“…twist1 has been implicated in mesoderm formation, as well as in a number of developmental events. twist1 haploinsufficiency leads to skeletal dysplasia (Miraoui and Marie, 2010). In the mouse, Twist1 is required for cranial neural crest migration as well as for the suppression of apoptosis (Chen and Behringer, 1995;Soo et al, 2002).…”
Section: Introductionmentioning
confidence: 99%
“…In the mouse, Twist1 is required for cranial neural crest migration as well as for the suppression of apoptosis (Chen and Behringer, 1995;Soo et al, 2002). In humans, mutations in TWIST have been implicated in mesenchymal stem cell differentiation and skeletal malformations (craniosynostosis) (Miraoui and Marie, 2010). There are two closely related snail-like genes in vertebrates, snail1 and snail2 (previously known as slug), as well as a number of more distantly related genes (BarralloGimeno and Nieto, 2009;Manzanares et al, 2001;Nieto, 2002).…”
SUMMARYThe neural crest is an induced tissue that is unique to vertebrates. In the clawed frog Xenopus laevis, neural crest induction depends on signals secreted from the prospective dorsolateral mesodermal zone during gastrulation. The transcription factors Snail2 (Slug), Snail1 and Twist1 are expressed in this region. It is known that Snail2 and Twist1 are required for both mesoderm formation and neural crest induction. Using targeted blastomere injection, morpholino-based loss of function and explant studies, we show that: (1) Snail1 is also required for mesoderm and neural crest formation; (2) loss of snail1, snail2 or twist1 function in the C2/C3 lineage of 32-cell embryos blocks mesoderm formation, but neural crest is lost only in the case of snail2 loss of function; (3) snail2 mutant loss of neural crest involves mesoderm-derived secreted factors and can be rescued synergistically by bmp4 and wnt8 RNAs; and (4) loss of snail2 activity leads to changes in the RNA levels of a number of BMP and Wnt agonists and antagonists. Taken together, these results identify Snail2 as a key regulator of the signals involved in mesodermal induction of neural crest.
“…twist1 has been implicated in mesoderm formation, as well as in a number of developmental events. twist1 haploinsufficiency leads to skeletal dysplasia (Miraoui and Marie, 2010). In the mouse, Twist1 is required for cranial neural crest migration as well as for the suppression of apoptosis (Chen and Behringer, 1995;Soo et al, 2002).…”
Section: Introductionmentioning
confidence: 99%
“…In the mouse, Twist1 is required for cranial neural crest migration as well as for the suppression of apoptosis (Chen and Behringer, 1995;Soo et al, 2002). In humans, mutations in TWIST have been implicated in mesenchymal stem cell differentiation and skeletal malformations (craniosynostosis) (Miraoui and Marie, 2010). There are two closely related snail-like genes in vertebrates, snail1 and snail2 (previously known as slug), as well as a number of more distantly related genes (BarralloGimeno and Nieto, 2009;Manzanares et al, 2001;Nieto, 2002).…”
SUMMARYThe neural crest is an induced tissue that is unique to vertebrates. In the clawed frog Xenopus laevis, neural crest induction depends on signals secreted from the prospective dorsolateral mesodermal zone during gastrulation. The transcription factors Snail2 (Slug), Snail1 and Twist1 are expressed in this region. It is known that Snail2 and Twist1 are required for both mesoderm formation and neural crest induction. Using targeted blastomere injection, morpholino-based loss of function and explant studies, we show that: (1) Snail1 is also required for mesoderm and neural crest formation; (2) loss of snail1, snail2 or twist1 function in the C2/C3 lineage of 32-cell embryos blocks mesoderm formation, but neural crest is lost only in the case of snail2 loss of function; (3) snail2 mutant loss of neural crest involves mesoderm-derived secreted factors and can be rescued synergistically by bmp4 and wnt8 RNAs; and (4) loss of snail2 activity leads to changes in the RNA levels of a number of BMP and Wnt agonists and antagonists. Taken together, these results identify Snail2 as a key regulator of the signals involved in mesodermal induction of neural crest.
“…Twist1 represents a critical modulator of mesenchymal cell fate during skeletal development, inducing differentiation toward both the chondrogenic and the osteogenic lineages, while inhibiting myogenesis (Miraoui & Marie, 2010). In Drosophila, twist homozygous mutations are associated to a lethal phenotype, due to disruption of gastrulation and failure in mesodermal-derived organ development and leading to complete eversion of head; the embryo was twisted in the egg, hence the name given to the gene www.intechopen.com (Simpson, 1983).…”
Section: Twistmentioning
confidence: 99%
“…Such findings, allowed to confirm TWIST1 as the candidate gene for the SaethreChotzen syndrome (MIM#101400, autosomal dominant), characterized by craniofacial and limb malformations and indicated a key role of TWIST in n the mesodermal development of the head and limbs (El Ghouzzi et al, 1997;Gripp et al, 2000; see following sections). Thereafter, Twist role in calvarial bone/suture patterning and development has been intensively investigated (Miraoui & Marie, 2010). In this context.…”
“…Twist-1 plays a crucial role during the development of the embryo. It is expressed during embryonic development, and it has been found to be involved in developmental processes such as myogenesis, neurogenesis, cardiogenesis, cranial tube morphogenesis and mesoderm formation (Miraoui and Marie, 2010). Twist-1 has also been found to be involved in the process of epithelial-to-mesenchymal transition, which plays an essential role in cancer metastasis (Yang et al, 2004).…”
Twist-1 is mostly expressed during development and has been previously shown to control myogenesis. Because its regulation in muscle has not been fully exploited, the aim of this project was to identify micro (mi)RNAs in muscle that regulate Twist-1. miR-206, one of the most important muscle-specific miRNAs (myomiRs), was identified as a possible regulator of Twist-1 mRNA. Luciferase assays and transfections in human foetal myoblasts showed that Twist-1 is a direct target of miR-206 and that through this pathway muscle cell differentiation is promoted. We next investigated whether MyoD, a major myogenic transcription factor, regulates Twist-1 because it is known that MyoD induces expression of the miR-206 gene. We found that forced MyoD expression induced miR-206 upregulation and Twist-1 downregulation through binding to the miR-206 promoter, followed by increased muscle cell differentiation. Finally, experiments were performed in muscle cells from subjects with congenital myotonic dystrophy type 1, in which myoblasts fail to differentiate into myotubes. MyoD overexpression inhibited Twist-1 through miR-206 induction, which was followed by an increase in muscle cell differentiation. These results reveal a previously unidentified mechanism of myogenesis that might also play an important role in muscle disease.
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