Researchers may be nearer to understanding how genes could influence severe health conditions. They found that failure to turn off a precise gene at the right time during development of an embryo could cause illness in later life. The research might one day help possibly to fix the genetic switch.
There are already growing evidence which suggest that while you carry the same set of genes for life, the environmental aspects such as diet or even health of mother while you were in the womb, could affect the activity and the chances of getting certain illnesses later in life.
A research team from the Gladstone Institute in San Francisco focused on two genes and their role in cardiomyopathy. Cardiomyopath is an expanding and weakening of the heart muscle that plays the lead role in life-threatening heart defects in children and adults. One of the genes known as Six1 seems to play a significant role in embryonic heart development.
The other gene Ezh2 seems to have performed the job of turning off genes including Six2, when they are needed no longer. Their precise relationship has been tested by researchers by halting Ezh2 from functioning in the embryo and foetus at various levels during pregnancy, in this manner allowing Six1 gene to continue working for longer than normal.
They found that mice in which the gene was left active were born apparently normal and healthy, but in later life they developed the signs of cardiomyopathy. This suggested that though leaving Six1 switched on in human being might produce an apparently healthy baby, but it could be storing up heart problems for later in life.
The study analysis revealed that in a healthy pregnancy, Six1 should only normally be switched on momentarily during heart development. Dr Paul Delgado-Olguin, one of the team researchers stated when Six1 remains active for too long in Ezh2-deficient mice, boosts the activity of other genes that should not be activated in heart muscle cells such as genes that make skeletal muscle.
The enlargement and thickening of the hearts in mice over time ultimately led to heart failure. They are expectant that more work will disclose more about the roots of congenital heart problems in early life, added Dr Delgado-Olguin. The study is reported in a Nature Genetics.
According Prof Peter Weissberg from the British Heart Foundation, the research shows that a crucial step in normal heart development is the switching off of genes. There was the possibility thatcould be corrected, although it would be some years before such techniques could be used in humans.