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XB-ART-48813
Development April 1, 2014; 141 (8): 1683-93.

Spalt-like 4 promotes posterior neural fates via repression of pou5f3 family members in Xenopus.

Young JJ , Kjolby RA , Kong NR , Monica SD , Harland RM .


Abstract
Amphibian neural development occurs as a two-step process: (1) induction specifies a neural fate in undifferentiated ectoderm; and (2) transformation induces posterior spinal cord and hindbrain. Signaling through the Fgf, retinoic acid (RA) and Wnt/β-catenin pathways is necessary and sufficient to induce posterior fates in the neural plate, yet a mechanistic understanding of the process is lacking. Here, we screened for factors enriched in posterior neural tissue and identify spalt-like 4 (sall4), which is induced by Fgf. Knockdown of Sall4 results in loss of spinal cord marker expression and increased expression of pou5f3.2 (oct25), pou5f3.3 (oct60) and pou5f3.1 (oct91) (collectively, pou5f3 genes), the closest Xenopus homologs of mammalian stem cell factor Pou5f1 (Oct4). Overexpression of the pou5f3 genes results in the loss of spinal cord identity and knockdown of pou5f3 function restores spinal cord marker expression in Sall4 morphants. Finally, knockdown of Sall4 blocks the posteriorizing effects of Fgf and RA signaling in the neurectoderm. These results suggest that Sall4, activated by posteriorizing signals, represses the pou5f3 genes to provide a permissive environment allowing for additional Wnt/Fgf/RA signals to posteriorize the neural plate.

PubMed ID: 24715458
PMC ID: PMC3978834
Article link: Development
Grant support: [+]
Genes referenced: acod1 acta4 actc1 alcam ccs cdx2 churc1 dkk1 eef1a1 efna4 egr2 eif3a en2 fgf8 foxi4.2 gbx2.1 gbx2.2 glul h3-3b hnrnph3 hnrnpk hoxb9 hoxc10 hoxd10 krt12.4 mafb meis3 mki67 mpzl2 myl2 myod1 nkx6-1 nol12 odc1 otx2 pax2 pip4k2a pou5f3.1 pou5f3.2 pou5f3.3 ppp1ca prickle1 sall1 sall4 sf3b4 smad4.1 smad4.2 snai2 sox2 srsf6 srsf7 tnpo2 tub tubb2b znf384
Morpholinos: pou5f3.1 MO2 pou5f3.2 MO3 pou5f3.3 MO3 sall4 MO1


Article Images: [+] show captions
References:
Archer, 2011, Pubmed, Xenbase [+]


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