A miR‐372/let‐7 Axis Regulates Human Germ Versus Somatic Cell Fates

The embryonic stem cell cycle (ESCC) and let‐7 families of miRNAs function antagonistically in the switch between mouse embryonic stem cell self‐renewal and somatic differentiation. Here, we report that the human ESCC miRNA miR‐372 and let‐7 act antagonistically in germline differentiation from huma...

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Published inStem cells (Dayton, Ohio) Vol. 34; no. 7; pp. 1985 - 1991
Main Authors Tran, Nam D., Kissner, Michael, Subramanyam, Deepa, Parchem, Ronald J., Laird, Diana J., Blelloch, Robert H.
Format Journal Article
LanguageEnglish
Published United States Oxford University Press 01.07.2016
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Abstract The embryonic stem cell cycle (ESCC) and let‐7 families of miRNAs function antagonistically in the switch between mouse embryonic stem cell self‐renewal and somatic differentiation. Here, we report that the human ESCC miRNA miR‐372 and let‐7 act antagonistically in germline differentiation from human embryonic stem cells (hESCs) and human induced pluripotent stem cells (iPSCs). hESC and iPSC‐derived primordial germ cell‐like cells (PGCLCs) expressed high levels of miR‐372 and conversely, somatic cells expressed high levels of let‐7. Manipulation of miRNA levels by introduction of miRNA mimics or knockdown with miRNA sponges demonstrated that miR‐372 promotes whereas let‐7 antagonizes PGCLC differentiation. Knockdown of the individual miR‐372 targets SMARCC1, MECP2, CDKN1, RBL2, RHOC, and TGFBR2 increased PGCLC production, whereas knockdown of the let‐7 targets CMYC and NMYC suppressed PGCLC differentiation. These findings uncover a miR‐372/let‐7 axis regulating human primordial germ cell (PGC) specification. Stem Cells 2016;34:1985–1991 Let‐7 and miR‐294 antagonistically regulate somatic versus germline fates through their influence on multiple cellular pathways.
AbstractList Abstract The embryonic stem cell cycle (ESCC) and let-7 families of miRNAs function antagonistically in the switch between mouse embryonic stem cell self-renewal and somatic differentiation. Here, we report that the human ESCC miRNA miR-372 and let-7 act antagonistically in germline differentiation from human embryonic stem cells (hESCs) and human induced pluripotent stem cells (iPSCs). hESC and iPSC-derived primordial germ cell-like cells (PGCLCs) expressed high levels of miR-372 and conversely, somatic cells expressed high levels of let-7. Manipulation of miRNA levels by introduction of miRNA mimics or knockdown with miRNA sponges demonstrated that miR-372 promotes whereas let-7 antagonizes PGCLC differentiation. Knockdown of the individual miR-372 targets SMARCC1, MECP2, CDKN1, RBL2, RHOC, and TGFBR2 increased PGCLC production, whereas knockdown of the let-7 targets CMYC and NMYC suppressed PGCLC differentiation. These findings uncover a miR-372/let-7 axis regulating human primordial germ cell (PGC) specification.
The embryonic stem cell cycle (ESCC) and let-7 families of miRNAs function antagonistically in the switch between mouse embryonic stem cell self-renewal and somatic differentiation. Here, we report that the human ESCC miRNA miR-372 and let-7 act antagonistically in germline differentiation from human embryonic stem cells (hESCs) and human induced pluripotent stem cells (iPSCs). hESC and iPSC-derived primordial germ cell-like cells (PGCLCs) expressed high levels of miR-372 and conversely, somatic cells expressed high levels of let-7. Manipulation of miRNA levels by introduction of miRNA mimics or knockdown with miRNA sponges demonstrated that miR-372 promotes whereas let-7 antagonizes PGCLC differentiation. Knockdown of the individual miR-372 targets SMARCC1, MECP2, CDKN1, RBL2, RHOC, and TGFBR2 increased PGCLC production, whereas knockdown of the let-7 targets CMYC and NMYC suppressed PGCLC differentiation. These findings uncover a miR-372/let-7 axis regulating human primordial germ cell (PGC) specification. Stem Cells 2016; 34:1985-1991 Let-7 and miR-294 antagonistically regulate somatic versus germline fates through their influence on multiple cellular pathways.
The embryonic stem cell cycle (ESCC) and let-7 families of miRNAs function antagonistically in the switch between mouse embryonic stem cell self-renewal and somatic differentiation. Here, we report that the human ESCC miRNA miR-372 and let-7 act antagonistically in germline differentiation from human embryonic stem cells (hESCs) and human induced pluripotent stem cells (iPSCs). hESC and iPSC-derived primordial germ cell-like cells (PGCLCs) expressed high levels of miR-372 and conversely, somatic cells expressed high levels of let-7. Manipulation of miRNA levels by introduction of miRNA mimics or knockdown with miRNA sponges demonstrated that miR-372 promotes whereas let-7 antagonizes PGCLC differentiation. Knockdown of the individual miR-372 targets SMARCC1, MECP2, CDKN1, RBL2, RHOC, and TGFBR2 increased PGCLC production, whereas knockdown of the let-7 targets CMYC and NMYC suppressed PGCLC differentiation. These findings uncover a miR-372/let-7 axis regulating human primordial germ cell (PGC) specification. Stem Cells 2016;34:1985-1991.
The embryonic stem cell cycle (ESCC) and let‐7 families of miRNAs function antagonistically in the switch between mouse embryonic stem cell self‐renewal and somatic differentiation. Here, we report that the human ESCC miRNA miR‐372 and let‐7 act antagonistically in germline differentiation from human embryonic stem cells (hESCs) and human induced pluripotent stem cells (iPSCs). hESC and iPSC‐derived primordial germ cell‐like cells (PGCLCs) expressed high levels of miR‐372 and conversely, somatic cells expressed high levels of let‐7. Manipulation of miRNA levels by introduction of miRNA mimics or knockdown with miRNA sponges demonstrated that miR‐372 promotes whereas let‐7 antagonizes PGCLC differentiation. Knockdown of the individual miR‐372 targets SMARCC1, MECP2, CDKN1, RBL2, RHOC, and TGFBR2 increased PGCLC production, whereas knockdown of the let‐7 targets CMYC and NMYC suppressed PGCLC differentiation. These findings uncover a miR‐372/let‐7 axis regulating human primordial germ cell (PGC) specification. Stem Cells 2016;34:1985–1991 Let‐7 and miR‐294 antagonistically regulate somatic versus germline fates through their influence on multiple cellular pathways.
The embryonic stem cell cycle (ESCC) and let-7 families of miRNAs function antagonistically in the switch between mouse embryonic stem cell (mESC) self-renewal and somatic differentiation. Here we report that the human ESCC miRNA miR-372 and let-7 act antagonistically in germline differentiation from human embryonic stem cells (hESCs) and human induced pluripotent stem cells (iPSCs). hESC and iPSC-derived primordial germ cell-like cells (PGCLCs) expressed high levels of miR-372 and conversely, somatic cells expressed high levels of let-7. Manipulation of miRNA levels by introduction of miRNA mimics or knockdown with miRNA sponges demonstrated that miR-372 promotes while let-7 antagonizes PGCLC differentiation. Knockdown of the individual miR-372 targets SMARCC1 , MECP2 , CDKN1 , RBL2 , RHOC , and TGFBR2 increased PGCLC production, while knockdown of the let-7 targets CMYC and NMYC suppressed PGCLC differentiation. These findings uncover a miR-372/let-7 axis common to induced pluripotency and primordial germ cell (PGC) specification. Let-7 and miR-294 antagonistically regulate somatic versus germline fates through their influence on multiple cellular pathways.
The embryonic stem cell cycle (ESCC) and let-7 families of miRNAs function antagonistically in the switch between mouse embryonic stem cell self-renewal and somatic differentiation. Here, we report that the human ESCC miRNA miR-372 and let-7 act antagonistically in germline differentiation from human embryonic stem cells (hESCs) and human induced pluripotent stem cells (iPSCs). hESC and iPSC-derived primordial germ cell-like cells (PGCLCs) expressed high levels of miR-372 and conversely, somatic cells expressed high levels of let-7. Manipulation of miRNA levels by introduction of miRNA mimics or knockdown with miRNA sponges demonstrated that miR-372 promotes whereas let-7 antagonizes PGCLC differentiation. Knockdown of the individual miR-372 targets SMARCC1, MECP2, CDKN1, RBL2, RHOC, and TGFBR2 increased PGCLC production, whereas knockdown of the let-7 targets CMYC and NMYC suppressed PGCLC differentiation. These findings uncover a miR-372/let-7 axis regulating human primordial germ cell (PGC) specification. Stem Cells 2016;34:1985-1991
Author Kissner, Michael
Tran, Nam D.
Blelloch, Robert H.
Subramanyam, Deepa
Parchem, Ronald J.
Laird, Diana J.
AuthorAffiliation 1 Departments of OB/Gyn and Urology, Center for Reproductive Sciences, and the Eli and Edythe Broad Center for Regeneration Medicine and Stem Cell Research, University of California, San Francisco, San Francisco, CA. USA
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Issue 7
Keywords mir-372
microRNA
Primordial germ cells
let-7
Embryonic stem cells
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Snippet The embryonic stem cell cycle (ESCC) and let‐7 families of miRNAs function antagonistically in the switch between mouse embryonic stem cell self‐renewal and...
The embryonic stem cell cycle (ESCC) and let-7 families of miRNAs function antagonistically in the switch between mouse embryonic stem cell self-renewal and...
Abstract The embryonic stem cell cycle (ESCC) and let-7 families of miRNAs function antagonistically in the switch between mouse embryonic stem cell...
The embryonic stem cell cycle (ESCC) and let-7 families of miRNAs function antagonistically in the switch between mouse embryonic stem cell (mESC) self-renewal...
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StartPage 1985
SubjectTerms Biomarkers - metabolism
Cell cycle
Cell Lineage
Cell self-renewal
Differentiation
Embryo cells
Embryonic stem cells
Embryos
Germ Cells - cytology
Germ Cells - metabolism
Humans
let‐7
MeCP2 protein
Methyl-CpG binding protein
microRNA
MicroRNAs - genetics
MicroRNAs - metabolism
miRNA
mir‐372
Pluripotency
Primordial germ cells
Signal Transduction - genetics
Somatic cells
Sponges
Stem cell transplantation
Stem cells
Title A miR‐372/let‐7 Axis Regulates Human Germ Versus Somatic Cell Fates
URI https://onlinelibrary.wiley.com/doi/abs/10.1002%2Fstem.2378
https://www.ncbi.nlm.nih.gov/pubmed/27066911
https://www.proquest.com/docview/1801399378
https://www.proquest.com/docview/1897632182
https://search.proquest.com/docview/1801864962
https://search.proquest.com/docview/1808684701
https://pubmed.ncbi.nlm.nih.gov/PMC5145290
Volume 34
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