Start Date
15-12-2020 3:20 PM
Description
During an embryo’s development period, multiple groups of cells interact to form the anatomical structures that we ultimately see. One of these groups of cells, the cardiac neural crest, plays a major role in heart development. Cardiac neural crest cells are known to give rise to various cardiac structures, of which the heart’s ventricular septum (the feature that separates oxygenated and deoxygenated blood in some vertebrates) is a key component. While normal human and chicken hearts possess this septum, both normal turtle hearts and human hearts with congenital heart disease exhibit incomplete cardiac septation. Research has shown that abnormal neural crest cell migration, differentiation, or growth are responsible for the malformation or complete lack of formation of this cardiac septum. Thus, my project aims to use both chicken and turtle embryos as models to comparatively track where and how these cardiac neural crest cells move to better understand the evolutionary and molecular mechanisms behind congenital heart disease in humans.
A Comparative Study of Cardiac Neural Crest Cell Migration in Chicken and Turtle Embryos
During an embryo’s development period, multiple groups of cells interact to form the anatomical structures that we ultimately see. One of these groups of cells, the cardiac neural crest, plays a major role in heart development. Cardiac neural crest cells are known to give rise to various cardiac structures, of which the heart’s ventricular septum (the feature that separates oxygenated and deoxygenated blood in some vertebrates) is a key component. While normal human and chicken hearts possess this septum, both normal turtle hearts and human hearts with congenital heart disease exhibit incomplete cardiac septation. Research has shown that abnormal neural crest cell migration, differentiation, or growth are responsible for the malformation or complete lack of formation of this cardiac septum. Thus, my project aims to use both chicken and turtle embryos as models to comparatively track where and how these cardiac neural crest cells move to better understand the evolutionary and molecular mechanisms behind congenital heart disease in humans.
Comments
Mentor: Max Ezin