In addition to being a marker for muscle connective tissue, Odd skipped-related 2 (OSR2) is expressed in differentiated muscle cells during chick development

ABSTRACTThe zinc finger transcription factor, Odd skipped-related 2 (OSR2) is a recognized marker of connective tissue in chick embryos. OSR2 gain- and loss-of-function experiments indicate a role in irregular connective tissue differentiation in chick limb undifferentiated cells. Re-investigation of OSR2 transcript location during chick development with in situ hybridization experiments showed that OSR2 was also expressed in differentiated muscle cells in limbs and head. OSR2 expression was also observed in differentiated myotubes in chick foetal myoblast cultures. This shows that in addition to being a marker of connective tissue, OSR2 is also expressed in muscle fibres during chick development.

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Embryonic development of the heart

Development ◽

10.1242/dev.22.3.333 ◽

1969 ◽

Vol 22 (3) ◽

pp. 333-348

Author(s):

Francis J. Manasek

Keyword(s):

Cell Layer ◽

Embryonic Heart ◽

Outer Cell ◽

Chick Embryos ◽

Myocardial Wall ◽

Undifferentiated Cells ◽

Epicardial Layer ◽

Outer Cell Layer ◽

Heart Wall

The mature heart may be thought of as consisting of three layers, endocardium, myocardium, and an outer investing tissue called the epicardium. During early formation of the tubular heart of chick embryos, at about the 8-somite stage, two tissue layers become clearly discernible with the light microscope: the endocardium and the developing myocardial wall. The outer epicardial layer does not appear until later in development. It is generally accepted that embryonic heart wall or ‘epimyocardium’ is composed of muscle and undifferentiated cells. As its name implies, the epimyocardium is thought to give rise to myocardium and epicardium. Kurkiewicz (1909) suggested that the epicardium was not an epimyocardial derivative but rather is formed from cells originating in the sinus venosus region, which migrate over the surface of the heart. Nevertheless, it has become generally accepted that the outer cell layer of the embryonic heart wall differentiates in situ to give rise to the definitive visceral epicardium (Patten, 1953).

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CASZ1 loss-of-function mutation contributes to familial dilated cardiomyopathy

Clinical Chemistry and Laboratory Medicine (CCLM) ◽

10.1515/cclm-2016-0612 ◽

2017 ◽

Vol 55 (9) ◽

Cited By ~ 11

Author(s):

Xing-Biao Qiu ◽

Xin-Kai Qu ◽

Ruo-Gu Li ◽

Hua Liu ◽

Ying-Jia Xu ◽

...

Keyword(s):

Transcription Factor ◽

Transcriptional Activity ◽

Autosomal Dominant ◽

Cardiac Development ◽

Index Patient ◽

Loss Of Function ◽

Zinc Finger Transcription Factor ◽

Complete Penetrance ◽

Familial Dilated Cardiomyopathy ◽

Postnatal Adaptation

AbstractBackground:The zinc finger transcription factor CASZ1 plays a key role in cardiac development and postnatal adaptation, and in mice, deletion of theMethods:The coding exons and splicing junction sites of theResults:A novel heterozygous CASZ1 mutation, p.K351X, was identified in an index patient with DCM. Genetic analysis of the mutation carrier’s family showed that the mutation co-segregated with DCM, which was transmitted in an autosomal dominant pattern with complete penetrance. The nonsense mutation, which was absent in 400 referential chromosomes, altered the amino acid that was highly conserved evolutionarily. Biological investigations revealed that the mutant CASZ1 had no transcriptional activity.Conclusions:The current study reveals

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Identification and disruption of an Arabidopsis zinc finger gene controlling seed germination

Genes & Development ◽

10.1101/gad.14.1.28 ◽

2000 ◽

Vol 14 (1) ◽

pp. 28-33 ◽

Cited By ~ 1

Author(s):

Maura Papi ◽

Sabrina Sabatini ◽

David Bouchez ◽

Christine Camilleri ◽

Paolo Costantino ◽

...

Keyword(s):

Transcription Factor ◽

Seed Germination ◽

Zinc Finger ◽

Segregation Analysis ◽

Reverse Genetics ◽

Vascular Tissue ◽

Zinc Finger Transcription Factor ◽

Zinc Finger Gene ◽

Dna Insertion

We describe here the Arabidopsis gene DAG1, encoding a zinc finger transcription factor of the Dof family, and show that it is involved in the control of seed germination. By a reverse genetics approach, we isolated an Arabidopsis mutant line with one T-DNA insertion in DAG1. Seeds from homozygous knockoutdag1-1 plants do not develop dormancy and germinate also in the absence of light. Segregation analysis indicates that the effect of the mutation is maternal. Accordingly, in situ mRNA hybridizations reveal expression of DAG1 in the vascular tissue of the flower and maturing fruit but not in the seed.

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myoblasts incompetent encodes a zinc finger transcription factor required to specify fusion-competent myoblasts in Drosophila

Development ◽

10.1242/dev.129.1.133 ◽

2002 ◽

Vol 129 (1) ◽

pp. 133-141 ◽

Cited By ~ 7

Author(s):

Mar Ruiz-Gómez ◽

Nikola Coutts ◽

Maximiliano L. Suster ◽

Matthias Landgraf ◽

Michael Bate

Keyword(s):

Transcription Factor ◽

Zinc Finger ◽

Myoblast Fusion ◽

Loss Of Function ◽

Cubitus Interruptus ◽

Zinc Finger Transcription Factor ◽

General Pathway ◽

Twist Expression ◽

Fusion Competent Myoblasts ◽

Normal Differentiation

We report a new gene, myoblasts incompetent, essential for normal myogenesis and myoblast fusion in Drosophila. myoblasts incompetent encodes a putative zinc finger transcription factor related to vertebrate Gli proteins and to Drosophila Cubitus interruptus. myoblasts incompetent is expressed in immature somatic and visceral myoblasts. Expression is predominantly in fusion-competent myoblasts and a loss-of-function mutation in myoblasts incompetent leads to a failure in the normal differentiation of these cells and a complete lack of myoblast fusion. In the mutant embryos, founder myoblasts differentiate normally and form mononucleate muscles, but genes that are specifically expressed in fusion-competent cells are not activated and the normal downregulation of twist expression in these cells fails to occur. In addition, fusion-competent myoblasts fail to express proteins characteristic of the general pathway of myogenesis such as myosin and Dmef2. Thus myoblasts incompetent appears to function specifically in the general pathway of myogenesis to control the differentiation of fusion-competent myoblasts.

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Identification of ZBP-89 as a Novel GATA-1-Associated Transcription Factor Involved in Megakaryocytic and Erythroid Development

Molecular and Cellular Biology ◽

10.1128/mcb.01945-07 ◽

2008 ◽

Vol 28 (8) ◽

pp. 2675-2689 ◽

Cited By ~ 49

Author(s):

Andrew J. Woo ◽

Tyler B. Moran ◽

Yocheved L. Schindler ◽

Seong-Kyu Choe ◽

Nathaniel B. Langer ◽

...

Keyword(s):

Transcription Factor ◽

Zinc Finger ◽

Regulatory Elements ◽

Loss Of Function ◽

Zinc Finger Transcription Factor ◽

Novel Proteins ◽

Proteomic Approach ◽

Primitive Erythropoiesis ◽

Definitive Erythropoiesis

ABSTRACT A complete understanding of the transcriptional regulation of developmental lineages requires that all relevant factors be identified. Here, we have taken a proteomic approach to identify novel proteins associated with GATA-1, a lineage-restricted zinc finger transcription factor required for terminal erythroid and megakaryocytic maturation. We identify the Krüppel-type zinc finger transcription factor ZBP-89 as being a component of multiprotein complexes involving GATA-1 and its essential cofactor Friend of GATA-1 (FOG-1). Using chromatin immunoprecipitation assays, we show that GATA-1 and ZBP-89 cooccupy cis-regulatory elements of certain erythroid and megakaryocyte-specific genes, including an enhancer of the GATA-1 gene itself. Loss-of-function studies in zebrafish and mice demonstrate an in vivo requirement for ZBP-89 in megakaryopoiesis and definitive erythropoiesis but not primitive erythropoiesis, phenocopying aspects of FOG-1- and GATA-1-deficient animals. These findings identify ZBP-89 as being a novel transcription factor involved in erythroid and megakaryocytic development and suggest that it serves a cooperative function with GATA-1 and/or FOG-1 in a developmental stage-specific manner.

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In situ localization of muscle insulin-like growth factor-II mRNA in developing bovine fetuses

Journal of Endocrinology ◽

10.1677/joe.0.1400179 ◽

1994 ◽

Vol 140 (2) ◽

pp. 179-187 ◽

Cited By ~ 4

Author(s):

A Listrat ◽

D E Gerrard ◽

N Boulle ◽

A Groyer ◽

J Robelin

Keyword(s):

Growth Factor ◽

Connective Tissue ◽

Muscle Tissue ◽

Muscle Cells ◽

Insulin Like Growth Factor ◽

Bovine Muscle ◽

Factor Ii ◽

Bovine Fetuses ◽

Developing Muscle

Abstract Insulin-like growth factor-II (IGF-II) modulates myogenesis in muscle cell cultures, in utero. IGF-II gene expression is developmentally regulated in several tissues including muscle. Determining whether IGF-II is expressed by developing muscle cells or by neighbouring cells in developing muscle tissue is crucial for determining whether IGF-II exerts a paracrine or an autocrine affect on myogenesis. Semitendinosus muscle samples from 12 bovine fetuses ranging from 60 to 274 days post conception (pc) were analysed for the amount and localization of muscle IGF-II mRNA using Northern, dot blot and in situ hybridization analyses. Northern blot analysis revealed multiple IGF-II transcripts of 5·1, 3·7, 2·6, 2·0, 1·7 and 1·1 kb in developing bovine muscle tissue. The relative amount of muscle IGF-II mRNA increased (P<0·05) until 162 days pc, then decreased (P<0·01) to near undetectable levels by the end of gestation (approximately 284 days pc). Between 60 and 162 days pc, in situ hybridization revealed that the majority of the IGF-II transcripts were localized to developing muscle cells rather than connective tissue. After 162 days pc the IGF-II hybridization signal shifted away from muscle cells and greater accumulation was observed in the connective tissue at 274 days pc. These data confirm that the expression of IGF-II in developing bovine muscle tissue is primarily localized in muscle cells and support the claim that IGF-II acts as an autocrineacting growth factor during myogenesis in vivo. Journal of Endocrinology (1994) 140, 179–187

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