Etchevers:Cardiac morphogenesis/2008/10/09
Cardiac morphogenesis | Main project page Previous entry Next entry |
SetbacksChristelle was not able to complete the luciferase induction experiments because the tissue culture facility at Necker has been infected by molds and yeast. One of the hoods apparently had not been cleaned as it should and was contaminating everything. She has thawed out some new HeLa cells. I wished for Candice to learn how to electroporate and perhaps process the eggs, if she has the time - and it seems she may. But we need to do some re-thinking about what to demonstrate with the dominant negative construction that Christelle has made. Christelle sent me this article Yes, it does. Thinking about this.
From same article (remember, they have deleted Fgf8 from the Isl1-expressing OFT mesoderm): "Neural crest cells modulate FGF8 signaling in the pharynx and influence not only the addition of myocardium to the OFT from the
SHF (Hutson et al., 2006), but also the contractile and secretory function of the myocardium itself, including its ability to produce
cardiac jelly (Stottmann et al., 2004; Waldo et al., 1999). Thus, in affected Fgf8, FGFR and Spry2 gain-of-function mutants, initial
myocardial dysfunction and subsequent abnormal CNC behavior might interact in a cycle that progressively impairs OFT morphogenesis." I don't see how that can be true with respect to Fgfr2 at least, given their own results? It should interrupt the cycle effectively.
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