Cardiac expression of the drosophila <i>Transglutaminase</i> (<i>CG7356</i>) gene is directly controlled by myocyte enhancer factor‐2

Ikle, Jennifer M.; Elwell, Jennifer A.; Bryantsev, Anton L.; Cripps, Richard M.

doi:10.1002/dvdy.21624

Cited by 17 publications

(10 citation statements)

References 88 publications

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“…Tg is expressed in all Svp cells of the embryonic dorsal vessel (Iklé et al, 2008), and we found that this pattern of expression persisted until the adult stage in Tg-lacZ animals. In fillets of young transgenic adults stained for ß-galactosidase (ß-gal) activity, we observed five sets of cardial cells stained, spanning from the posterior of the thorax, to abdominal segment A5 (Figure 2A).…”

Section: Resultsmentioning

confidence: 64%

Cardiac remodeling in Drosophila arises from changes in actin gene expression and from a contribution of lymph gland-like cells to the heart musculature

Shah

Nongthomba

Kelly

et al. 2011

Mechanisms of Development

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Understanding the basis of normal heart remodeling can provide insight into the plasticity of the cardiac state, and into the potential for treating diseased tissue. In Drosophila, the adult heart arises during metamorphosis from a series of events, that include the remodeling of an existing cardiac tube, the elaboration of new inflow tracts, and the addition of a layer of longitudinal muscle fibers. We have identified genes active in all these three processes, and studied their expression in order to characterize in greater detail normal cardiac remodeling. Using a Transglutaminase-lacZ transgenic line, that is expressed in the inflow tracts of the larval and adult heart, we confirm the existence of five inflow tracts in the adult structure. In addition, expression of the Actin87E actin gene is initiated in the remodeling cardiac tube, but not in the longitudinal fibers, and we have identified an Act87E promoter fragment that recapitulates this switch in expression. We also establish that the longitudinal fibers are multinucleated, characterizing these cells as specialized skeletal muscles. Furthermore, we have defined the origin of the longitudinal fibers, as a subset of lymph gland cells associated with the larval dorsal vessel. These studies underline the myriad contributors to the formation of the adult Drosophila heart, and provide new molecular insights into the development of this complex organ.

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Section: Resultsmentioning

confidence: 64%

Cardiac remodeling in Drosophila arises from changes in actin gene expression and from a contribution of lymph gland-like cells to the heart musculature

Shah

Nongthomba

Kelly

et al. 2011

Mechanisms of Development

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“…8) As a first step in the study on dTG functions, we established transgenic fly lines overexpressing dTG-A in various tissues and at various developmental stages utilizing a GAL4-UAS targeted expression system. Recently, we found that overexpression of dTG-A in the eye imaginal disc of Drosophila larvae caused a rough eye phenotype in adult compound eyes, and that the induced phenotype is probably due to the occurrence of apoptosis and enhancement of the JNK signaling pathway.…”

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confidence: 99%

Overexpression of Transglutaminase in theDrosophilaWing Imaginal Disc Induced an Extra Wing Crossvein Phenotype

Ichikawa

Yamada

Sakamoto

et al. 2010

Bioscience, Biotechnology, and Biochemistry

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“…5A). One transglutaminase ( Tg ) gene has been identified in Drosophila (CG7356) that appears to be expressed predominantly in cardiac tissue (Iklé et al, 2008) but whether this functions in the CNS remains unknown. It is tempting to hypothesize that inhibiting TG activity under conditions of excess 5-HT prevents neurotransmitter binding to cytoplasmic proteins that would initiate spheroid formation.…”

Section: Discussionmentioning

confidence: 99%

Serotonergic dystrophy induced by excess serotonin

Daubert¹,

Heffron²,

Mandell³

et al. 2010

Molecular and Cellular Neuroscience

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Administration of certain serotonin-releasing amphetamine derivatives (fenfluramine and/or 3,4-methylenedioxymethamphetamine, MDMA, 'ecstasy') results in dystrophic serotonergic morphology in the mammalian brain. In addition to drug administration, dystrophic serotonergic neurites are also associated with neurodegenerative disorders. We demonstrate here that endogenously elevated serotonin in the Drosophila CNS induces aberrant enlarged varicosities, or spheroids, that are morphologically similar to dystrophic mammalian serotonergic fibers. In Drosophila these spheroids are specific to serotonergic neurons, distinct from typical varicosities, and form only after prolonged increases in cytoplasmic serotonin. Our results also suggest that serotonin levels during early development determine later sensitivity of spheroid formation to manipulations of the serotonin transporter (SERT). Elevated serotonin also interacts with canonical protein aggregation and autophagic pathways to form spheroids. The data presented here support a model in which excess cytoplasmic neurotransmitter triggers a cell-specific pathway inducing aberrant morphology in fly serotonergic neurons that may be shared in certain mammalian pathologies.

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Cardiac expression of the drosophila Transglutaminase (CG7356) gene is directly controlled by myocyte enhancer factor‐2

Cited by 17 publications

References 88 publications

Cardiac remodeling in Drosophila arises from changes in actin gene expression and from a contribution of lymph gland-like cells to the heart musculature

Cardiac remodeling in Drosophila arises from changes in actin gene expression and from a contribution of lymph gland-like cells to the heart musculature

Overexpression of Transglutaminase in theDrosophilaWing Imaginal Disc Induced an Extra Wing Crossvein Phenotype

Serotonergic dystrophy induced by excess serotonin

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