Developmental Signals - Tbx

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Introduction

Mouse forelimb Tbx5 expression.[1]
Mouse hindlimb Tbx4 expression.[1]

Genes in the TBX gene family provide instructions for making proteins called T-box proteins that play critical roles during embryonic development. These proteins are especially important for normal development of the arms, hands, and heart. T-box proteins regulate the activity of other genes by attaching (binding) to specific regions of DNA. On the basis of this action, T-box proteins are called transcription factors. Genes in the T-box family are grouped together because the proteins produced from these genes share a similar segment called a T box. The T box is the part of the protein that binds to DNA. T-box proteins often interact with one another or with other transcription factors that regulate gene activity.


Researchers have identified at least 17 genes in the T-box gene family. Mutations in these genes lead to disorders that involve the abnormal development of tissues in which a particular T-box gene is active (expressed). Many genetic disorders caused by T-box gene mutations are characterized by heart problems and/or skeletal abnormalities of the hands and arms.


(text from Genetics Home Reference http://ghr.nlm.nih.gov/geneFamily/tbx)


Factor Links: AMH | hCG | BMP | sonic hedgehog | bHLH | HOX | FGF | FOX | Hippo | LIM | Nanog | NGF | Nodal | Notch | PAX | retinoic acid | SIX | Slit2/Robo1 | SOX | TBX | TGF-beta | VEGF | WNT | Category:Molecular

| Category:Tbx

Some Recent Findings

  • Tbx15 controls skeletal muscle fibre-type determination and muscle metabolism[2] "Skeletal muscle is composed of both slow-twitch oxidative myofibers and fast-twitch glycolytic myofibers that differentially impact muscle metabolism, function and eventually whole-body physiology. Here we show that the mesodermal transcription factor T-box 15 (Tbx15) is highly and specifically expressed in glycolytic myofibers. Ablation of Tbx15 in vivo leads to a decrease in muscle size due to a decrease in the number of glycolytic fibres, associated with a small increase in the number of oxidative fibres. This shift in fibre composition results in muscles with slower myofiber contraction and relaxation, and also decreases whole-body oxygen consumption, reduces spontaneous activity, increases adiposity and glucose intolerance. Mechanistically, ablation of Tbx15 leads to activation of AMPK signalling and a decrease in Igf2 expression. Thus, Tbx15 is one of a limited number of transcription factors to be identified with a critical role in regulating glycolytic fibre identity and muscle metabolism." Muscle Development
  • Tbx1 controls the morphogenesis of pharyngeal pouch epithelia through mesodermal Wnt11r and Fgf8a[3] "The pharyngeal pouches are a segmental series of epithelial structures that organize the embryonic vertebrate face. In mice and zebrafish that carry mutations in homologs of the DiGeorge syndrome gene TBX1, a lack of pouches correlates with severe craniofacial defects, yet how Tbx1 controls pouch development remains unclear. Using mutant and transgenic rescue experiments in zebrafish, we show that Tbx1 functions in the mesoderm to promote the morphogenesis of pouch-forming endoderm through wnt11r and fgf8a expression. Consistently, compound losses of wnt11r and fgf8a phenocopy tbx1 mutant pouch defects, and mesoderm-specific restoration of Wnt11r and Fgf8a rescues tbx1 mutant pouches. Time-lapse imaging further reveals that Fgf8a acts as a Wnt11r-dependent guidance cue for migrating pouch cells. We therefore propose a two-step model in which Tbx1 coordinates the Wnt-dependent epithelial destabilization of pouch-forming cells with their collective migration towards Fgf8a-expressing mesodermal guideposts."
  • Tbx1 regulates oral epithelial adhesion and palatal development[4] "Cleft palate, the most frequent congenital craniofacial birth defect, is a multifactorial condition induced by the interaction of genetic and environmental factors. In addition to complete cleft palate, a large number of human cases involve soft palate cleft and submucosal cleft palate. ...These findings suggest that Tbx1 regulates the balance between proliferation and differentiation of keratinocytes and is essential for palatal fusion and oral mucosal differentiation. The impaired adhesion separation of the oral epithelium together with compromised palatal mesenchymal growth is an underlying cause for various forms of cleft palate phenotypes in Tbx1(-/-) mice. Our present study reveals new pathogenesis of incomplete and submucous cleft palate during mammalian palatogenesis."
More recent papers
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<pubmed limit=5>Tbx Embryology</pubmed>

Limb Development

Mouse- forelimb-bud-Tbx3-Tbx2.jpg

Mouse forelimb bud Tbx3 and Tbx2 expression[5]

Chicken limb gene expression 02.jpg

Chicken stage 21 wing bud[6]

Hindlimb Tbx2 model

Hindlimb Tbx2 model[7]


Links: Limb Development

Respiratory Development

Mouse respiratory Tbx4 and Tbx5.jpg Mouse respiratory Tbx4 and Tbx5 model[8]
  • A - Lung and trachea specification begins at E9.0 in the ventral foregut and at this time Tbx5 expression (light purple) is adjacent to the presumptive endoderm. Later, Tbx4 and Tbx5 expression (dark purple) is in mesenchyme associated with the lung and trachea. Tbx5 but not Tbx4 is important for specification of bilateral lung buds and the trachea.
  • B - Magnification of box shown in (A) representing the events in the growing tip during branching morphogenesis. Grey denotes epithelium and purple denotes mesenchyme. Tbx4 and Tbx5 interact with each other and act upstream of the Fgf10 signaling pathway. Decrease in Tbx4 and Tbx5 affects mesenchymal Fgf10 expression and expression of its targets in the epithelium – Bmp4, Spry2 and Etv5 – but not the expression of the epithelial Fgf10 receptor Fgfr2. In addition to Fgf10 expression in the mesenchyme, Tbx4 and Tbx5 also control the expression of an unknown factor(s) (X) that is essential for activation of the Fgf10 signaling pathway. Furthermore, Tbx4 and Tbx5 act upstream of Wnt2 in the mesenchyme.
  • C - In the trachea and the main stem bronchi Tbx4 and Tbx5 either control Sox9 expression, which in turn regulates cartilage condensation, or Tbx4 and Tbx5 regulate another factor (X) essential for chondrogenesis secondarily affecting Sox9 expression.

(Text from figure legend)

Links: Respiratory System Development

Heart Development

Cardiac conduction system[9] "Here, we assessed the genome-wide occupation of conduction system-regulating transcription factors TBX3, NKX2-5, and GATA4 and of enhancer-associated coactivator p300 in the mouse heart, uncovering cardiac enhancers throughout the genome. Many of the enhancers colocalized with ion channel genes repressed by TBX3, including the clustered sodium channel genes Scn5a, essential for cardiac function, and Scn10a. We identified 2 enhancers in the Scn5a/Scn10a locus, which were regulated by TBX3 and its family member and activator, TBX5, and are functionally conserved in humans. We also provided evidence that a SNP in the SCN10A enhancer associated with alterations in cardiac conduction patterns in humans disrupts TBX3/TBX5 binding and reduces the cardiac activity of the enhancer in vivo."

References

  1. 1.0 1.1 <pubmed>22174793</pubmed>| PMC3235105 | PLoS One.
  2. <pubmed>26299309</pubmed>
  3. <pubmed>25142463</pubmed>| Development
  4. <pubmed>22371266</pubmed>
  5. <pubmed>20386744</pubmed>| PLoS Genet.
  6. <pubmed>21526123</pubmed>| PLoS One.
  7. 23633963</pubmed>| PLoS Genet.
  8. <pubmed>22876201</pubmed>| PLoS Genet.
  9. <pubmed>22706305</pubmed>

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Reviews

<pubmed>17506689</pubmed> <pubmed>10197584</pubmed>

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Cite this page: Hill, M.A. (2024, March 28) Embryology Developmental Signals - Tbx. Retrieved from https://embryology.med.unsw.edu.au/embryology/index.php/Developmental_Signals_-_Tbx

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