Richard Harvey received a PhD from the University of Adelaide in the Department of Biochemistry, under the late Julian RE Wells. After briefly exploring life in biotechnology in France, he proceeded to Harvard University in Boston, training in embryology with Doug Melton. He returned to Australia in 1988, spending 10 years at the Walter and Eliza Hall Institute of Medical Research in Melbourne, where his identification of Nkx2-5, a regulatory gene in the cardiac genetic hierarchy, established a new field of research in heart development. He has continued his work on the heart after moving to the Victor Chang Cardiac Research Institute in Sydney, where he is Deputy Director and Head of the Developmental Biology Program. He also holds the Sir Peter Finley Professorship at the University of New South Wales in Sydney.

Cell to organ: Exploring the genetic basis of the origins and patterning of the mammalian heart
by Professor Richard Harvey

The heart and blood vessels comprise the first organ system to function in the developing embryo. Remarkably, the heart begins to pump blood when it is merely a rudimentary muscular tube, and as demands on the heart increase with foetal growth, pumping efficiency must advance hand-in-hand with major progressions in heart size and architecture. The formation of the heart from a small group of embryonic cells committed to this fate is guided by the genetic program – gene circuits flash on and off as cells specialise and collaborate in the generation of form.

Nearly one in 100 children are born with some form of structural heart disease, most arising as a result of genetic misfortune and many requiring complex surgeries and a lifetime of care. Understanding the genetic pathways guiding heart formation can help in many ways, including counselling, genetic screening, and in the future, tissue engineering from stem cells. My laboratory has used the tools of genetic engineering and cell biology to unravel the genetic circuit diagrams that determine how heart cells come into being, how heart form is achieved and how this process goes wrong in structural heart disease. More recently, we have begun to reflect on how adult heart stem cells might be coaxed into regenerating the diseased adult heart via similar pathways.

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