A novel insulin-like growth factor 2 mutation in mice increases body and tissue weights

Karuhn, Meagan A; Boler, Dustin; Beever, Jonathan

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https://hdl.handle.net/2142/99967 Copy

Description

Title

A novel insulin-like growth factor 2 mutation in mice increases body and tissue weights

Author(s)

• Karuhn, Meagan A
• Boler, Dustin
• Beever, Jonathan

Contributor(s)

Dilger, Anna C.

Issue Date

2018-04

Keyword(s)

• Animal Sciences
• IGF2
• Insulin-like growth factor 2

Abstract

This objective was to characterize effects of a novel mutation in mice on muscle and organ weights. Insulin-like growth factor 2 (IGF2), is a major regulator of growth. A mutation in the pig IGF2 gene (g.G3072A) disrupts the binding site of a transcriptional repressor of IGF2, subsequently increasing postnatal IGF2 expression. This results in increased muscle growth and reduced fat deposition. To further investigate the role of this mutation in animal development, mice with a homologous mutation were created by gene-editing. Eight male mice with or without the mutation were weaned at 21 days of age and group-housed with free access to food and water until 77 (±2d) of age. Mice were weighed, euthanized, and then dissected to collect heart, liver, inguinal fat, epididymal fat and individual muscle weights. Our hypothesis was that mice with the IGF2 mutation would display increased muscle mass but similar overall body weights, comparable to the phenotype of pigs. However, in the mice, body weight was increased (P<0.01) in mutant IGF2 mice compared with wild type mice. Tibialis anterior muscle weight was also increased (P=0.03) and liver weight tended to be increased (P=0.06) in mutant compared with wild type mice. When expressed as a percentage of body weight, organ, muscle, and fat pad weights were also not different (P>0.23) between genotypes. These data suggest that, in contrast to the phenotype of IGF2 mutant pigs, IGF2 mutant mice experience an overall increase in growth. This increase is not restricted to muscle growth.

Type of Resource

image

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http://hdl.handle.net/2142/99967

Copyright and License Information

• Copyright 2018 Meagan A. Karuhn
• Copyright 2018 Dustin Boler
• Copyright 2018 Jonathan Beever

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