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Fig. 2 | Molecular Medicine

Fig. 2

From: Expression of Human GLI in Mice Results in Failure to Thrive, Early Death, and Patchy Hirschsprung-like Gastrointestinal Dilatation

Fig. 2

Failure to thrive and premature death in homozygous GLI transgenic mice

(A) Four-week old mice, from right to left: normal wild-type CD-1 mouse, homozygous noninduced transgenic mouse, three Zn++-induced homozygous transgenic mice. (B) Growth curves of male (top) and female (bottom) mice illustrate failure to thrive in a subset of Zn++-induced homozygous transgenic animals. Growth of small animals remains parallel to the growth of unaffected animals. Points represent mean values. : wild-type Zn++-noninduced, n = 17 females, 24 males; : wild-type Zn++-induced, n = 12 females, 9 males; : heterozygous Zn++-noninduced, n = 16 females, 6 males; : heterozygous Zn++-induced, n = 11 females, 11 males; □: homozygous Zn++-noninduced, n = 7 females, 7 males; ■: homozygous small-sized animals Zn++-induced, n = 14 females, 5 males; : homozygous normal sized animals Zn++-induced, n = 9 females, 13 males. There is no significant difference between wild type Zn++-induced and the other groups except homozygous GLI transgenic small-sized animals Zn++-induced. P < .05 for both male and female (t-test). (C) Failure to thrive was defined as weight smaller than 2 SD below wild-type weight. The phenotype was more prevalent in females than in males. P < .03 (Fisher’s. exact test). (D) Cumulative premature death in homozygous GLI transgenic mice. Zn++ (+): homozygous transgenic mice fed 25 mM ZnSO4 in drinking water since conception; Zn++ (−): homozygous transgenic mice without supplemental zinc; control group: wild-type animals with Zn++-induction. The y-axis is cumulative mortality in percentage.

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