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. 2004 May;24(10):4448–4464. doi: 10.1128/MCB.24.10.4448-4464.2004

FIG. 4.

FIG. 4.

Pre- and postnatal growth retardation of IMP1-deficient mice. (A) Photographs of wild-type and Imp1−/− littermates at 3 and 12 days of age. (B) Embryonal growth. Mean body weight ± standard error of the mean of wild-type, Imp1+/−, and Imp1−/− embryos from E12.5, E14.5, E17.5, and P0 mice. Growth was significantly (P < 0.05) reduced in Imp1−/− E17.5 embryos and P0 mice. (C) Postnatal growth. Wild-type, Imp1+/−, and Imp1−/− male and female mice were weighed over a period of 6 weeks. Results are plotted as the mean body weight ± standard error of the mean. Growth was significantly (P < 0.05) reduced in Imp1−/− postnatal and adult mice. (D) Organs were proportionally reduced in size. Mean organ weights ± standard error of the mean for Imp1+/− (open columns) and Imp1−/− (solid columns) mice at 2 to 3 weeks of age (except placenta, which was from E17.5 embryos) are plotted as a percentage of the weights for the organs and placentas from wild-type mice. The size of all Imp1−/− organs was significantly (P < 0.05) reduced. (E) Macroscopic appearance of selected organs from IMP1-deficient mice. Hypoplasia was observed in various organs, including brain (a), small intestine (b), kidney (c), and spleen (d).