. Author manuscript; available in PMC: 2007 Apr 10.

Published in final edited form as: Dev Biol. 2006 Apr 4;295(2):559–570. doi: 10.1016/j.ydbio.2006.03.044

Table 3.

Frequency of aortic arch defects at E18.5 after timed ablation of Fgf8 in the Tbx1 domain

Genotype	E7.5	E8.5	E9.5

	Abnormal/Total
Tbx1^mcm^/⁺; Fgf8⁺^/⁺		16/41 (39%)*,^
Tbx1^mcm^/⁺; Fgf8⁺^/−		29/37 (78%)*
Tbx1^mcm^/⁺; Fgf8^flox^/⁺	16/31 (52%)	10/31 (32%)	19/31 (63%)^
Tbx1^mcm^/⁺; Fgf8^flox^/−	21/26 (81%)	28/32 (88%)	33/37 (89%)

Comparison of Tbx1^mcm^/⁺; Fgf8⁺^/⁺ and Tbx1^mcm^/⁺; Fgf8⁺^/− reconfirmed that Tbx1 and Fgf8 interact in vivo as the frequency of defects increases significantly in Tbx1^mcm^/⁺; Fgf8⁺^/− embryos (*P = 0.006). Tbx1-driven deletion of one copy of Fgf8 in Tbx1^mcm^/⁺; Fgf8^flox^/⁺ embryos exposed to TM at E9.5 is sufficient to recapitulate the effect of germ-line ablation of Fgf8, since the frequency of defects in E9.5 induced Tbx1^mcm^/⁺; Fgf8^flox^/⁺ embryos is significantly greater that in Tbx1^mcm^/⁺; Fgf8⁺^/⁺ (^P = 0.04) and closely approached the frequency seen in Tbx1^mcm^/⁺; Fgf8⁺^/− (78% vs. 63%; P = 0.2).