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. Author manuscript; available in PMC: 2010 Mar 1.
Published in final edited form as: Nat Med. 2009 Aug 23;15(9):1062–1065. doi: 10.1038/nm.2020

Fig. 2. Kif3a suppresses Gli2ΔN-driven medulloblastoma formation.

Fig. 2

(a–c) Hematoxylin and eosin (H&E) stained sagittal sections of control and mutant cerebella at P23. (a) hGFAP::Cre; CLEG2fl/+ mice have ectopic clusters of cells (arrows) without tumor formation. (b) All hGFAP::Cre; CLEG2fl/+; Kif3afl/fl mice develop medulloblastomas between P11 and P30. A green dotted line in b demarcates domains of the tumors containing type 1 and type 2 tumor cells (see text). (c) High magnification of red box in b, showing the two domains with different cell types. (d) Western blot analysis of Gli3 proteins isolated from P23 cerebella shows the decrease of Gli3 repressor (Gli3R) in hGFAP::Cre; CLEG2fl/+; Kif3afl/fl mice compared with wild-type and hGFAP::Cre; CLEG2fl/+ mice. Asterisk indicates a nonspecific band, which serves as a loading control. This banding pattern is similar to a previous report, which showed that this Gli3 antibody detects specific Gli3 bands that are absent in Gli3 mutants and non-specific bands38. (e,f) BrdU-labeling (1h survival) reveals that the ectopic clusters in hGFAP::Cre; CLEG2fl/+ mice are not proliferating (arrows), while tumors in hGFAP::Cre; CLEG2fl/+; Kif3afl/fl mice contained many proliferating cells. (g) hGFAP::Cre; CLEG2fl/+; Kif3afl/fl mice (P < 0.001) and hGFAP::Cre; CLEG2fl/+; Gli3Xt/+ mice (P < 0.02) die significantly earlier than hGFAP::Cre; CLEG2fl/+ mice. (h) Hh-responsive genes are up-regulated in both SmoM2- and Gli2ΔN-driven tumors (see text). *: P < 0.05. Scale bar = 0.5 mm (a,b,e,f), 10 µm (c).