Edith Heard

Born March 5, 1965 in London, England.

Edith Heard trained as a geneticist. She studied natural sciences at Cambridge University in the UK, and completed her doctorate at the Imperial Cancer Research Fund in London. Edith Heard joined the Institut Pasteur in France in 1990. Today, she heads the Institut Curie's Genetics and Developmental Biology Unit and the Mammalian Epigenesis and Development team.

She has received numerous awards for her research work, including the CNRS Silver Medal in 2008, the Prix Jean Hamburger from the City of Paris in 2009, the ERC Advanced Investigator Award from the European Research Council in 2010 and the FRM Grand Prix in 2011. She has also been an elected member of the prestigious European Molecular Biology Organization (EMBO) since 2005. In 2012, she was appointed Professor at the Collège de France. She was also awarded the Inserm Grand Prix in 2017. On January^1, 2019, Ms. Heard becameExecutive Director of EMBL.

Edith Heard has devoted many years to the study of epigenetic processes such as X chromosome inactivation in mammals, a classic model in this field. Her work has contributed to our understanding of the initial events that accompany X chromosome inactivation during embryogenesis. Her team has highlighted the remarkable dynamics of epigenetic changes during early development and elucidated some of the mechanisms responsible for the X inactivation process. She has also demonstrated the diversity of strategies implemented in this process between even very closely related mammals in the course of evolution. Her work is widely recognized in the field, as similar mechanisms appear to be involved in other epigenetic processes.

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Edith Heard's work over the last ten years has led to many important conceptual advances, particularly in the field of X chromosome inactivation and epigenetics in general, thanks to her analysis of nuclear organization and epigenetic changes in early mammalian development. Her team's major discoveries include: the remarkable dynamics of epigenetic changes on the X chromosome in early mouse embryos (Okamoto et al., 2004; Patrat et al, 2009); the demonstration that the specific form of paternal X chromosome inactivation in mice can occur de novo and independently of meiotic inactivation in male germ cells (Okamoto et al., 2005); and more recently, the discovery of major differences in the nature and timing of events underlying the initiation of X inactivation between different species such as mouse, rabbit and human (Okamoto et al, 2011). This study demonstrates the extent to which epigenetic processes such as X chromosome inactivation can adapt to developmental needs and constraints in different mammals.

Edith Heard and her team have also shed light on the role of nuclear organization in X inactivation. She demonstrated that one of the first functions of non-coding Xist RNA - which triggers the X inactivation process - is to create a silent compartment in the nucleus, in which genes are recruited (Chaumeil et al., 2006). Shortly afterwards, her laboratory highlighted the fact that certain repetitive elements, long considered to be "junk" DNA such as LINEs, undoubtedly play an important role in this compartmentalization of the nucleus and in silencing throughout the chromosome (Chow et al, 2010). She and her team also discovered that the X chromosome passes through transient homologous associations, at a particular stage of the cell cycle and differentiation, which facilitate the coordination of random mono-allelic regulation of the Xist locus, and thus, the process of X inactivation (Bacher et al., 2006; Augui et al., 2007; Masui et al, 2011). This is one of the first examples of homologous chromosome interactions in early mammalian development. This discovery paved the way for the study of other parts of the mammalian genome to see if they too go through similar transient pairing phases, and if so, does this participate in the establishment of random mono-allelic expression and epigenetic regulation. Following these discoveries, Edith Heard was awarded an ERC Advanced Research Fellowship to further investigate the genome-wide prevalence of random mono-allelic expression and chromosome pairing events.

The most recent work carried out by Edith Heard and her team on the X chromosome inactivation center, using technologies to study chromosome conformation at the molecular level with a very high level of resolution, has revealed a new level of chromosome architecture involving sub-megabase scale domains of preferential interactions (Nora et al, 2012). This work has important implications, not only for the regulatory context of the X-inactivation center, but also for our understanding of genomic and epigenomic organization in general. The discovery of these chromosomal domains makes it possible to predict the long-term regulatory elements of disease loci, as well as the coordination of gene expression patterns during development.

In addition to her work on fundamental aspects of epigenetics, Edith Heard is actively involved in the search for epigenetic abnormalities in cancer patients. She has established close collaborations with the Institut Curie hospital, to study the role that epigenetic changes might play in breast cancer (Vincent-Salomon et al, 2007) and to propose biomarkers useful for prognosis and diagnosis, as well as treatment strategies using "epi-drugs" capable of reversing genetic aberrations. By combining its expertise in the field of X-inactivation and developmental epigenetics, Edith Heard's team hopes to gain a better understanding of the epigenetic deregulation that occurs in cancer, and its link with genetic mutations.

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Edith Heard