Figure 2.

Activation of Tbx1-GFP by Foxg1-Cre and Pax2-Cre. (A)Foxg1-Cre;Tbx1-GFPflox/+ mutants have thymic aplasia and nasal malformations at E15.5, and eye and pharyngeal defects at E11.5. (B)Pax2-Cre;Tbx1-GFPflox/+ mutants die shortly after birth. They have microcephaly and ocular defects. Thymus (T), heart (H), lungs (L), forebrain (FB). (C) Paintfilling of inner ears in Pax2-Cre;Tbx1-GFPflox/+ and Foxg1-Cre;Tbx1-GFPflox/+ mutants. The endolymphatic duct (ED) and common crus (CC) are enlarged. The lateral semicircular canal (LC), utricle (U), and saccule (S) are missing. The cochlea (C) is shortened to varying degrees. BAC316.23 mice show similarities in inner ear morphological defects. Anterior canal (AC), posterior canal (PC). (D) Wholemount RNA in situ hybridization at E9.5 for NeuroD, expressed in neuroblasts of the cranial ganglia. Wholemount immunohistochemistry stains cranial sensory ganglia with anti-Neurofilament (NF) at E10.5. Red brackets indicate olfactory placode. Otic vesicle is circled in yellow.

Freyer et al. BMC Developmental Biology 2013 13:33   doi:10.1186/1471-213X-13-33
Download authors' original image