Forebrain-specific promoter/enhancer D6 derived from the mouse Dach1 gene controls expression in neural stem cells

Machoň, Ondřej; Bout, Christiaan J. van den; Backman, Mattias; Røsok, Øystein; Caubit, Xavier; Fromm, Sigurd H.; Geronimo, Benedicto; Krauß, Stefan

doi:10.1016/s0306-4522(02)00053-2

Cited by 53 publications

(50 citation statements)

References 49 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Li and colleagues demonstrated murine Dach1 regulated retinogenesis and pituitary development through tissue-specific gene regulation by recruiting the corepressors (39,40). Functional relevance of DACH1 expression in development and neural differentiation of both invertebrates and vertebrates has been reported (39)(40)(41)(42)(43)(44)(45)(46). DACH1-expressed embryonic and postnatal brain-derived cells displayed neural stem cell-like property (44), suggesting that DACH1 functions in neural differentiation.…”

Section: Dach1-spanning Region Is Indicated As a Target Of Copy Numbementioning

confidence: 99%

“…Functional relevance of DACH1 expression in development and neural differentiation of both invertebrates and vertebrates has been reported (39)(40)(41)(42)(43)(44)(45)(46). DACH1-expressed embryonic and postnatal brain-derived cells displayed neural stem cell-like property (44), suggesting that DACH1 functions in neural differentiation. From these facts together, we think that DACH1 act as a guardian of differentiation in the glial lineage, and loss of DACH1 would result in dysregulation of normal differentiation and drive gliomagenesis.…”

Section: Dach1-spanning Region Is Indicated As a Target Of Copy Numbementioning

confidence: 99%

See 1 more Smart Citation

Homozygously deleted gene DACH1 regulates tumor-initiating activity of glioma cells

Watanabe

Ogiwara

Ehata³

et al. 2011

Proc. Natl. Acad. Sci. U.S.A.

View full text Add to dashboard Cite

Loss or reduction in function of tumor suppressor genes contributes to tumorigenesis. Here, by allelic DNA copy number analysis using single-nucleotide polymorphism genotyping array and mass spectrometry, we report homozygous deletion in glioblastoma multiformes at chromosome 13q21, where DACH1 gene is located. We found decreased cell proliferation of a series of glioma cell lines by forced expression of DACH1. We then generated U87TR-Da glioma cells, where DACH1 expression could be activated by exposure of the cells to doxycycline. Both ex vivo cellular proliferation and in vivo growth of s.c. transplanted tumors in mice are reduced in U87TR-Da cells with DACH1 expression (U87-DACH1-high), compared with DACH1-nonexpressing U87TR-Da cells (U87-DACH1-low). U87-DACH1-low cells form spheroids with CD133 and Nestin expression in serum-free medium but U87-DACH1-high cells do not. Compared with spheroid-forming U87-DACH1-low cells, adherent U87-DACH1-high cells display lower tumorigenicity, indicating DACH1 decreases the number of tumor-initiating cells. Gene expression analysis and chromatin immunoprecipitation assay reveal that fibroblast growth factor 2 (FGF2/bFGF) is transcriptionally repressed by DACH1, especially in cells cultured in serum-free medium. Exogenous bFGF rescues spheroid-forming activity and tumorigenicity of the U87-DACH1-high cells, suggesting that loss of DACH1 increases the number of tumor-initiating cells through transcriptional activation of bFGF. These results illustrate that DACH1 is a distinctive tumor suppressor, which does not only suppress growth of tumor cells but also regulates bFGF-mediated tumor-initiating activity of glioma cells.neural differentiation | gliomagenesis

show abstract

Section: Dach1-spanning Region Is Indicated As a Target Of Copy Numbementioning

confidence: 99%

Section: Dach1-spanning Region Is Indicated As a Target Of Copy Numbementioning

confidence: 99%

Homozygously deleted gene DACH1 regulates tumor-initiating activity of glioma cells

Watanabe

Ogiwara

Ehata³

et al. 2011

Proc. Natl. Acad. Sci. U.S.A.

View full text Add to dashboard Cite

show abstract

“…47 Anti-GFP (A-11120, Molecular Probes) was used as primary antibody (1.67 mg/ml concentration) and Alexat594 anti-mouse IgG (A-11005, Molecular Probes) was used as secondary antibody (1/500 dilution).…”

Section: Immunocytochemistrymentioning

confidence: 99%

Branched oligonucleotides induce in vivo gene conversion of a mutated EGFP reporter

Olsen¹,

McKeen

Krauß³

2003

Gene Ther

Self Cite

View full text Add to dashboard Cite

UKBranched oligonucleotides (b-oligonucleotides) based on a novel branching monomer were used for site-specific sequence alteration in vivo. With a stable integrated mutated enhanced green fluorescent protein (EGFP) template in Chinese hamster ovary cells, up to 0.1% EGFP-positive cells were counted after transfection with b-oligonucleotides. The presence of EGFP protein in converted cells was demonstrated by anti-EGFP immunocytochemistry. Genomic sequencing of converted cells showed in 40% of the analysed clones the corrected wild-type codon, while 9.3% of the sequences showed a corrected wild-type sequence and an additional collateral mutation. Despite the stable corrected genomic locus, converted cells entered selective apoptosis after 3-6 days. The cell line Irs-1 that is deficient in the homologous recombination pathway showed a reduced frequency of boligonucleotide-induced site-specific sequence conversion. The reduced conversion rates in the mutant cell line could be partly rescued by complementation with XRCC2 cDNA.

show abstract

“…WT mice for expression studies were MF1 × MF1, rats were Sprague-Dawley (Charles River Laboratories), and Ikaros mutant mice (30) were on the CBA/CaH background. For generation of D6-Ikaros and D6-Ikaros 159A mice, Ikaros-IRES-GFP and Ikaros 159A -IRES-GFP sequences were PCR-amplified from retroviral vectors (41), and cloned into the Not1 site of the D6 vector (39). Transgenic mice were generated by pronuclear injection of Sal1 linearized vector in CBA × C57BL6 F1 zygotes, and transgenic lines were established in the same genetic background.…”

Section: Methodsmentioning

confidence: 99%

“…To this end, we generated transgenic mice expressing Ikaros from the D6 enhancer. This 6-kblong genomic fragment from the promoter region of the mouse Dach1 gene mediates specific cortical and hippocampal expression in progenitor cells and neurons starting at E10 and lasting throughout development (39,40). For easier visualization of transgene expression, an internal ribosome entry site (IRES)-GFP sequence was also included (Fig.…”

Section: Ikaros-expressing Cortical Progenitor Cells Give Rise To Promentioning

confidence: 99%

Ikaros promotes early-born neuronal fates in the cerebral cortex

Alsiö

Tarchini

Cayouette

et al. 2013

Proc. Natl. Acad. Sci. U.S.A.

110

View full text Add to dashboard Cite

During cerebral cortex development, a series of projection neuron types is generated in a fixed temporal order. In Drosophila neuroblasts, the transcription factor hunchback encodes first-born identity within neural lineages. One of its mammalian homologs, Ikaros, was recently reported to play an equivalent role in retinal progenitor cells, raising the question as to whether Ikaros/Hunchback proteins could be general factors regulating the development of early-born fates throughout the nervous system. Ikaros is also expressed in progenitor cells of the mouse cerebral cortex, and this expression is highest during the early stages of neurogenesis and thereafter decreases over time. Transgenic mice with sustained Ikaros expression in cortical progenitor cells and neurons have developmental defects, including displaced progenitor cells within the cortical plate, increased early neural differentiation, and disrupted cortical lamination. Sustained Ikaros expression results in a prolonged period of generation of deep layer neurons into the stages when, normally, only late-born upper layer neurons are generated, as well as a delayed production of late-born neurons. Consequently, more early-born and fewer late-born neurons are present in the cortex of these mice at birth. This phenotype was observed in all parts of the cortex, including those with minimal structural defects, demonstrating that it is not secondary to abnormalities in cortical morphogenesis. These data suggest that Ikaros plays a similar role in regulating early temporal fates in the mammalian cerebral cortex as Ikaros/Hunchback proteins do in the Drosophila nerve cord.

show abstract

Forebrain-specific promoter/enhancer D6 derived from the mouse Dach1 gene controls expression in neural stem cells

Cited by 53 publications

References 49 publications

Homozygously deleted gene DACH1 regulates tumor-initiating activity of glioma cells

Homozygously deleted gene DACH1 regulates tumor-initiating activity of glioma cells

Branched oligonucleotides induce in vivo gene conversion of a mutated EGFP reporter

Ikaros promotes early-born neuronal fates in the cerebral cortex

Contact Info

Product

Resources

About