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. Author manuscript; available in PMC: 2009 Nov 1.
Published in final edited form as: Dev Biol. 2008 Aug 29;323(1):6–18. doi: 10.1016/j.ydbio.2008.08.019

Fig. 6.

Fig. 6

Tsg is epistatic over Cv2: the loss of Tsg in Cv2−/− suppresses most of the Cv2 mutant skeletal phenotypes. Skeletal preparations of wild-type (A, E, I, M), Cv2−/− (B, F, J, N), Tsg−/− (C, G, K, O) and Cv2−/−;Tsg−/− (D, H, L, P) neonates stained with Alizarin Red and Alcian Blue. (A–D) The cervical neural arches (na) are reduced in Cv2−/− but are rescued in Cv2−/−;Tsg−/− double mutants. The tracheal rings (tr) are missing in Cv2−/− (red asterisk in B), but the tracheal (t) cartilage develops like wild-type (A) in Cv2−/−;Tsg−/− double mutants (D). (E–H). Cv2−/− lack the humerus deltoid tuberosity (dt), which is rescued in Cv2−/−;Tsg−/−. (I–L) The posterior homeotic transformation of T13 (black asterisks) in Cv2−/− (J) is rescued in Cv2−/−;Tsg−/− (L); however the ossification centers (oc) remain defective. (M–P) Side views of the lumbar region. Neural arches (na) are reduced in Cv2−/− (N) but are only mildly affected in Cv2−/−;Tsg−/− (P), as is the case in Tsg−/− mutants (O).

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