Microarray Screening for Genes Involved in Oligodendrocyte Differentiation in the Zebrafish CNS

Chung, Ah-Young; Kim, Suhyun; Kim, Ho; Bae, Young-Ki; Park, Hae-Chul

doi:10.5607/en.2011.20.2.85

Cited by 10 publications

(9 citation statements)

References 30 publications

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“…Of note, one of the altered genes derived from microarray data analysis and verified by qRT-PCR and IHC was Dlg1 (Fig. 9B) (Chung, 2011). Previous studies reported that physical interaction between scaffolding protein DLG1 (Discs large homolog 1, also termed synapse-associated protein 97, SAP97) and APC is required for polarization of the microtubule cytoskeleton in astrocytes (Etienne-Manneville et al, 2005; Nathke, 2006).…”

Section: Resultsmentioning

confidence: 97%

Adenomatous Polyposis Coli Regulates Oligodendroglial Development

et al. 2013

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The expression of the gut tumor suppressor gene adenomatous polyposis coli (Apc) and its’ role in the oligodendroglial lineage are poorly understood. We found that immunoreactive APC is transiently induced in the oligodendroglial lineage during both normal myelination and remyelination following toxin-induced, genetic or autoimmune demyelination murine models. Using the Cre/loxP system to conditionally ablate APC from the oligodendroglial lineage, we determined that APC enhances proliferation of oligodendroglial progenitor cells (OPCs) and is essential for oligodendrocyte differentiation in a cell-autonomous manner. Biallelic Apc disruption caused translocation of β-catenin into the nucleus and up-regulated β-catenin-mediated Wnt signaling in early postnatal but not adult oligodendroglial lineage cells. The results of conditional ablation of Apc or Ctnnb1 (the gene encoding β-catenin), and of simultaneous conditional ablation of Apc and Ctnnb1, revealed that β-catenin is dispensable for postnatal oligodendroglial differentiation, that Apc one-allele deficiency is not sufficient to dysregulate β-catenin-mediated Wnt signaling in oligodendroglial lineage cells, and that APC regulates oligodendrocyte differentiation through β-catenin-independent, as well as β-catenin-dependent mechanisms. Gene ontology analysis of microarray data suggested that the β-catenin-independent mechanism involves APC regulation of the cytoskeleton, a result compatible with established APC functions in neural precursors and with our observation that Apc-deleted OPCs develop fewer, shorter processes in vivo. Together, our data support the hypothesis that APC regulates oligodendrocyte differentiation through both β-catenin-dependent and additional β-catenin-independent mechanisms.

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Section: Resultsmentioning

confidence: 97%

Adenomatous Polyposis Coli Regulates Oligodendroglial Development

et al. 2013

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“…Although Sox10 is a robust marker for many neural crest lineages, Sox10-driven lines also label some other non-neural crest-derived cell populations at later time points. For example, multiple studies have used Sox10:eGFP and Sox10:mRFP to mark oligodendrocytes (Chung, Kim, Kim, Bae, & Park, 2011;Kucenas, Snell, & Appel, 2008) and otic epithelial cells (Carney et al, 2006;Kwak et al, 2013). To determine if Sox10:zFucci is also expressed in these cell types, we crossed the Sox10:zFucci line with either the Sox10:mRFP or Sox10:eGFP line.…”

Section: Resultsmentioning

confidence: 99%

Tracking neural crest cell cycle progression in vivo

Rajan

Gallik

Monaghan

et al. 2018

Genesis

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Analysis of cell cycle entry/exit and progression can provide fundamental insights into stem cell propagation, maintenance, and differentiation. The neural crest is a unique stem cell population in vertebrate embryos that undergoes long-distance collective migration and differentiation into a wide variety of derivatives. Using traditional techniques such as immunohistochemistry to track cell cycle changes in such a dynamic population is challenging, as static time points provide an incomplete spatiotemporal picture. In contrast, the fluorescent, ubiquitination-based cell cycle indicator (Fucci) system provides in vivo readouts of cell cycle progression and has been previously adapted for use in zebrafish. The most commonly used Fucci systems are ubiquitously expressed, making tracking of a specific cell population challenging. Therefore, we generated a transgenic zebrafish line, Tg(-4.9sox10:mAG-gmnn(1/100)-2A-mCherry-cdt1(1/190)), in which the Fucci system is specifically expressed in delaminating and migrating neural crest cells. Here, we demonstrate validation of this new tool and its use in live high-resolution tracking of cell cycle progression in the neural crest and derivative populations.

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“…Several groups have also taken a microarray approach to discover novel genes in oligodendrocyte development (Chung et al, ; Takada and Appel, ). One microarray screen (Takada and Appel, ) looked at transcripts from cells purified by fluorescent activated cell (FAC) sorting from tg( olig2 :EGFP) zebrafish.…”

Section: Zebrafish As a Model For Studying Myelinationmentioning

confidence: 99%

Zebrafish as a model to investigate CNS myelination

Preston

Macklin

2014

Glia

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Myelin plays a critical role in proper neuronal function by providing trophic and metabolic support to axons and facilitating energy-efficient saltatory conduction. Myelination is influenced by numerous molecules including growth factors, hormones, transmembrane receptors and extracellular molecules, which activate signaling cascades that drive cellular maturation. Key signaling molecules and downstream signaling cascades controlling myelination have been identified in cell culture systems. However, in vitro systems are not able to faithfully replicate the complex in vivo signaling environment that occurs during development or following injury. Currently, it remains time-consuming and expensive to investigate myelination in vivo in rodents, the most widely used model for studying mammalian myelination. As such, there is a need for alternative in vivo myelination models, particularly ones that can test molecular mechanisms without removing oligodendrocyte lineage cells from their native signaling environment or disrupting intercellular interactions with other cell types present during myelination. Here, we review the ever-increasing role of zebrafish in studies uncovering novel mechanisms controlling vertebrate myelination. These innovative studies range from observations of the behavior of single cells during in vivo myelination as well as mutagenesis- and pharmacology-based screens in whole animals. Additionally, we discuss recent efforts to develop novel models of demyelination and oligodendrocyte cell death in adult zebrafish for the study of cellular behavior in real time during repair and regeneration of damaged nervous systems.

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Microarray Screening for Genes Involved in Oligodendrocyte Differentiation in the Zebrafish CNS

Cited by 10 publications

References 30 publications

Adenomatous Polyposis Coli Regulates Oligodendroglial Development

Adenomatous Polyposis Coli Regulates Oligodendroglial Development

Tracking neural crest cell cycle progression in vivo

Zebrafish as a model to investigate CNS myelination

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