Dissociation of Cardiogenic and Postnatal Myocardial Activities of GATA4

Gallagher, Joseph M.; Komati, Hiba; Roy, Emmanuel; Nemer, Mona; Latinkic, Branko

doi:10.1128/mcb.00218-12

Cited by 28 publications

(40 citation statements)

References 51 publications

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“…Here, we show that CycD2 but not CycD1 enhances transcriptional activity of GATA4 and potentiates GATA4-dependent cardiomyogenesis. Moreover, CycD2 interacts physically with a GATA4 N-terminal activation domain that overlaps with a recently identified GATA4 cardiogenic domain (33). We find that mutations within this domain that reduce CycD2-GATA4 synergy are associated with decreased GATA4 cardiogenic activity and with human congenial heart disease.…”

Section: Discussionmentioning

confidence: 62%

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Cyclin D2 is a GATA4 cofactor in cardiogenesis

Yamak

Latinkic

Dali

et al. 2014

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

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The G1 cyclins play a pivotal role in regulation of cell differentiation and proliferation. The mechanisms underlying their cellspecific roles are incompletely understood. Here, we show that a G1 cyclin, cyclin D2 (CycD2), enhances the activity of transcription factor GATA4, a key regulator of cardiomyocyte growth and differentiation. GATA4 recruits CycD2 to its target promoters, and their interaction results in synergistic activation of GATA-dependent transcription. This effect is specific to CycD2 because CycD1 is unable to potentiate activity of GATA4 and is CDK-independent. GATA4 physically interacts with CycD2 through a discreet N-terminal activation domain that is essential for the cardiogenic activity of GATA4. Human mutations in this domain that are linked to congenital heart disease interfere with CycD2-GATA4 synergy. Cardiogenesis assays in Xenopus embryos indicate that CycD2 enhances the cardiogenic function of GATA4. Together, our data uncover a role for CycD2 as a cardiogenic coactivator of GATA4 and suggest a paradigm for cell-specific effects of cyclin Ds.

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Section: Discussionmentioning

confidence: 62%

“…The CycD2 interaction domain overlaps with a region of GATA4 that was recently found to be essential for its cardiogenic activity (33), and mutations therein that decrease synergy with CycD2 have been associated with congenital heart disease ( Fig. 3).…”

Section: Yv P Shs Gs M T L Gg a S S S T H Pmentioning

confidence: 99%

Cyclin D2 is a GATA4 cofactor in cardiogenesis

Yamak

Latinkic

Dali

et al. 2014

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

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“…The respective BAF60 subunit present in the BAF complex appears to be a commonly employed recruiter via its direct interaction with specific transcription factors (Ito et al 2001;Hsiao et al 2003;Debril et al 2004;Takeuchi et al 2007;Oh et al 2008;Chen et al 2012;Forcales et al 2012;Gallagher et al 2012). Such recruitment is thought to be a prerequisite to enable transcription or to allow access of additional transacting factors (Sudarsanam and Winston 2000).…”

mentioning

confidence: 99%

The SWI/SNF Chromatin Remodeling Complex Selectively Affects Multiple Aspects of Serotonergic Neuron Differentiation

et al. 2013

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Regulatory programs that control the specification of serotonergic neurons have been investigated by genetic mutant screens in the nematode Caenorhabditis elegans. Loss of a previously uncloned gene, ham-3, affects migration and serotonin antibody staining of the hermaphrodite-specific neuron (HSN) pair. We characterize these defects here in more detail, showing that the defects in serotonin antibody staining are paralleled by a loss of the transcription of all genes involved in serotonin synthesis and transport. This loss is specific to the HSN class as other serotonergic neurons appear to differentiate normally in ham-3 null mutants. Besides failing to migrate appropriately, the HSNs also display axon pathfinding defects in ham-3 mutants. However, the HSNs are still generated and express a subset of their terminal differentiation features in ham-3 null mutants, demonstrating that ham-3 is a specific regulator of select features of the HSNs. We show that ham-3 codes for the C. elegans ortholog of human BAF60, Drosophila Bap60, and yeast Swp73/Rsc6, which are subunits of the yeast SWI/SNF and vertebrate BAF chromatin remodeling complex. We show that the effect of ham-3 on serotonergic fate can be explained by ham-3 regulating the expression of the Spalt/SALL-type Zn finger transcription factor sem-4, a previously identified regulator of serotonin expression in HSNs and of the ham-2 Zn transcription factor, a previously identified regulator of HSN migration and axon outgrowth. Our findings provide the first evidence for the involvement of the BAF complex in the acquisition of terminal neuronal identity and constitute genetic proof by germline knockout that a BAF complex component can have cell-type-specific roles during development. N EURONS that express the neurotransmitter serotonin fulfill a number of critical functions in all nervous systems examined to date. In vertebrates, serotonergic neurons modulate anxiety, cognitive processes, mood, body temperature, sleep, sexual behavior, appetite, and metabolism, and their dysfunction has been connected to a variety of human disorders (Muller and Jacobs 2010). In the hermaphroditic Caenorhabditis elegans nervous system, serotonin also controls a number of distinct behaviors (Schafer 2005;Chase and Koelle 2007). Serotonin is utilized as a neurotransmitter under normal conditions by seven neuron types, the sensory neuron ADF; the interneurons AIM and RIH; the motor neurons hermaphroditespecific neurons (HSNs), the ventral cord motor neurons VC4 and VC5; and the neurosecretory NSM cells (Schafer 2005;Chase and Koelle 2007). Under stress conditions, serotonin is used by an additional neuron type, ASG (Pocock and Hobert 2010). One of the serotonergic neurons, the hermaphrodite-specific motor neuron, HSN, utilizes serotonin to signal to vulval muscles to control egg-laying behavior (Schafer 2005). Unlike most other neurons in the C. elegans nervous system, the two bilaterally symmetric HSNs undergo long-range migration. After terminating migration, they extend th...

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“…These observations indicate that the molecular mechanisms underlying normal stem cell differentiation and embryo development do not quit after birth but are still in part operating and remodeled throughout the adult life to maintain the self-identity of and the interplay between tissues and organs. Supporting this view, the transcription factor GATA4 has been shown to act as a critical regulator of both embryonic and postnatal heart development and morphogenic maintenance due to a fine tuning of its structural/regulatory domains [104]. Whereas the N-terminal domain of GATA4 is required for inducing cardiogenesis and for promoting postnatal cardiomyocyte survival, distinct residues and domains therein are necessary to mediate these effects [104].…”

Section: Cancer Stem Cell Reprogrammingmentioning

confidence: 99%

Cancer Stem Cells: Foe or Reprogrammable Cells for Efficient Cancer Therapy?

Ventura¹,

Olivi²,

Cavallini³

et al. 2015

NanoWorld J

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Embryonic development and carcinogenesis share many molecular pathways and regulatory molecules. While the induction of a pluripotent state involves a significant oncogenic risk, as in induced pluripotent stem cells (iPSCs), the embryonic environment in vivo has been shown to suppress tumor development. In this review, we discuss the subtle equilibrium between the nanotopography (niche) of the hosting tissue resident stem cells and their biological dynamics, including the transformation in cancer stem cells. We review consistent findings indicating the potential for modulating the biology of human cancer stem cells by the aid of naturally occurring or synthetic molecules, including developmental stage zebrafish embryo extracts, hyaluronan, butyric acid (BA) and retinoic acid (RA), hyaluronan mixed esters of BA and RA, melatonin, vitamin D3, and endorphin peptides. Within this context, we dissect the multifaceted mechanisms orchestrated by endorphinergic systems, including paracrine cellto-cell communication, as well as the establishment of autocrine and intracrine (intracellular) peptide actions driving transcriptional responses and self-sustaining loops that behave as long-lived signals imparting features characteristic of differentiation, growth regulation and cell memory.Based upon the remarkable action of electromagnetic fields and mechanical vibration on (stem) cell signaling, differentiation, and senescence, we also consider the potential for using these physical energies as a tool to afford a fine tuning of cancer stem cell fate.On the whole, we forecast future deployment of the physical and/or chemical approaches described herein aiming at reprogramming, rather than destroying cancer stem cells, eventually placing cancer therapy within the context of Regenerative Medicine.

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Dissociation of Cardiogenic and Postnatal Myocardial Activities of GATA4

Cited by 28 publications

References 51 publications

Cyclin D2 is a GATA4 cofactor in cardiogenesis

Cyclin D2 is a GATA4 cofactor in cardiogenesis

The SWI/SNF Chromatin Remodeling Complex Selectively Affects Multiple Aspects of Serotonergic Neuron Differentiation

Cancer Stem Cells: Foe or Reprogrammable Cells for Efficient Cancer Therapy?

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