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Characterize Disease-related Mutants of RAF Family Kinases by Using a Set of Practical and Feasible Methods
Published on: July 17, 2019
Characterization of mice deficient in the Src family nonreceptor tyrosine kinase Frk/rak
Subhashini Chandrasekharan1, Ting Hu Qiu, Nawal Alkharouf
1Curriculum in Genetics and Molecular Biology, University of North Carolina at Chapel Hill, Chapel Hill, NC 27599, USA.
Abstract:
Frk/rak belongs to a novel family of Src kinases with epithelial tissue-specific expression. Although developmental expression patterns and functional overexpression in vitro have associated these kinases with growth suppression and differentiation, their physiological functions remain largely unknown. We therefore generated mice carrying a null mutation in iyk, the mouse homolog of Frk/rak. We report here that frk/rak(-/-) mice are viable, show similar growth rates to wild-type animals, and are fertile. Furthermore, a 2-year study of health and survival did not identify differences in the incidence and spectrum of spontaneous tumors or provide evidence of hyperplasias in frk/rak(-/-) epithelial tissues. Histological analysis of organs failed to reveal any morphological changes in epithelial tissues that normally express high levels of Frk/rak. Ultrastructural analysis of intestinal enterocytes did not identify defects in brush border morphology or structural polarization, demonstrating that Frk/rak is dispensable for intestinal cytodifferentiation. Additionally, frk/rak-null mice do not display altered sensitivity to intestinal damage induced by ionizing radiation. cDNA microarray analysis revealed an increase in c-src expression and identified subtle changes in the expression of genes regulated by thyroid hormones. Significant decreases in the circulating levels of T3 but not T4 hormone are consistent with this observation and reminiscent of euthyroid sick syndrome, a stress-associated clinical condition.
Insights
The Frk/rak kinase, despite its epithelial specificity, is not essential for mouse growth, differentiation, or tumor suppression. Frk/rak-null mice exhibit normal health and development, indicating dispensability for these physiological processes.
Area of Science:
- Molecular Biology
- Cell Biology
- Genetics
Background:
- Frk/rak is a novel Src kinase family member with epithelial tissue-specific expression.
- In vitro studies suggest roles in growth suppression and differentiation, but physiological functions are unknown.
Purpose of the Study:
- To investigate the physiological roles of Frk/rak by generating and analyzing knockout mice.
- To determine the necessity of Frk/rak in epithelial tissue development, homeostasis, and response to stress.
Main Methods:
- Generation of frk/rak-null mice.
- Long-term health and survival studies (2 years).
- Histological and ultrastructural analyses of epithelial tissues.
- cDNA microarray analysis and hormone level measurements.
Main Results:
- Frk/rak-null mice are viable, fertile, and exhibit normal growth rates without spontaneous tumors or hyperplasias.
- No morphological defects were observed in epithelial tissues, including intestinal enterocytes.
- No altered sensitivity to radiation-induced intestinal damage was detected.
- Microarray analysis revealed increased c-src expression and altered thyroid hormone-regulated gene expression, with decreased T3 levels.
Conclusions:
- Frk/rak is dispensable for normal epithelial tissue development, differentiation, and overall health in mice.
- The kinase is not required for intestinal cytodifferentiation or radiation resistance.
- Loss of Frk/rak leads to subtle metabolic changes, including decreased T3 levels, resembling euthyroid sick syndrome.
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