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. 2001 Sep 15;15(18):2433–2444. doi: 10.1101/gad.205001

Figure 5.

Figure 5

The Hoxb7–Ret51 transgene fails to rescue kidney development in Ret.k−/Ret.k− mice, or to induce dominant hypodysplasia in wild-type mice, unlike the Hoxb7–Ret9 transgene (Srinivas et al. 1999). (A) Northern blot of 5 μg of poly(A)+ RNA from adult brain and kidney of wild-type and Hoxb7–Ret51 Tg mice, hybridized with a c-Ret probe. The major endogenous c-Ret transcripts are indicated at left. The transgene encodes a major 4.3-kb mRNA, and several larger bands of unknown origin. (WT) Wild-type control. RET51-20, RET51-23, and RET51-43 are three different Tg lines. Brain RNA (B) expresses endogenous c-Ret mRNA in wild-type and Tg mice, whereas kidney (K) does not express detectable c-Ret mRNA in wild-type adult, but expresses the Tg mRNA. (B,C) Kidney sizes in newborn mice (a value of zero indicates no kidney). (B) Although the Hoxb7–Ret9 transgene increased kidney size in Ret.k−/Ret.k− mice, occasionally into the normal range, the Hoxb7–Ret51 transgene had only a small beneficial effect. (C) On a wild-type background, although the Hoxb7–Ret9 transgene caused renal hypodysplasia in ∼50% of Tg mice, Hoxb7–Ret51 had no significant effect. Data for Ret.k− homozygotes (ret−/−) and Hoxb7–Ret9 Tg mice are from Srinivas et al. (1999). ret−/−, n = 38; +/+, n = 138; Ret9 Tg, ret−/−, n = 92; Ret51 Tg, ret−/−, n = 32; Ret9 Tg, n = 76; Ret51 Tg, n = 128. Data were pooled for three Hoxb7–Ret51 and three Hoxb7–Ret9 Tg lines.