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Robert Lloyd is a bacterial geneticist who applied molecular, biochemical and structural methods over a 42-year career at Nottingham to study DNA recombination, replication and repair. He modeled how the genetic material of an organism - its genome - is transmitted faithfully from one generation to the next.
Recombination is a vital evolutionary process that acts both to preserve genome integrity and to generate genetic diversity. Robert discovered many of the key genes associated with homologous recombination and recombination-dependent repair of damaged DNA in the bacterium Escherichia coli. His studies of the recR and recN genes shed light on the factors that facilitate initiation of recombination and DNA-break repair while his studies of ruv and recG established the critical role of the RuvABC protein complex and of the RecG helicase in processing DNA Holliday junction structures. This work paved the way towards an understanding of equivalent processes in human cells.
His discovery of the sbcC and sbcD genes and of their role in palindrome-mediated inviability laid the foundations for analysis of the SbcCD proteins in E. coli and of their RAD50 and MRE11 homologues in yeast and man where they orchestrate repair of DNA double-strand breaks and V(D)J recombination within the immune system.
Damage to DNA is unavoidable and can destabilise the genome, a common cause of cancer in human cells. Robert discovered that the E. coli enzyme RecG - which unwinds Holliday junctions and a number of other branched DNA structures - is an important player in genome maintenance. His research has also described how how conflicts between the protein machines associated with DNA replication and transcription are avoided or limited, or resolved when such conflicts do occur and threaten viability.
Recombination is a vital evolutionary process that acts both to preserve genome integrity and to generate genetic diversity. Robert discovered many of the key genes associated with homologous recombination and recombination-dependent repair of damaged DNA in the bacterium Escherichia coli. His studies of the recR and recN genes shed light on the factors that facilitate initiation of recombination and DNA-break repair while his studies of ruv and recG established the critical role of the RuvABC protein complex and of the RecG helicase in processing DNA Holliday junction structures. This work paved the way towards an understanding of equivalent processes in human cells.
His discovery of the sbcC and sbcD genes and of their role in palindrome-mediated inviability laid the foundations for analysis of the SbcCD proteins in E. coli and of their RAD50 and MRE11 homologues in yeast and man where they orchestrate repair of DNA double-strand breaks and V(D)J recombination within the immune system.
Damage to DNA is unavoidable and can destabilise the genome, a common cause of cancer in human cells. Robert discovered that the E. coli enzyme RecG - which unwinds Holliday junctions and a number of other branched DNA structures - is an important player in genome maintenance. His research has also described how how conflicts between the protein machines associated with DNA replication and transcription are avoided or limited, or resolved when such conflicts do occur and threaten viability.
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JOURNAL OF MANAGEMENT HISTORYno. 1 (2024): 41-59
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crossref(2020)
The Palgrave Handbook of Management Historypp.245-269, (2020)
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