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University Lecturer (1976-96), Professor of Developmental Anatomy (1996)

GilliamMorrissKay.jpgProfessor Gillian Morriss-Kay came to Oxford in Michaelmas term 1976 as a University Lecturer in the Department of Human Anatomy and Fellow of Balliol College, having previously been a University Demonstrator in Anatomy at Cambridge. She taught first-year anatomy, histology and embryology, and organised the final year Developmental Biology course. She was awarded DSc in 1995 and the title Professor of Developmental Anatomy in 1996. She served on the committee of the British Society for Developmental Biology, was secretary of the Anatomical Society and Editor-in-Chief of the Journal of Anatomy (2002-2012). In 2013, she was elected to one of the first Honorary Fellowships of the Anatomical Society. She published over 130 research articles and edited several books and symposium volumes.

Professor Morriss-Kay's long-term research interest has been to use rodent models for understanding the developmental basis of human congenital abnormalities, with a major focus on craniofacial development. This interest was seeded by observations made during her PhD on the effects of excess retinoids (vitamin A) on prenatal development in the rat. She began to analyse early craniofacial morphogenesis (J Embryol. Exp Morph, 65, 1981) using scanning electron microscopy, whole embryo culture, immunohistochemistry, and both conventional and high voltage transmission EM. Her research student Seong-Seng Tan used these and other techniques to define, for the first time, cranial neural cell migration pathways in a mammalian embryo (Trends in Genetics, 3, 1987). In the late 1980s, the molecular revolution meant that her knowledge of mammalian morphogenesis could enhance the work of pioneering molecular biologists. She enjoyed several fruitful years of collaboration with Pierre Chambon’s CNRS Institute in Strasbourg, analysing the expression patterns of retinoid receptors and binding proteins in mouse development (Development, 108, 1990). This was the first of several enjoyable and fruitful multidisciplinary interactions, both international and local.

Gillian Morris-Kay 1976.jpg© Ramsey and Muspratt on behalf of Balliol College, 1976Professor Morriss-Kay's major contribution was on the genetic control of skull development (Journal of Anatomy, 207, 2005) mainly with the clinical molecular geneticist Andrew Wilkie and the Oxford Craniofacial Surgery Unit. Andrew discovered that craniosynostosis syndromes involving premature fusion of the coronal suture were caused by mutations of fibroblast growth factor receptor (FGFR) genes that engender ligand-independent activity. Sachiko Iseki, a Japanese post-doc in the Morriss-Kay laboratory, used expression analysis and intra-abdominal microsurgery in mice to explore the expression patterns of Fgfr1 and Fgfr2 in the developing coronal suture and the dynamic nature of Fgfr interactions with Fgf ligands. Their work revealed a balance between the differentiation and proliferation roles of Fgfr1 and Fgfr2 in the coronal suture (Development, 124, 1997) and showed that enhancing Fgfr signalling altered this balance.

Understanding the dynamic nature of cell interactions in the coronal suture required knowledge of the tissue origins and interactions there. Professor Morriss-Kay collaborated with Henry Sucov (University of Southern California) to explore the relative contributions of neural crest and mesodermal cells using a transgenic mouse with the permanent neural crest marker Wnt1-Cre/R26R. She discovered that the coronal suture formed at a clear tissue boundary between these two distinct tissues (Developmental Biology, 241, 2002), revealing that the long-accepted description based on avian developmental studies had been misinterpreted. When a mesodermal marker also became available, it showed a complementary pattern to that of neural crest, not only in the skull vault (Mechanisms of Development, 125, 2008), but also in the developing synchondroses of the skull base (Developmental Biology, 322, 2008). The first mouse model of an Fgfr2 mutation that accurately mimicked a human craniosynostosis syndrome (Crouzon syndrome) was constructed in Peter Lonai’s laboratory at the Weizmann Institute, Israel. Professor Morriss-Kay spent several weeks there analysing the mutant embryos, before importing the mice to her laboratory for further work (Development, 129, 2002).

"I am grateful to all my collaborators, students and post-docs, now scattered around the world in leading research, academic, industrial and clinical positions; they greatly enriched my intellectual life. I am also grateful to my departmental colleagues, especially the late Ray Guillery, who created an enabling and encouraging atmosphere." (Professor Morriss-Kay)