Cyclin‐dependent kinase 9 forms a complex with GATA4 and is involved in the differentiation of mouse ES cells into cardiomyocytes

Kaichi, Shinji; Takaya, Tomohide; Morimoto, Tatsuya; Sunagawa, Yoichi; Kawamura, Teruhisa; Ono, Koh; Shimatsu, Akira; Baba, Shiro; Heike, Toshio; Nakahata, Tatsutoshi; Hasegawa, Koji

doi:10.1002/jcp.22336

Cited by 24 publications

(16 citation statements)

References 26 publications

(41 reference statements)

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“…We previously reported that TSA, a histone deacetylase inhibitor, enhances the differentiation of mouse and monkey ES cells into cardiac myocytes. 21,22,24 As shown in Figure 1B, TSA dose-dependently reduced the levels of the cardiac miRNAs, miR-1, miR-133, and miR-143. However, TSA did not affect the level of miR-24, which is ubiquitously expressed in various tissues.…”

Section: Expression Profiles Of Cardiac Mirnas During Differentiationmentioning

confidence: 80%

“…23 The kinase activity of Cdk9 plays an important role in the p300-induced GATA4 acetylation, and, finally, the myocardial differentiation of mouse ES cells. 24 In the present study, we investigated the expression profiles of miR-1, miR-133, and miR-143 during the myocardial differentiation of 2-D cultured mouse ES cells, and found that all of these miRNAs were increased during spontaneous differentiation, but reduced during TSA-induced myocardial differentiation. The overexpression of miR-1 or miR-133, but not that of miR-143, inhibited the expression of cardiac genes.…”

Section: Editorial P 1397mentioning

confidence: 87%

“…18,19 Recently, we found that Cdk9 forms a transcriptional complex with p300/GATA4, to activate the expression of cardiac-specific genes such as Nkx2.5, ANF, and β-MHC. 23,24 The kinase activity of Cdk9 is required for the acetylation of GATA4 and for the myocardial differentiation of mouse ES cells. The administration of Cdk9 inhibitor or the forced expression of the dominant-negative form of Cdk9 suppresses cardiac gene transcription and the myocardial differentiation of mouse ES cells cultured, 24 as noted in the present study.…”

Section: Discussionmentioning

confidence: 99%

“…23,24 The kinase activity of Cdk9 is required for the acetylation of GATA4 and for the myocardial differentiation of mouse ES cells. The administration of Cdk9 inhibitor or the forced expression of the dominant-negative form of Cdk9 suppresses cardiac gene transcription and the myocardial differentiation of mouse ES cells cultured, 24 as noted in the present study. Therefore, it is possible that the miR-1-dependent decrease of Cdk9 protein suppresses cardiac gene expression in ES cells during spontaneous differentiation.…”

Section: Discussionmentioning

confidence: 99%

“…GATA4, which activates cardiac gene expression with Cdk9, begins to be expressed from day 5 in 2-D culture. 24 However, in an EB-forming system, a significant amount of GATA4 is expressed even on day 3. 21 Therefore, 2-D cultured ES cells, which express lower levels of GATA4, may be more sensitive to the minimal reduction of Cdk9 by miR-1 rather than the EBs expressing higher levels of GATA4.…”

Section: Discussionmentioning

confidence: 99%

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MicroRNA-1 and MicroRNA-133 in Spontaneous Myocardial Differentiation of Mouse Embryonic Stem Cells

Takaya

Ono

Kawamura

et al. 2009

Circ J

Self Cite

118

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Background: MicroRNAs (miRNAs) regulate various biological processes through inhibiting the translation of RNA transcripts. Although miRNA-1 (miR-1) and miRNA-133 (miR-133) are abundantly expressed in the adult heart and involved in cardiac hypertrophy, the roles of these miRNAs in spontaneous myocardial differentiation are unknown. Methods and Results:The levels of miR-1 and miR-133 in mouse embryonic stem (ES) cells were increased during spontaneous differentiation by 2-dimensional culture, but reduced during forced myocardial differentiation by a histone deacetylase inhibitor, trichostatin A. The overexpression of miR-1 or miR-133 by lentiviral infection reduced the expression of a cardiac-specific gene, Nkx2.5, during differentiation of ES cells. In addition, miR-1 also inhibited α-myosin heavy chain expression. The results of luciferase assays revealed that miR-1 recognizes and targets the 3' untranslated region of cyclin-dependent kinase-9 (Cdk9) in ES cells. Overexpression of miR-1 decreased the protein amounts of Cdk9 without affecting the mRNA levels, indicating that miR-1 post-transcriptionally inhibits Cdk9 translation. Conclusions: miR-1 and miR-133 may play significant roles in the myocardial differentiation of mouse ES cells, and Cdk9 may be involved in this process as a target of miR-1. (Circ J 2009; 73: 1492 -1497

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Section: Expression Profiles Of Cardiac Mirnas During Differentiationmentioning

confidence: 80%

Section: Editorial P 1397mentioning

confidence: 87%

Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

See 3 more Smart Citations

MicroRNA-1 and MicroRNA-133 in Spontaneous Myocardial Differentiation of Mouse Embryonic Stem Cells

Takaya

Ono

Kawamura

et al. 2009

Circ J

Self Cite

118

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Phosphorylation of histone H1 by P‐TEFb is a necessary step in skeletal muscle differentiation

O'Brien

Knight

Rana

2011

Journal Cellular Physiology

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Positive transcription elongation factor b (P-TEFb), the complex of Cyclin T1 and CDK9, activates the transcription of many viral and eukaryotic genes at the point of mRNA elongation. The activity of P-TEFb has been implicated in the differentiation of a number of cell types, including skeletal muscle. In order to promote transcription, P-TEFb hyperphosphorylates RNA Pol II, thereby increasing its processivity. Our previous work identified histone H1 as a P-TEFb substrate during HIV-1 and immediate-early transcription. Here, we examine the role of P-TEFb phosphorylation of histone H1 during differentiation, using the myoblast cell line C2C12 as a model for skeletal muscle differentiation. We found that H1 phosphorylation is elevated in differentiating C2C12, and this phosphorylation is sensitive to P-TEFb inhibition. H1 phosphorylation was also necessary for the induction of three muscle marker genes that require P-TEFb for expression. Additionally, ChIP experiments demonstrate that H1 dissociates from muscle differentiation marker genes in C2C12 cells under active P-TEFb conditions. We determine that both P-TEFb activity and H1 phosphorylation are necessary for the full differentiation of C2C12 myoblasts into myotubes.

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Cardiomyocyte proliferation in zebrafish and mammals: lessons for human disease

Matrone

Tucker

Denvir

2016

Cell. Mol. Life Sci.

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Cardiomyocytes proliferate profusely during early development and for a brief period after birth in mammals. Within a month after birth, this proliferative capability is dramatically reduced in mammals unlike lower vertebrates where it persists into adult life. The zebrafish, for example, retains the ability to regenerate the apex of the heart following resection by a mechanism predominantly driven by cardiomyocyte proliferation. Differences in proliferative capacity of cardiomyocytes in adulthood between mammals and lower vertebrates are closely liked to ontogenetic or phylogenetic factors. Elucidation of these factors has the potential to provide enormous benefits if they lead to the development of therapeutic strategies that facilitate cardiomyocyte proliferation. In this review, we highlight the differences between Mammalian and Zebrafish cardiomyocytes, which could explain at least in part the different proliferative capacities in these two species. We discuss the advantages of the zebrafish as a model of cardiomyocyte proliferation, particularly at the embryonic stage. We also identify a number of key molecular pathways with potential to reveal key steps in switching cardiomyocytes from a quiescent to a proliferative phenotype.Electronic supplementary materialThe online version of this article (doi:10.1007/s00018-016-2404-x) contains supplementary material, which is available to authorized users.

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Cyclin‐dependent kinase 9 forms a complex with GATA4 and is involved in the differentiation of mouse ES cells into cardiomyocytes

Cited by 24 publications

References 26 publications

MicroRNA-1 and MicroRNA-133 in Spontaneous Myocardial Differentiation of Mouse Embryonic Stem Cells

MicroRNA-1 and MicroRNA-133 in Spontaneous Myocardial Differentiation of Mouse Embryonic Stem Cells

Phosphorylation of histone H1 by P‐TEFb is a necessary step in skeletal muscle differentiation

Cardiomyocyte proliferation in zebrafish and mammals: lessons for human disease

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