Dwarfism and Impaired Gut Development in Insulin-Like Growth Factor II mRNA-Binding Protein 1-Deficient Mice

Thomas V. O. Hansen; Niels A. Hammer; Jacob Nielsen; Mette Madsen; Charlotte Dalbaeck; Ulla M. Wewer; Jan Christiansen; Finn C. Nielsen

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Dwarfism and Impaired Gut Development in Insulin-Like Growth Factor II mRNA-Binding Protein 1-Deficient Mice

机译：侏儒症和胰岛素样生长因子II mRNA结合蛋白1缺陷小鼠肠道的受损。

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Insulin-like growth factor II mRNA-binding protein 1 (IMP1) belongs to a family of RNA-binding proteins implicated in mRNA localization, turnover, and translational control. Mouse IMP1 is expressed during early development, and an increase in expression occurs around embryonic day 12.5 (E12.5). To characterize the physiological role of IMP1, we generated IMP1-deficient mice carrying a gene trap insertion in the Imp1 gene. Imp1?/? mice were on average 40% smaller than wild-type and heterozygous sex-matched littermates. Growth retardation was apparent from E17.5 and remained permanent into adult life. Moreover, Imp1?/? mice exhibited high perinatal mortality, and only 50% were alive 3 days after birth. In contrast to most other organs, intestinal epithelial cells continue to express IMP1 postnatally, and Imp1?/? mice exhibited impaired development of the intestine, with small and misshapen villi and twisted colon crypts. Analysis of target mRNAs and global expression profiling at E12.5 indicated that Igf2 translation was downregulated, whereas the postnatal intestine showed reduced expression of transcripts encoding extracellular matrix components, such as galectin- 1, lumican, tenascin-C, procollagen transcripts, and the Hsp47 procollagen chaperone. Taken together, the results demonstrate that IMP1 is essential for normal growth and development. Moreover, IMP1 may facilitate intestinal morphogenesis via regulation of extracellular matrix formation.

机译：胰岛素样生长因子II mRNA结合蛋白1（IMP1）属于RNA结合蛋白家族，与mRNA定位，更新和翻译控制有关。小鼠IMP1在早期发育中表达，在胚胎第12.5天（E12.5）左右表达增加。为了表征IMP1的生理作用，我们生成了在 Imp1 基因中带有基因陷阱插入的IMP1缺陷小鼠。 Imp1 ？/？小鼠平均比野生型和杂合性别匹配同窝幼崽小40％。从E17.5开始，生长迟缓很明显，并一直持续到成年生活。此外， Imp1 ？/？小鼠表现出较高的围产期死亡率，出生后3天仅存活50％。与大多数其他器官相比，肠上皮细胞在出生后仍继续表达IMP1，而 Imp1 ？/？小鼠的肠发育受损，绒毛小而畸形且扭曲结肠隐窝。对目标mRNA的分析和E12.5处的整体表达谱分析表明， Igf2 翻译被下调，而产后肠道显示出编码细胞外基质成分（例如半乳凝素-1，卢米肯，腱生蛋白- C，原胶原蛋白转录物和 Hsp47 原胶原蛋白伴侣。两者合计，结果表明IMP1对于正常的生长发育至关重要。此外，IMP1可能通过调节细胞外基质的形成促进肠道形态发生。 展开▼

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《Molecular and Cellular Biology》 |2004年第10期|共17页

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Thomas V. O. Hansen; Niels A. Hammer; Jacob Nielsen; Mette Madsen; Charlotte Dalbaeck; Ulla M. Wewer; Jan Christiansen; Finn C. Nielsen;
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中图分类细胞生物学;

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2. RNA-binding Protein Insulin-like Growth Factor mRNA-binding Protein 3 (IMP-3) Promotes Cell Survival via Insulin-like Growth Factor II Signaling after Ionizing Radiation [J] . Baisong Liao, Yan Hu, Gary Brewer The Journal of biological chemistry . 2011,第36期

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6. Dwarfism and Impaired Gut Development in Insulin-Like Growth Factor II mRNA-Binding Protein 1-Deficient Mice [O] . Thomas V. O. Hansen, Niels A. Hammer, Jacob Nielsen, 2004

机译：侏儒症和胰岛素样生长因子II mRNA结合蛋白1缺陷小鼠肠道的受损。

7. Dwarfism and Impaired Gut Development in Insulin-Like Growth Factor II mRNA-Binding Protein 1-Deficient Mice [O] . Hansen, Thomas V. O., Hammer, Niels A., Nielsen, Jacob, 2004

机译：侏儒症和胰岛素样生长因子II mRNA结合蛋白1缺陷小鼠肠道的受损。

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Dwarfism and Impaired Gut Development in Insulin-Like Growth Factor II mRNA-Binding Protein 1-Deficient Mice

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