Cdh2 stabilizes FGFR1 and contributes to primed-state pluripotency in mouse epiblast stem cells

Toshiyuki Takehara; Takeshi Teramura; Yuta Onodera; John Frampton; Kanji Fukuda

doi:10.1038/srep14722

Cdh2 stabilizes FGFR1 and contributes to primed-state pluripotency in mouse epiblast stem cells

Toshiyuki Takehara, Takeshi Teramura, Yuta Onodera, John Frampton, Kanji Fukuda

Medicine

Résultat de recherche: Article › examen par les pairs

16 Citations (Scopus)

Résumé

The cell adhesion molecule Cadherin 2 (Cdh2) plays important roles in somatic cell adhesion, proliferation and migration. Cdh2 is also highly expressed in mouse epiblast stem cells (mEpiSCs), but its function in these cells is unknown. To understand the function of Cdh2 in mEpiSCs, we compared the expression of pluripotency-related genes in mEpiSCs and mouse embryonic stem cells (mESCs) after either Cdh2 knockdown or Cdh2 over-expression. Introduction of specific siRNA against Cdh2 led to attenuation of pluripotency-related genes. Pluripotent gene expression was not recovered by over-expression of Cdh1 following Cdh2 knockdown. Western blot analysis and co-immunoprecipitation assays revealed that Cdh2 stabilizes FGFR1 in mEpiSCs. Furthermore, stable transfection of mESCs with Cdh2 cDNA followed by FGF2 supplementation accelerated cell differentiation. Thus, Cdh2 contributes to the establishment and maintenance of FGF signaling-dependent self-renewal in mEpiSCs through stabilization of FGFR1.

Langue d'origine	English
Numéro d'article	14722
Journal	Scientific Reports
Volume	5
DOI	https://doi.org/10.1038/srep14722
Statut de publication	Published - sept. 30 2015

Note bibliographique

Funding Information:
We gratefully acknowledge Dr. Hitoshi Niwa, M.D., Ph.D., RIKEN Center for Developmental Biology, for kindly providing the pCAG-Ecadherin-IRES-Puromycin plasmid and Dr. Hirofumi Suemori, Institute for Frontier Medical Science, Kyoto University, for kindly providing the pCAG-IRES-Puro plasmid. We also thank Ms. Naomi Backes Kamimura and Ms. Julia Walhelm-Kimura, Department of Biology-Oriented Science and Technology, Kinki University, for English language editing. This study was supported by JSPS KAKENHI 26861216 and 26861217.

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title = "Cdh2 stabilizes FGFR1 and contributes to primed-state pluripotency in mouse epiblast stem cells",

abstract = "The cell adhesion molecule Cadherin 2 (Cdh2) plays important roles in somatic cell adhesion, proliferation and migration. Cdh2 is also highly expressed in mouse epiblast stem cells (mEpiSCs), but its function in these cells is unknown. To understand the function of Cdh2 in mEpiSCs, we compared the expression of pluripotency-related genes in mEpiSCs and mouse embryonic stem cells (mESCs) after either Cdh2 knockdown or Cdh2 over-expression. Introduction of specific siRNA against Cdh2 led to attenuation of pluripotency-related genes. Pluripotent gene expression was not recovered by over-expression of Cdh1 following Cdh2 knockdown. Western blot analysis and co-immunoprecipitation assays revealed that Cdh2 stabilizes FGFR1 in mEpiSCs. Furthermore, stable transfection of mESCs with Cdh2 cDNA followed by FGF2 supplementation accelerated cell differentiation. Thus, Cdh2 contributes to the establishment and maintenance of FGF signaling-dependent self-renewal in mEpiSCs through stabilization of FGFR1.",

author = "Toshiyuki Takehara and Takeshi Teramura and Yuta Onodera and John Frampton and Kanji Fukuda",

note = "Funding Information: We gratefully acknowledge Dr. Hitoshi Niwa, M.D., Ph.D., RIKEN Center for Developmental Biology, for kindly providing the pCAG-Ecadherin-IRES-Puromycin plasmid and Dr. Hirofumi Suemori, Institute for Frontier Medical Science, Kyoto University, for kindly providing the pCAG-IRES-Puro plasmid. We also thank Ms. Naomi Backes Kamimura and Ms. Julia Walhelm-Kimura, Department of Biology-Oriented Science and Technology, Kinki University, for English language editing. This study was supported by JSPS KAKENHI 26861216 and 26861217.",

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AU - Takehara, Toshiyuki

AU - Teramura, Takeshi

AU - Onodera, Yuta

AU - Frampton, John

AU - Fukuda, Kanji

N1 - Funding Information: We gratefully acknowledge Dr. Hitoshi Niwa, M.D., Ph.D., RIKEN Center for Developmental Biology, for kindly providing the pCAG-Ecadherin-IRES-Puromycin plasmid and Dr. Hirofumi Suemori, Institute for Frontier Medical Science, Kyoto University, for kindly providing the pCAG-IRES-Puro plasmid. We also thank Ms. Naomi Backes Kamimura and Ms. Julia Walhelm-Kimura, Department of Biology-Oriented Science and Technology, Kinki University, for English language editing. This study was supported by JSPS KAKENHI 26861216 and 26861217.

PY - 2015/9/30

Y1 - 2015/9/30

N2 - The cell adhesion molecule Cadherin 2 (Cdh2) plays important roles in somatic cell adhesion, proliferation and migration. Cdh2 is also highly expressed in mouse epiblast stem cells (mEpiSCs), but its function in these cells is unknown. To understand the function of Cdh2 in mEpiSCs, we compared the expression of pluripotency-related genes in mEpiSCs and mouse embryonic stem cells (mESCs) after either Cdh2 knockdown or Cdh2 over-expression. Introduction of specific siRNA against Cdh2 led to attenuation of pluripotency-related genes. Pluripotent gene expression was not recovered by over-expression of Cdh1 following Cdh2 knockdown. Western blot analysis and co-immunoprecipitation assays revealed that Cdh2 stabilizes FGFR1 in mEpiSCs. Furthermore, stable transfection of mESCs with Cdh2 cDNA followed by FGF2 supplementation accelerated cell differentiation. Thus, Cdh2 contributes to the establishment and maintenance of FGF signaling-dependent self-renewal in mEpiSCs through stabilization of FGFR1.

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Cdh2 stabilizes FGFR1 and contributes to primed-state pluripotency in mouse epiblast stem cells

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