Heart Development in Drosophila Requires the Segment Polarity Gene wingless

Wu, Xiushan; Golden, Krista; Bodmer, Rolf

doi:10.1006/dbio.1995.1174

Cited by 207 publications

(137 citation statements)

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“…1 A and C). tin expression is restricted to the cardiac mesoderm just after stage 11 by means of the ectodermally secreted signaling molecules Wg and Dpp and then becomes restricted to four of six cardiac cells (7,9,23,24) (Fig. 1 B and D).…”

Section: Results Dsur Expression In the Developing Heart Is Regulatedmentioning

confidence: 99%

The ATP-sensitive potassium (K _ATP ) channel-encoded dSUR gene is required for Drosophila heart function and is regulated by tinman

Akasaka

Klinedinst

Ocorr

et al. 2006

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

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The homeobox transcription factor Tinman plays an important role in the initiation of heart development. Later functions of Tinman, including the target genes involved in cardiac physiology, are less well studied. We focused on the dSUR gene, which encodes an ATP-binding cassette transmembrane protein that is expressed in the heart. Mammalian SUR genes are associated with K ATP (ATPsensitive potassium) channels, which are involved in metabolic homeostasis. We provide experimental evidence that Tinman directly regulates dSUR expression in the developing heart. We identified a cis-regulatory element in the first intron of dSUR, which contains Tinman consensus binding sites and is sufficient for faithful dSUR expression in the fly's myocardium. Site-directed mutagenesis of this element shows that these Tinman sites are critical to dSUR expression, and further genetic manipulations suggest that the GATA transcription factor Pannier is synergistically involved in cardiac-restricted dSUR expression in vivo. Physiological analysis of dSUR knock-down flies supports the idea that dSUR plays a protective role against hypoxic stress and pacinginduced heart failure. Because dSUR expression dramatically decreases with age, it is likely to be a factor involved in the cardiac aging phenotype of Drosophila. dSUR provides a model for addressing how embryonic regulators of myocardial cell commitment can contribute to the establishment and maintenance of cardiac performance.aging ͉ hypoxia ͉ sulfonylurea receptor

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Section: Results Dsur Expression In the Developing Heart Is Regulatedmentioning

confidence: 99%

The ATP-sensitive potassium (K _ATP ) channel-encoded dSUR gene is required for Drosophila heart function and is regulated by tinman

Akasaka

Klinedinst

Ocorr

et al. 2006

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

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“…3GЈ-JЈ). Sibling embryos injected with each of these mRNAs, but not dissected for VMZ explants, developed malformations characteristic of each inhibitor, indicating that the injected mRNAs yielded functional protein (Wu et al 1995;Salic et al 1997;Hsieh et al 1999; data not shown). Thus, of the Wnt antagonists examined, only Dkk-1 and Crescent induced ectopic cardiogenesis in VMZ tissue.…”

Section: Wnt Antagonists Other Than Dkk-1 and Crescent Are Unable To mentioning

confidence: 91%

Wnt antagonism initiates cardiogenesis in Xenopus laevis

Schneider¹,

Mercola²

2001

Genes Dev.

458

393

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Heart induction in Xenopus occurs in paired regions of the dorsoanterior mesoderm in response to signals from the Spemann organizer and underlying dorsoanterior endoderm. These tissues together are sufficient to induce heart formation in noncardiogenic ventral marginal zone mesoderm. Similarly, in avians the underlying definitive endoderm induces cardiogenesis in precardiac mesoderm. Heart-inducing factors in amphibians are not known, and although certain BMPs and FGFs can mimic aspects of cardiogenesis in avians, neither can induce the full range of activities elicited by the inducing tissues. Here we report that the Wnt antagonists Dkk-1 and Crescent can induce heart formation in explants of ventral marginal zone mesoderm. Other Wnt antagonists, including the frizzled domain-containing proteins Frzb and Szl, lacked this activity. Unlike Wnt antagonism, inhibition of BMP signaling did not promote cardiogenesis. Ectopic expression of GSK3␤, which inhibits ␤-catenin-mediated Wnt signaling, also induced cardiogenesis in ventral mesoderm. Analysis of Wnt proteins expressed during gastrulation revealed that Wnt3A and Wnt8, but not Wnt5A or Wnt11, inhibited endogenous heart induction. These results indicate that diffusion of Dkk-1 and Crescent from the organizer initiate cardiogenesis in adjacent mesoderm by establishing a zone of low Wnt3A and Wnt8 activity.

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“…Maintenance of the Dro-sophila NK-2 gene tinman is required for specification of the cardiac mesoderm, and its expression depends upon the Wnt homologue, wingless (wg), and the BMP homologue, decapentaplegic (dpp; Azpiazu and Frasch 1993;Bodmer 1993;Wu et al 1995;Park et al 1996). Similarly, formation of the vertebrate heart requires the tinman related genes Nkx-2.3 or 2.5 (Fu et al 1998;Grow and Krieg 1998).…”

Section: Evolutionary Differences Between Heart-inducing Signals In Fmentioning

confidence: 99%

Inhibition of Wnt activity induces heart formation from posterior mesoderm

Marvin¹,

Rocco²,

Gardiner³

et al. 2001

Genes Dev.

539

459

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In the chick, heart mesoderm is induced by signals from the anterior endoderm. Although BMP-2 is expressed in the anterior endoderm, BMP activity is necessary but not sufficient for heart formation. Previous work from our lab has suggested that one or more additional factors from anterior endoderm are required. Crescent is a Frizzled-related protein that inhibits Wnt-8c and is expressed in anterior endoderm during gastrulation. At the same stages, expression of Wnt-3a and Wnt-8c is restricted to the primitive streak and posterior lateral plate, and is absent from the anterior region where crescent is expressed. Posterior lateral plate mesoderm normally forms blood, but coculture of this tissue with anterior endoderm or infection with RCAS-crescent induces formation of beating heart muscle and represses formation of blood. Dkk-1, a Wnt inhibitor of a different protein family, similarly induces heart-specific gene expression in posterior lateral plate mesoderm. Furthermore, we have found that ectopic Wnt signals can repress heart formation from anterior mesoderm in vitro and in vivo and that forced expression of either Wnt-3a or Wnt-8c can promote development of primitive erythrocytes from the precardiac region. We conclude that inhibition of Wnt signaling promotes heart formation in the anterior lateral mesoderm, whereas active Wnt signaling in the posterior lateral mesoderm promotes blood development. We propose a model in which two orthogonal gradients, one of Wnt activity along the anterior-posterior axis and the other of BMP signals along the dorsal-ventral axis, intersect in the heart-forming region to induce cardiogenesis in a region of high BMP and low Wnt activity.

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Heart Development in Drosophila Requires the Segment Polarity Gene wingless

Cited by 207 publications

References 0 publications

The ATP-sensitive potassium (K _ATP ) channel-encoded dSUR gene is required for Drosophila heart function and is regulated by tinman

The ATP-sensitive potassium (K _ATP ) channel-encoded dSUR gene is required for Drosophila heart function and is regulated by tinman

Wnt antagonism initiates cardiogenesis in Xenopus laevis

Inhibition of Wnt activity induces heart formation from posterior mesoderm

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Heart Development in Drosophila Requires the Segment Polarity Gene wingless

Cited by 207 publications

References 0 publications

The ATP-sensitive potassium (K ATP ) channel-encoded dSUR gene is required for Drosophila heart function and is regulated by tinman

The ATP-sensitive potassium (K ATP ) channel-encoded dSUR gene is required for Drosophila heart function and is regulated by tinman

Wnt antagonism initiates cardiogenesis in Xenopus laevis

Inhibition of Wnt activity induces heart formation from posterior mesoderm

Contact Info

Product

Resources

About

The ATP-sensitive potassium (K _ATP ) channel-encoded dSUR gene is required for Drosophila heart function and is regulated by tinman

The ATP-sensitive potassium (K _ATP ) channel-encoded dSUR gene is required for Drosophila heart function and is regulated by tinman