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Discussion with Christelle, Jeanne and Stanislas
Wondering about the paper Park et al. cited in last entry, given there is no FGFR2 expressed in early cardiac mesoderm and it is in the NCC, how the mesodermal FGF10 has an effect on heart morphogenesis?
In light of two papers about FRS2a (floxed) crossed to Nkx2.5-Cre mice for instance, and the FGFR2iiib +/- c floxed crossed to Wnt1-Cre show that the FGFR2 signaling is not critical to the NCC invasion and appropriate formation of great arteries from outflow tract from within the neural crest cells, but rather from within the secondary heart field mesoderm.
However, we notice that we do not ourselves nor has anyone else shown what must be a dynamic and temporary expression of FGFR2 in the cardiac mesoderm. Need to discuss this with Margaret and/or Fanny. I am wondering if it is a rostral continuation of the strong expression seen by Orr-Urtreger et al in their figure 3 in the intermediate mesoderm (pronephros). What does that become more rostrally?
Tania, Jeanne and Stan were brainstorming with us. Are there deletions around FGFR2, someone wondered? (on 10q) no leading to craniostenoses.
I wrote “if lofunction -> fibros” which I no longer know what it means. Transfect the QT6 as below, I think I meant, to get locally secreting sink for FGFR2b. Oh, I remember – I was thinking could do Affymetrix expression chips to get changes before/after transfection in neural crest cells. Or something like that.
hCCN and fibros de caille (QT6) – FGFR2 iiib soluble get them to express.
What other targets besides ISL1 in the heart? (BMP2 very early in SHF - cf paper with Delphine Duprez)