Brian Michael Wilkins, geneticist: born Cheltenham, Gloucestershire 3 April 1939; Assistant Lecturer and Lecturer, Queen Mary College, London 1965-66; Research Associate, Radiobiology Laboratories, Yale University School of Medicine 1966-69; Lecturer, Department of Genetics, Leicester University 1969-80, Senior Lecturer 1980-96, Reader 1996-2000, Head of Department 1996-2000, Professor of Microbial Genetics 2000-03; married 1972 Susan Hollom (one son); died Leicester 7 April 2003.
Brian Wilkins used genetics to study the mechanisms controlling the horizontal spread of genes in bacterial populations. His work was of great intrinsic interest as a study of complex biological phenomena, but also had broader impact in revealing mechanisms driving the spread of antibiotic resistance in bacterial populations and events in important infectious diseases.
Wilkins was born in Cheltenham in 1939 and brought up in Bristol, where he attended Clifton College. He read Botany as a Neale Exhibitioner at Queen's College, Oxford, graduating with second class honours in 1962. He was awarded a Christopher Welch Scholarship to support his DPhil research on genetic recombination in bacteria, under the supervision of E.A. Bevan. During his postgraduate training he attended a course in Naples on the genetics and physiology of bacterial viruses that had a lasting influence on his scientific interests and his experimental design.
After a brief period at Queen Mary College, London, Wilkins joined the laboratory of Paul Howard-Flanders in the Radiobiology Laboratories, Yale University School of Medicine, as a postdoctoral research associate. Howard-Flanders was a British-born geneticist who was established amongst the international network of scientists interested in the mechanisms of replication, recombination and repair of DNA molecules. Together with Dean Rupp and others, they published several important papers on the replication and recombination of bacterial DNA that had been damaged by UV irradiation.
In 1969, Wilkins was recruited by Bob Pritchard to join the emerging new Department of Genetics at Leicester University. There he continued to work on processes related to DNA recombination, with increasing emphasis on the role of plasmid-borne genes in the transfer of DNA between bacterial cells.
As early as 1975, he produced evidence for a genetic interaction between certain plasmid genes and host genes encoding components of the cellular DNA replication machinery. Developments of this observation in his laboratory led to the discovery of a plasmid gene encoding DNA primase, an enzyme crucially involved in the initiation of DNA replication. Wilkins and his colleagues established that the plasmid-specified primase protein was transferred from the donor to the recipient cell during the bacterial "mating" event, and that this could occur in the absence of DNA transfer.
The importance of these observations on plasmid-mediated protein export is emphasised by the genetic homology between the cognate transport proteins and components of secretion systems associated with several clinically important bacterial pathogens, including Legionella pneumophila, the cause of legionnaires' disease.
Wilkins's interest in plasmid biology and horizontal gene-transfer fuelled a continuing study of the genetic interactions between the plasmid and the recipient cell, in which the newly transferred DNA encounters a potentially antagonistic environment. He pioneered the studies that have shown that the first few plasmid genes transferred are immediately expressed in the recipient cell to produce proteins that help to protect and establish the incoming DNA in the hostile environment.
Plasmid-encoded proteins block host-specific degradation ("restriction") of the incoming DNA, inhibit the potentially suicidal "SOS" response and augment a potentially limiting host protein that is necessary for DNA replication. The relevant plasmid genes are expressed in a transient burst by a mechanism that unusually involves utilisation of the single-stranded transferred DNA as the template for RNA polymerase.
Wilkins's most recent studies, in collaboration with biochemical colleagues, involved exploration of the hypothesis that the single-stranded DNA folds into a unique secondary structure that creates a temporary template for RNA polymerase. Replication of the transferred strand in the recipient would necessarily destroy this special secondary structure and self-limit the burst of gene-expression.
Brian Wilkins's approach to laboratory investigation was reflective and careful. He relished the planning process, designing the controlled experiment that would test the current hypothesis. Early in his career a referee assessed him as "interested, original, ingenious and effective": that perceptive description remained true throughout his career. He worked with a small team, often a technician and a PhD student, sometimes a single postdoctoral associate, but was able to make an internationally recognised scientific contribution over two decades.
His status in the field was well recognised. He received frequent invitations to speak or chair sessions at international meetings and to write reviews for leading journals. He was also a very effective university teacher, caring deeply about the welfare of his students and the quality of their educational experience. He was a painstaking administrator and had an integrating influence on his beloved Department of Genetics while acting as its Head from 1996 to 2000.
Wilkins had productive interactions with a wide circle of professional colleagues in Europe, Australia and North America, whom he referred to as his "friends". He was magnanimous in his relationships and seemed constitutionally incapable of making enemies.
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