A first of its kind study revealed that mammals are genetically more like their fathers.
The research at UNC School of Medicine shows that although we inherit equal amounts of genetic mutations from our parents, the mutations that make us who we are and not some other person, we actually use more of the DNA that we inherit from our dads.
The research has wide implications for the study of human disease, especially when using mammalian research models, but the UNC research shows that inheriting a mutation has different consequences in mammals, depending on whether the genetic variant is inherited from the mother or father.
Senior author Fernando Pardo-Manuel de Villena said that this is an exceptional new research finding that opens the door to an entirely new area of exploration in human genetics. They've known that there are 95 genes that are subject to this parent-of-origin effect. They're called imprinted genes, and they can play roles in diseases, depending on whether the genetic mutation came from the father or the mother. Now they've found that in addition to them, there are thousands of other genes that have a novel parent-of-origin effect.
These genetic mutations that are handed down from parents show up in many common but complex diseases that involve many genes, such as type-2 diabetes, heart disease, schizophrenia, obesity, and cancers. Studying them in genetically diverse mouse models that take parent-of-origin into account will give scientists more precise insights into the underlying causes of disease and the creation of therapeutics or other interventions.
Pardo-Manuel de Villena said that these types of genetic mutations across hundreds of genes are hard to study and a major bottleneck to realizing the promises of the post-genome era, but thanks to the Collaborative Cross, the mouse can be used to model how these genes work and how they impact health and disease in any kind of tissue in the body.
The study is published in the journal Nature Genetics.
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