NDLI: Differential organ phenotypes after postnatal Igf1r gene conditional deletion induced by tamoxifen in UBC-CreERT2; Igf1r $^{ fl/fl }$ double transgenic mice

Content Provider	Springer Nature Link
Author	López, Icíar Paula Rodriguez de la Rosa, Lourdes Pais, Rosete Sofia Piñeiro Hermida, Sergio Torrens, Raquel Contreras, Julio Varela Nieto, Isabel Pichel, José García
Copyright Year	2014
Abstract	Insulin-like growth factor type 1 receptor (IGF1R) is a ubiquitously expressed tyrosine kinase that regulates cell proliferation, differentiation and survival. It controls body growth and organ homeostasis, but with specific functions depending on developmental time and cell type. Human deficiency in IGF1R is involved in growth failure, microcephaly, mental retardation and deafness, and its overactivation is implicated in oncogenesis. Igf1r-deficient mice die at birth due to growth retardation and respiratory failure. Although multiple Igf1r tissue-specific mutant lines have been analyzed postnatally, using Igf1r-floxed (Igf1r $^{ fl/fl }$) mice mated with diverse cell-type recombinase Cre-expressing transgenics, no mouse models for the study of generalized Igf1r deficiency in adults have been reported. To this end we generated UBC-CreERT2; Igf1r $^{ fl/fl }$ transgenic mice with an inducible deletion of Igf1r activated by tamoxifen. Tamoxifen administration to 4 week-old prepuberal male mice delayed their growth, producing a distinct impact on organ size 4 weeks later. Whereas testes were smaller, spleen and heart showed an increased organ to body weight ratio. Mosaic Igf1r genomic deletions caused a significant reduction in Igf1r mRNA in all organs analyzed, resulting in diverse phenotypes. While kidneys, spleen and cochlea had unaltered gross morphology, testes revealed halted spermatogenesis, and liver and alveolar lung parenchyma showed increased cell proliferation rates without affecting apoptosis. We demonstrate that UBC-CreERT2 transgenic mice efficiently delete Igf1r upon postnatal tamoxifen treatment in multiple mouse organs, and corroborate that IGF1R function is highly dependent on cell, tissue and organ type.
Starting Page	279
Ending Page	294
Page Count	16
File Format	PDF
ISSN	09628819
Journal	Transgenic Research
Volume Number	24
Issue Number	2
e-ISSN	15739368
Language	English
Publisher	Springer International Publishing
Publisher Date	2014-09-20
Publisher Place	Cham
Access Restriction	One Nation One Subscription (ONOS)
Subject Keyword	IGF1R Transgenic mouse Cre/lox system UBC-CreERT2 mice Cochlea Lung Molecular Medicine Plant Genetics & Genomics Animal Genetics and Genomics Plant Sciences Transgenics
Content Type	Text
Resource Type	Article
Subject	Genetics Animal Science and Zoology Biotechnology Agronomy and Crop Science

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