Tissue-specific derepression of TCF/LEF controls the activity of the Wnt/β-catenin pathway

Lu, Fu I.; Sun, Yuhan; Wei, Chang Yong; Thisse, Christine; Thisse, Bernard

doi:10.1038/ncomms6368

Cited by 48 publications

(40 citation statements)

References 43 publications

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“…For example, O‐GlcNAc Transferase (OGT) has been reported to promote TLE repression by direct interaction with TLEs, and this interaction was attenuated by Wnt signaling in mammalian cell culture . The transcription factor Ladybird homeobox 2 (Lbx2) activated Wnt transcriptional readouts in zebrafish by binding to the WD40 domain of TLEs, blocking their ability to bind to TCFs . In another recent report, the selenoenzyme Glutathione peroxidase 4 (GPX4) was shown to bind to TCFs and prevent their association with chromatin.…”

Section: Other Potential Factors Acting In the Switchmentioning

confidence: 99%

The Wnt Transcriptional Switch: TLE Removal or Inactivation?

et al. 2017

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Many targets of the Wnt/β-catenin signaling pathway are regulated by TCF transcription factors, which play important roles in animal development, stem cell biology, and oncogenesis. TCFs can regulate Wnt targets through a "transcriptional switch," repressing gene expression in unstimulated cells and promoting transcription upon Wnt signaling. However, it is not clear whether this switch mechanism is a general feature of Wnt gene regulation or limited to a subset of Wnt targets. Co-repressors of the TLE family are known to contribute to the repression of Wnt targets in the absence of signaling, but how they are inactivated or displaced by Wnt signaling is poorly understood. In this mini-review, we discuss several recent reports that address the prevalence and molecular mechanisms of the Wnt transcription switch, including the finding of Wnt-dependent ubiquitination/inactivation of TLEs. Together, these findings highlight the growing complexity of the regulation of gene expression by the Wnt pathway.

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Section: Other Potential Factors Acting In the Switchmentioning

confidence: 99%

The Wnt Transcriptional Switch: TLE Removal or Inactivation?

et al. 2017

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“…The whole mount in situ hybridization in zebrafish embryo with ff1b 26, 38 or star (BioCat GmbH) was done as described before 39, 40 . Briefly, the embryos were fixed with 4% paraformaldehyde in PBS for overnight at 4 °C and then dehydrated by 100% methanol and stored at −20 °C.…”

Section: Methodsmentioning

confidence: 99%

Lysosomal activity maintains glycolysis and cyclin E1 expression by mediating Ad4BP/SF-1 stability for proper steroidogenic cell growth

Syu

Baba

Huang

et al. 2017

Sci Rep

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The development and differentiation of steroidogenic organs are controlled by Ad4BP/SF-1 (adrenal 4 binding protein/steroidogenic factor 1). Besides, lysosomal activity is required for steroidogenesis and also enables adrenocortical cell to survive during stress. However, the role of lysosomal activity on steroidogenic cell growth is as yet unknown. Here, we showed that lysosomal activity maintained Ad4BP/SF-1 protein stability for proper steroidogenic cell growth. Treatment of cells with lysosomal inhibitors reduced steroidogenic cell growth in vitro. Suppression of autophagy did not affect cell growth indicating that autophagy was dispensable for steroidogenic cell growth. When lysosomal activity was inhibited, the protein stability of Ad4BP/SF-1 was reduced leading to reduced S phase entry. Interestingly, treatment of cells with lysosomal inhibitors reduced glycolytic gene expression and supplying the cells with pyruvate alleviated the growth defect. ChIP-sequence/ChIP studies indicated that Ad4BP/SF-1 binds to the upstream region of Ccne1 (cyclin E1) gene during G1/S phase. In addition, treatment of zebrafish embryo with lysosomal inhibitor reduced the levels of the interrenal (adrenal) gland markers. Thus lysosomal activity maintains steroidogenic cell growth via stabilizing Ad4BP/SF-1 protein.

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“…Analysis of gene expression in zebrafish by RT-PCR was performed as previously described in Lu et al (24). Primer sequences used for measuring gene expression were arfgef1 forward, 59-TGTGCGTAGCGCTGTCTAAA-39, and reverse, 59-TTGCTCTCCTGCTCTGAAGG-39; and arfgef2 forward, 59-AC-GGTTCGCCTTGTCTCAG-39, and reverse, 59-GCGCAACT-CATGAGACTTTGG-39; elfa forward, 59-CTTCTCAGGCT-GACTGTGC-39, and reverse, 59-CCGCTAGCATTACCCTCC-39 was used as an internal control.…”

Section: Cell Culture and Transfectionmentioning

confidence: 99%

“…S4). RT-PCR was performed as previously described (24). The target sites of single-guide (sg) RNA3 (59-GAAACATGCTCTTGGTGCTC-39) or sgRNA4 (59-GAAAATCCTCGCGGATAAAG-39) were designed by CHOPCHOP software (http://chopchop.cbu.uib.no/), and PCR and RNA synthesis followed the procedure of the previous study (31).…”

Section: Fish Maintenance and Microinjectionmentioning

confidence: 99%

Involvement of BIG1 and BIG2 in regulating VEGF expression and angiogenesis

Wang

et al. 2019

FASEB j.

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VEGF stimulates the formation of new blood vessels by inducing endothelial cell (EC) proliferation and migration. Brefeldin A (BFA)‐inhibited guanine nucleotide–exchange protein (BIG)1 and 2 accelerate the replacement of bound GDP with GTP to activate ADP‐ribosylation factor (Arf)1, which regulates vesicular transport between the Golgi and plasma membrane. Although it has been reported that treating cells with BFA interferes with Arf1 activation to inhibit VEGF secretion, the role of BIG1 and BIG2 in VEGF trafficking and expression, EC migration and proliferation, and vascular development remains unknown. Here, we found that inactivation of Arf1 reduced VEGF secretion but did not affect the levels of VEGF protein. Interestingly, however, BIG1 and BIG2 knockdown significantly decreased the levels of VEGF mRNA and protein in glioblastoma U251 cells and HUVECs. Furthermore, depletion of BIG1 and BIG2 inhibited HUVEC angiogenesis by diminishing cell migration. Angioblast migration and intersegmental vessel sprouting were also impaired when the BIG2 homolog, Arf guanine nucleotide exchange factor (arfgef)2, was knocked down in zebrafish with endothelial expression of green fluorescent protein (GFP). Depletion of arfgef2 by clustered regularly interspaced short palindromic repeat (CRISPR)/ CRISPR‐associated protein 9 (Cas9) also caused defects in vascular development of zebrafish embryos. Taken together, these data reveal that BIG1 and BIG2 participate in endothelial cell angiogenesis.—Lu, F.‐L, Wang, Y.‐T., Wang, Y.‐S., Wu, C.‐Y., Li, C.‐C. Involvement of BIG1 and BIG2 in regulating VEGF expression and angiogenesis. FASEB J. 33, 9959–9973 (2019). http://www.fasebj.org

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Tissue-specific derepression of TCF/LEF controls the activity of the Wnt/β-catenin pathway

Cited by 48 publications

References 43 publications

The Wnt Transcriptional Switch: TLE Removal or Inactivation?

The Wnt Transcriptional Switch: TLE Removal or Inactivation?

Lysosomal activity maintains glycolysis and cyclin E1 expression by mediating Ad4BP/SF-1 stability for proper steroidogenic cell growth

Involvement of BIG1 and BIG2 in regulating VEGF expression and angiogenesis

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