Adrian Bird has held the Buchanan Chair of Genetics at the University of Edinburgh since 1990. He was raised in the Midlands of England near Birmingham, graduated in Biochemistry from the University of Sussex and obtained his PhD at Edinburgh University. Following postdoctoral experience at the Universities of Yale (with Joe Gall) and Zurich (with Max Birnstiel), he joined the Medical Research Council’s Mammalian Genome Unit in Edinburgh. In 1987 Bird moved to Vienna to become a Senior Scientist at the newly created Institute for Molecular Pathology. Following his return to Edinburgh he became founding director of the Wellcome Trust Centre for Cell biology from 1999-2011. He was a governor of the Wellcome Trust from 2000-2010, becoming deputy chair in 2007. Subsequently he joined Cancer Research UK as a trustee and chair of the Research Strategy Committee. He is also a longstanding trustee of The Rett Syndrome Research Trust.

Research Interests

Adrian Bird has studied the biological and biomedical significance of DNA methylation. He introduced the use of restriction enzymes to map patterns of methylated CpG sites in genomic DNA. This led to the recognition that "CpG islands" - non-methylated CpG-rich genomic domains - are associated with the promoters of most mammalian genes and could be used as markers for early gene-discovery in mammalian DNA. The Bird laboratory later described a family of proteins with an affinity for the methyl-CpG sequence and demonstrated that several can mediate transcriptional repression. MeCP2 was the first methyl-CpG binding protein to be purified and was shown to recruit a transcriptional corepressor complex to DNA, providing a mechanistic connection between two different epigenetic marks - DNA methylation and histone acetylation. The report by others that mutations in the MECP2 gene cause of the autism spectrum disorder Rett Syndrome (RTT) led Bird to pursue the molecular basis of this disorder. His group created a convincing mouse model of RTT and established, unexpectedly, that the resulting severe neurological phenotype is reversible. Both terminally ill Mecp2-null males and chronically symptomatic heterozygous females lost all RTT-like signs, suggesting that this is potentially a curable disorder.

Membership Type

International Member

Election Year


Primary Section

Section 22: Cellular and Developmental Biology