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Human Molecular Genetics, Vol 7, 1997-2006, Copyright © 1998 by Oxford University Press

ARTICLES

The embryonic expression pattern of 40 murine cDNAs homologous to Drosophila mutant genes (Dres): a comparative and topographic approach to predict gene function

A Bulfone, C Gattuso, A Marchitiello, C Pardini, E Boncinelli, G Borsani, S Banfi and A Ballabio
Telethon Institute of Genetics of Medicine (TIGEM), San Raffaele Biomedical Science Park, via Olgettina 58, Milan 20132, Italy.

Nature often utilizes the same metabolic 'core groups' of interacting genes or 'pathways' in completely different organs, tissues and cellular compartments. Deciphering the physiological role of a particular gene in a living organism is therefore critical to understanding not only how a gene/protein works, but also where (in which tissue/organ) and when (at what developmental stage) it functions. We have performed systematic RNA in situ hybridization on a subset of murine genes homologous to Drosophila mutant genes, called Drosophila -related expressed sequences (Dres). This approach combines functional information derived from cross-species sequence comparisons and biochemical, physiological and pathological studies performed in the fly with knowledge of the spatial and temporal distribution of gene expression. Forty murine Dres were tested by RNA in situ hybridization on sagittal, coronal and transverse sections at three developmental stages, E10.5, E12.5 and E17.5. For some of them, whole mount in situ hybridization was performed at earlier stages. These data are valuable for establishing how the function of these genes and the genetic programs underlying the development of a particular tissue or organ have evolved during evolution. For example, six Dres genes showed restricted expression domains within the murine retina, suggesting a different role for each of these genes in eye development and functioning. Furthermore, the information derived from this combined approach will be instrumental in predicting the phenotypic consequences of gene dysfunction in both mouse mutants and human genetic diseases.
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