Didier Stainier

Last updated
Didier Stainier
Didier Stainier.jpg
Born1963 (age 6061)
Liège, Belgium
NationalityBelgian/American
Alma mater
Awards
Scientific career
Fields
Institutions
Doctoral advisor Walter Gilbert
Other academic advisors Mark Fishman

Didier Stainier (born 1963) is a Belgian/American developmental geneticist who is currently a director at the Max Planck Institute for Heart and Lung Research in Bad Nauheim, Germany. [1] [2]

Contents

Scientific career

Didier Stainier studied biology in Wales (United World College of the Atlantic), Belgium (University of Liège) and the USA (Brandeis University) where he got a BA in 1984. He has a PhD in biochemistry and biophysics from Harvard University (1990). During his PhD work, he investigated axon guidance and target recognition in the developing mouse with Walter Gilbert. Subsequently, he initiated the studies on zebrafish cardiac development as a Helen Hay Whitney postdoctoral fellow with Mark Fishman at the Massachusetts General Hospital (Boston).

Scientific interests

Together with the many students and postdocs in his laboratory, Stainier helped pioneer the use of the zebrafish model to study a wide range of questions pertaining to vertebrate organ development and function, [3] and has published extensively. [4] [5] [6] His forward genetic analyses of heart development revealed the unexpected role of several signaling pathways including sphingosine 1-phosphate signaling [7] and the discovery of the long-elusive sphingosine 1-phosphate transporter. [8] [9] Additional genetic screens led to the elucidation of transcriptional networks regulating endoderm formation [10] and endothelial cell specification [11] as well as extracellular signals regulating liver induction. [12] He pushed the frontiers of in vivo microscopy [13] to reveal new insights into cardiac valve formation [14] and cardiac trabeculation, and used cellular approaches to gain a detailed understanding of these processes. Stainier developed and used single-cell analyses to provide the first in vivo demonstration of the hemangioblast, [15] a formerly hypothetical cell that gives rise to both endothelial and blood cells, as well as the discovery of a new mode of blood vessel formation. [16] His studies on gut looping morphogenesis revealed the importance of tissue-level physical forces in shaping organs, [17] and his studies on gut lumen formation revealed the importance of fluid flow in this process. [18] He developed a number of cell ablation models that allowed him and others to gain new insights into the process of organ regeneration, with potential implications for novel disease therapies. [19] Most recently, he has also made significant contributions to the understanding of genetic compensation. [20] [21]

Selected awards and honors

Related Research Articles

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<span class="mw-page-title-main">Notch signaling pathway</span> Series of molecular signals

The Notch signaling pathway is a highly conserved cell signaling system present in most animals. Mammals possess four different notch receptors, referred to as NOTCH1, NOTCH2, NOTCH3, and NOTCH4. The notch receptor is a single-pass transmembrane receptor protein. It is a hetero-oligomer composed of a large extracellular portion, which associates in a calcium-dependent, non-covalent interaction with a smaller piece of the notch protein composed of a short extracellular region, a single transmembrane-pass, and a small intracellular region.

<span class="mw-page-title-main">ROCK1</span> Protein

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Cadherin-2 also known as Neural cadherin (N-cadherin), is a protein that in humans is encoded by the CDH2 gene. CDH2 has also been designated as CD325 . Cadherin-2 is a transmembrane protein expressed in multiple tissues and functions to mediate cell–cell adhesion. In cardiac muscle, Cadherin-2 is an integral component in adherens junctions residing at intercalated discs, which function to mechanically and electrically couple adjacent cardiomyocytes. Alterations in expression and integrity of Cadherin-2 has been observed in various forms of disease, including human dilated cardiomyopathy. Variants in CDH2 have also been identified to cause a syndromic neurodevelopmental disorder.

<span class="mw-page-title-main">S1PR1</span> Protein and coding gene in humans

Sphingosine-1-phosphate receptor 1, also known as endothelial differentiation gene 1 (EDG1) is a protein that in humans is encoded by the S1PR1 gene. S1PR1 is a G-protein-coupled receptor which binds the bioactive signaling molecule sphingosine 1-phosphate (S1P). S1PR1 belongs to a sphingosine-1-phosphate receptor subfamily comprising five members (S1PR1-5). S1PR1 was originally identified as an abundant transcript in endothelial cells and it has an important role in regulating endothelial cell cytoskeletal structure, migration, capillary-like network formation and vascular maturation. In addition, S1PR1 signaling is important in the regulation of lymphocyte maturation, migration and trafficking.

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References

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