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We caught up with Adrian Bird, Buchanan Chair of Genetics at the University of Edinburgh, to ask about his research into
Adrian Bird holds the Buchanan Chair of Genetics at the University of Edinburgh since 1990. He graduated in Biochemistry from the University of Sussex and obtained his PhD at Edinburgh University. Following postdoctoral experience at the Universities of Yale and Zurich, he joined the Medical Research Council's Mammalian Genome Unit in Edinburgh. In 1987 he moved to Vienna to become a Senior Scientist at the Institute for Molecular Pathology.
Adrian's research focuses on the basic biology of the genome, including the role of DNA methylation and other epigenetic processes. His laboratory identified CpG islands as gene markers in the vertebrate genome and discovered proteins that read the DNA methylation signal to influence chromatin structure. Mutations in one of these proteins, MeCP2, cause the severe neurological disorder Rett Syndrome. Adrian's group established a mouse model of this disorder and made the unexpected discovery that the resulting severe neurological phenotype is reversible.
Biology as taught at school was something of a turn-off, but away from the classroom I was very interested in natural history (birds, frogs, etc). I particularly remember watching a series of TV programs on Sunday mornings (a rather unusual thing in the early 1960s) with scientists from Cambridge explaining recent excitement in the new Molecular Biology.
The key thing was that the presenters were the actual scientists, there in black and white, telling us about the structure of myoglobin (John Kendrew) or viruses (Aaron Klug) and of course, DNA. DNA itself was not yet on any school curriculum and for some reason it caught my imagination. I decided then that I wanted to know more about it - and that remains true today.
We want to understand how global features of genomic DNA impact on genomic function. For example, it is known already that CpG islands share properties that make them stand out from the majority of the genome, notably a very high density of the non-methylated CpG dinucleotide. It turns out that CpG recruits proteins that modify chromatin and transcription. So CpG islands appear to function as platforms for gene regulation that simplify management of genome activity.
Our current work is based on the hypothesis that other short DNA sequence motifs are also recognized by sequence-specific DNA binding proteins and by doing so may direct aspects of chromatin structure. The early data is encouraging and, excitingly, may help explain some perplexing aspects of chromosome organization.
Epigenetics research is becoming more realistic as the questions being asked are more penetrating and the boundaries between epigenetics and other aspects of gene regulation are dissolving. Instead of arguing about what the word means, scientists are getting on with the job of deciphering how the genome actually works. This has to be a good thing. We are learning that epigenetics and genetics are inextricably linked.
Perhaps the most impressive example is the recent genome sequencing of DNA from children diagnosed with developmental delay and intellectual disability (e.g. Iossifov et al., 2014. Nature, 515, 216–221). A large fraction of the most frequently implicated rare mutations are in genes for chromatin/epigenetic components. We don't know why epigenetic mechanism are so important in the brain, but the accumulating data suggests that modulation of genome function is exquisitely finely-tuned in the nervous system.
I do science because of its potential to surprise, so predicting the next big thing based on what we already know takes away some of the fun. Fortunately the predictions are nearly always wrong. The CRISPR revolution illustrates this well, as did restriction enzymes, RNAi monoclonal antibodies and many of the other profound discoveries before them. Hardly anyone saw how things might develop, sometimes including the scientists involved in making the discoveries.
The imaginings and obsessions of talented individuals or small teams have always been the engines of real scientific progress. So if you ask me how biomedical research in general will go, I suggest that the current emphasis on headline exercises in large-scale data collection, screening, etc. will be re-balanced in favor of "smaller science" that is creative and necessarily undisciplined. Big data is obviously vital and here to stay, but it almost always poses far more questions than it answers. Getting the important answers remains an art-form.
Become literate in computation and statistics - without losing your love of experimentation.