|Presenting Author(s)||Megan Davey|
|Abstract Title||Patterning and vascularisation of the talpid3 chick limb.|
|Full author List||M. G. Davey, I. R Paton, D. R. Morrice, D. W. Burt, C. Tickle|
|Text of abstract||
Talpid3 is a novel chick mutation which affects Hedgehog signalling causing polydactyly, cyclopia, widespread haemorrhaging and oedema. A comparison between patterning of the limb and of the neural tube indicates that Gli-repressor activity is still present in talpid3 embryos but that Gli-activator function is severely inhibited. A consequence of the loss of GliA function is loss of high level Ptc expression, which, in the limb, leads to unrestrained spread of Shh protein thoughout thus inducing polydactyly. Ectopic Shh signalling in the limb also results in widespread expression of genes involved in vascularisation including members of the Bmp and VEGF family. These alterations in angiogenic gene expression explain why the talpid3 limb is hypervascularised. There is also abnormal junction formation between endothelial cells and changes in extracellular matrix around developing blood vessels.
Furthermore Np1 and Np2, genes associated with arteriovenous identity, are abnormally expressed suggesting that Shh signalling can specify endothelial identity in the limb. We further explored the role of Hedgehog signalling in limb vascularisation and found that that addition of Shh to normal limb buds results in dynamic local blood vessel remodelling which correlates with induced local Ang2 expression. This indicates that Hedgehogs play a central role in regulation of vascular growth during embryonic development.
|Which session is your work most relevant to:||Limb patterning or Vascularisation & innervation|
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