Grant: Travel Awards - Institute Community Support

Asthma is a common but complex heritable disease that is caused by genetic and environmental factors, and one of the most common chronic conditions occurring in childhood. Several studies have been performed to identify the genetic cause of asthma; yet despite the success of these studies, we are still unable to account for the heritability of asthma. A probable explanation for this gap are so-called "parent-of-origin" effects. Parent-of-origin effects occur when the parental origin of an allele has an effect on the phenotype of the offspring. Parent-of-origin effects can be caused by different mechanisms such as genomic imprinting. Each of us inherits two copies of our genes, one from the mother and one from the father. Usually both copies of each gene are active in cells. However, there are certain genes whose activity depends on the parent of origin: some genes are normally active only when they are inherited from the father, others are active only when inherited from the mother. This phenomenon is called 'genomic imprinting'. Imprinting occurs in early life during growth and development of the fetus. In my proposed research, I hypothesize that imprinting is involved in the origins of asthma and related phenotypes (atopy and airway hyperresponsiveness). I studied this hypothesis by analyzing data obtained in three genomic studies from Canada (The Canadian Asthma Primary Prevention Study, The Study of Asthma Genes and the Environment, The Saguenay-Lac-Saint-Jean Québec Familial Collection) and one from the Netherlands (The Dutch Asthma Study). The data coming from these studies include the genomes of both parents and their children. I studied parent-of-origin effects separately in each of the four family-based studies and combined the results in a meta-analysis. Our results suggest a possible role for long non-coding (lnc)RNA genes in parent-of-origin effects in asthma and allergic phenotypes. LncRNAs are known to be involved in genomic imprinting.