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Dev Biol 2010 Feb 01;3381:50-62. doi: 10.1016/j.ydbio.2009.11.024.
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Xenopus Meis3 protein lies at a nexus downstream to Zic1 and Pax3 proteins, regulating multiple cell-fates during early nervous system development.

Gutkovich YE , Ofir R , Elkouby YM , Dibner C , Gefen A , Elias S , Frank D .

In Xenopus embryos, XMeis3 protein activity is required for normal hindbrain formation. Our results show that XMeis3 protein knock down also causes a loss of primary neuron and neural crest cell lineages, without altering expression of Zic, Sox or Pax3 genes. Knock down or inhibition of the Pax3, Zic1 or Zic5 protein activities extinguishes embryonic expression of the XMeis3 gene, as well as triggering the loss of hindbrain, neural crest and primary neuron cell fates. Ectopic XMeis3 expression can rescue the Zic knock down phenotype. HoxD1 is an XMeis3 direct-target gene, and ectopic HoxD1 expression rescues cell fate losses in either XMeis3 or Zic protein knock down embryos. FGF3 and FGF8 are direct target genes of XMeis3 protein and their expression is lost in XMeis3 morphant embryos. In the genetic cascade controlling embryonic neural cell specification, XMeis3 lies below general-neuralizing, but upstream of FGF and regional-specific genes. Thus, XMeis3 protein is positioned at a key regulatory point, simultaneously regulating multiple neural cell fates during early vertebrate nervous system development.

PubMed ID: 19944089
Article link: Dev Biol

Species referenced: Xenopus laevis
Genes referenced: egr2 fgf3 fgf8 foxd1 foxd3 hesx1 hoxb3 hoxd1 id3 isl1 meis3 myc myt1 nes neurod1 neurog2 nrp1 pax3 snai2 sox15 sox2 tub tubb2b zic1 zic2 zic5
Morpholinos: meis3 MO1 pax3 MO1 zic1 MO1

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