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In addition, mutant embryos display a swollen pericardium and lack fin buds.
50 58% of Ppt1 mutant embryos display abnormal FasII-positive longitudinal connectives ranging from mild to severe (Table 3).
These γCOP mutant embryos display defects in the formation of the embryonic cuticle; denticles are barely made.
Indeed it has been reported that y10 (the zebra fish homologue of PLCγ1) mutant embryos display specific defect in the formation of arteries, but not veins [23].
Results indicate that Ppt1 mutant embryos display abnormal complement of EVE+ GMCs and their progeny in many hemisegments, as early as stage 11/12 of embryogenesis.
At earlier developmental stages, Hes1 mutant embryos display defects in second heart field proliferation, a reduction in cardiac neural crest cells and failure to completely extend the outflow tract.
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Upon administration of TM at E9.5, E10.5 or E11.5, mutant embryos displayed omphalocele and polydactyly phenotypes (Fig. 5B,B',D,D'; data not shown).
21/127 Hes1−/− embryos were recovered (expected 32/127; p>0.05)) and 8/21 (38%) mutant embryos displayed an externally visible dextraposed ascending aorta; this phenotype was not observed in Hes1+/− or Hes1+/+ embryos (Fig. 5A).
Moreover, the most severe class of Tbx3-null mutant embryos displays heart defects that are similar to zebrafish tbx3b morphants with respect to morphology and the degree of development, indicating that the mechanisms of AVC formation are conserved among vertebrates.
Additionally, staufenHL mutant embryos displayed a decrease in robust development [34], which could be due to another double-stranded RNA binding function of Staufen apart from bicoid or oskar.
We therefore wanted to determine whether the OCRL1 mutant embryos displayed elevated levels of PtdIns(4,5) P2.
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