Regulation of Intestinal Stem Cell Proliferation by Human Methyl-CpG-binding Protein-2 in Drosophila

Lee, Shin Hae; Kim, In Joo; Kim, Joong Gook; Park, Joung Sun; Kim, Young S.; Yamaguchi, Masamitsu; Kim, Cheol Min; Yoo, Mi‐Ae

doi:10.1247/csf.11027

Cited by 4 publications

(2 citation statements)

References 57 publications

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“…In the midgut, HP-1 was detected in all cell types, mainly as one strong focus per cell (Fig. 7C), as previously described (Lee et al, 2011). In esg ts >chn RNAi midguts, the HP-1 staining in the precursor cells became weaker and was present as more foci (Fig.…”

Section: Chn Regulates the Chromatin Of Precursor Cellssupporting

confidence: 84%

Gene expression profiling identifies the zinc-finger protein Charlatan as a regulator of intestinal stem cells in Drosophila

Amcheslavsky

Nie

et al. 2014

Development

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Intestinal stem cells (ISCs) in the adult Drosophila midgut can respond to tissue damage and support repair. We used genetic manipulation to increase the number of ISC-like cells in the adult midgut and performed gene expression profiling to identify potential ISC regulators. A detailed analysis of one of these potential regulators, the zinc-finger protein Charlatan, was carried out. MARCM clonal analysis and RNAi in precursor cells showed that loss of Chn function caused severe ISC division defects, including loss of EdU incorporation, phosphorylated histone 3 staining and expression of the mitotic protein Cdc2. Loss of Charlatan also led to a much reduced histone acetylation staining in precursor cells. Both the histone acetylation and ISC division defects could be rescued by the simultaneous decrease of the Histone Deacetylase 2. The overexpression of Charlatan blocked differentiation reversibly, but loss of Charlatan did not lead to automatic differentiation. The results together suggest that Charlatan does not simply act as an anti-differentiation factor but instead functions to maintain a chromatin structure that is compatible with stem cell properties, including proliferation.

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Section: Chn Regulates the Chromatin Of Precursor Cellssupporting

confidence: 84%

Gene expression profiling identifies the zinc-finger protein Charlatan as a regulator of intestinal stem cells in Drosophila

Amcheslavsky

Nie

et al. 2014

Development

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“…Interestingly, expression of human MeCP2 (hMeCP2) in Drosophila ECs in midgut alters the cytological distribution of heterochromatin protein-1 (HP-1), as determined by immunofluorescence, and stimulates ISC proliferation. These observations suggest that hMeCP2 misregulates genes important for ISC maintenance [69]. …”

Section: Introductionmentioning

confidence: 99%

Epigenetic regulation in adult stem cells and cancers

Tarayrah

Chen

2013

Cell Biosci

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Adult stem cells maintain tissue homeostasis by their ability to both self-renew and differentiate to distinct cell types. Multiple signaling pathways have been shown to play essential roles as extrinsic cues in maintaining adult stem cell identity and activity. Recent studies also show dynamic regulation by epigenetic mechanisms as intrinsic factors in multiple adult stem cell lineages. Emerging evidence demonstrates intimate crosstalk between these two mechanisms. Misregulation of adult stem cell activity could lead to tumorigenesis, and it has been proposed that cancer stem cells may be responsible for tumor growth and metastasis. However, it is unclear whether cancer stem cells share commonalities with normal adult stem cells. In this review, we will focus on recent discoveries of epigenetic regulation in multiple adult stem cell lineages. We will also discuss how epigenetic mechanisms regulate cancer stem cell activity and probe the common and different features between cancer stem cells and normal adult stem cells.

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Association of TGFβ signaling with the maintenance of a quiescent stem cell niche in human oral mucosa

Andl

Bras

Loomans

et al. 2016

Histochem Cell Biol

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A dogma in squamous epithelial biology is that proliferation occurs in the basal cell layer. Notable exceptions are squamous epithelia of the human oral cavity, esophagus, ectocervix, and vagina. In these human epithelia, proliferation is rare in the basal cell layer, and the vast majority of cells positive for Ki67 and other proliferation markers are found in para- and suprabasal cell layers. This unique human feature of a generally quiescent basal cell layer overlaid by highly proliferative cells offers the rare opportunity to study the molecular features of undifferentiated, quiescent, putative stem cells in their natural context. Here, we show that the quiescent human oral mucosa basal cell layer expresses putative markers of stemness, while para- and suprabasal cells are characterized by cell cycle genes. We identified a TGFβ signature in this quiescent basal cell layer. In in vitro organotypic cultures, human keratinocytes could be induced to express markers of these quiescent basal cells when TGFβ signaling is activated. The study suggests that the separation of basal cell layer and proliferation in human oral mucosa may function to accommodate high proliferation rates and the protection of a quiescent reserve stem cell pool. Psoriasis, an epidermal inflammatory hyperproliferative disease, exhibits features of a quiescent basal cell layer mimicking normal oral mucosa. Our data indicate that structural changes in the organization of epithelial proliferation could contribute to longevity and carcinogenesis.

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Regulation of Intestinal Stem Cell Proliferation by Human Methyl-CpG-binding Protein-2 in Drosophila

Cited by 4 publications

References 57 publications

Gene expression profiling identifies the zinc-finger protein Charlatan as a regulator of intestinal stem cells in Drosophila

Gene expression profiling identifies the zinc-finger protein Charlatan as a regulator of intestinal stem cells in Drosophila

Epigenetic regulation in adult stem cells and cancers

Association of TGFβ signaling with the maintenance of a quiescent stem cell niche in human oral mucosa

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