) and multipotent neural progenitor cells (NPCs); however, we currently lack a detailed understanding of how SOX2 controls these distinct stem cell populations. Here we show by genome-wide analysis that, while SOX2 bound to a distinct set of gene promoters in ESCs and NPCs, the majority of regions coincided with unique distal enhancer elements, important cis-acting regulators of tissue-specific gene expression programs. Notably, SOX2 bound the same consensus DNA motif in both cell types, suggesting that additional factors contribute to target specificity. We found that, similar to its association with OCT4 (Pou5f1) in ESCs, the related POU family member BRN2 (Pou3f2) co-occupied a large set of putative distal enhancers with SOX2 in NPCs. Forced expression of BRN2 in ESCs led to functional recruitment of SOX2 to a subset of NPC-specific targets and to precocious differentiation toward a neural-like state. Further analysis of the bound sequences revealed differences in the distances of SOX and POU peaks in the two cell types and identified motifs for additional transcription factors. Together, these data suggest that SOX2 controls a larger network of genes than previously anticipated through binding of distal enhancers and that transitions in POU partner factors may control tissue-specific transcriptional programs. Our findings have important implications for understanding lineage specification and somatic cell reprogramming, where SOX2, OCT4, and BRN2 have been shown to be key factors.

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Nuclear factor I gene expression in the developing forebrain

Abstract: Retrograde tracing of laterally projecting corticospinal neurons (blue) co‐labeled with NFIB (red). J. Comp. Neurol. 508:385–401, 2008. © 2008 Wiley‐Liss, Inc.

Cited by 20 publications

References 0 publications

Aspartoacylase deficiency affects early postnatal development of oligodendrocytes and myelination

Aspartoacylase deficiency affects early postnatal development of oligodendrocytes and myelination

DNER and NFIA are expressed by developing and mature AII amacrine cells in the mouse retina

SOX2 Co-Occupies Distal Enhancer Elements with Distinct POU Factors in ESCs and NPCs to Specify Cell State

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