Description
Analysis of the effects of an ectopically expressed human SRY (hSRY) on gene expression in the mouse heart. We hypothesize that aberrant expression of the human SRY gene could affect the development and physiology of transgenic mice. To test this hypothesis we have established a Cre-LoxP transgene activation system, thereby activating and expressing the hSRY transgene at the single-cell embryonic stage. Such transgenic mice were born of similar sizes as non-transgenic littermates, but retard in postnatal growth and all die within two weeks of age. To determine the molecular changes associated with such phenotypes, we have analyzed the transcriptomes of hearts of pups expressing (hSRY-ON) and not-expressing (hSRY-OFF) the hSRY transgene. The results provide important information demonstrating that ectopic expression of hSRY resulted in altered expression patterns of numerous genes associating with the development of cardiovascular system and pathogenesis of cardiovascular diseases in the heart.