High impact information on ptc1

• Morphological changes were accompanied by an expansion, followed by a reduction, in domains of shh expression and a rapid abolition of ptc1 expression [1].
• The expression domain of ptc1 is broader than that of shh and adjacent blastemal cells releasing the dermal bone matrix also express ptc1 [2].
• We find a striking correlation between the accumulation of patched1 transcripts and cells responding to sonic hedgehog activity both in the neurectoderm and mesoderm, suggesting that like its Drosophila counterpart, patched1 is regulated by sonic hedgehog activity [3].
• We find that at the sequence level Zf-ptc2 is more closely related than Zf-ptc1 to the ptc genes initially characterised in other vertebrate species [4].
• Triple uki/dre/lep mutants show neither an additive increase in PCNA expression nor enhanced embryonic phenotypes, suggesting that other negative regulators, possibly Ptc1, prevent further activation of the Hh signaling pathway [5].

Biological context of ptc1

• Although this suggested an involvement of Hh signaling in TCDD-mediated impairment of jaw growth, we did not observe downregulation of ptc1 and ptc2, receptors dependent on Hh signaling [6].

Other interactions of ptc1

• We have shown that RA exposure during the early stages of pectoral fin development first results in a rapid decrease or complete loss of shh/ptc1 expression [7].

References