Skip to main content
. Author manuscript; available in PMC: 2015 Jul 20.
Published in final edited form as: Development. 2012 Jan 4;139(4):731–739. doi: 10.1242/dev.075408

Fig. 5. Delay in the induction of Hoxa13 inactivation is sufficient to ensure proper development of the labyrinth and survival of the embryo.

Fig. 5

(A–C) CD31 immunostaining on placenta cryosections at E14.5. Hoxa13Cre/HoxAflox labyrinthine vasculature (B) is comparable to that of wild type (A) and Hoxa13Cre/Hoxa13Cre mutant (C). (D,E) Forelimbs (D) and hindlimbs (E) of control (left, HoxAflox/+) and mutant (right, Hoxa13Cre/HoxAflox) mice at 6 months of age. Mutant limbs show a fully penetrant phenotype associated with the loss of Hoxa13, such as lack of digit 1 (asterisk), shortening and malformation of the other digits in the forelimb (white arrow) and fusion of digits 2, 3 and 4 in the hindlimb (black arrows). Scale bars: 200 μm.

HHS Vulnerability Disclosure