Abstract
Aims
Mutations in the FERM domain containing 7 (FRMD7) genes are known to cause a significant number of cases of congenital idiopathic nystagmus (CIN). Only limited expression data exist suggesting low levels of expression in all tissues. In this study, we assess the expression profile of the murine homologue of FRMD7(Frmd7) in tissue from three murine organs during development.
Methods
cDNA was extracted from heart, lung, and brain tissues of MF-1 mice at 12 developmental time points, embryonic days 11–19, postnatal days 1 and 8, and from adult mice. Relative expression of Frmd7mRNA was calculated using quantitative real-time PCR techniques with two normalising genes (Gapdhand Actb).
Results
Expression of Frmd7was low in all tissues consistent with earlier reports. In heart and lung tissues, expression remained very low with an increase only in adult samples. In brain tissue, expression levels were higher at all time points with a significant increase at embryonic day 18, with no gender-specific influence on Frmd7expression.
Conclusions
Frmd7is expressed at low levels in all tissues studied suggesting a role in many tissue types. However, higher overall expression and a sharp increase at ED18 in the murine brain suggest a different role in this tissue.
Earlier studies have shown that genes expressed in the murine brain during development exhibit temporal functional clustering. The temporal pattern of Frmd7 expression found in this study mirrors that of genes involved in synapse formation/function, and genes related to axon growth/guidance. This suggests a role for Frmd7 in these processes and should direct further expression studies.
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Acknowledgements
We thank Angela Cree of the Gift of Sight Laboratory for technical and advisory support. Grant support was provided by an MRC clinical research fellowship, a grant from the Nystagmus Network, and support from the AAIR (Asthma, Allergy, and Inflammation Research) charity.
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Self, J., Haitchi, H., Griffiths, H. et al. Frmd7 expression in developing mouse brain. Eye 24, 165–169 (2010). https://doi.org/10.1038/eye.2009.44
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DOI: https://doi.org/10.1038/eye.2009.44