Andrew Jackson is fascinated with how study of human genetic diseases can shed light on fundamental biological mechanisms. His work has revealed that reduced brain and body size results when the processes that control DNA replication, cell division or genome stability are perturbed.
Andrew is also known for his work on Ribonuclease H2, mutations in which cause an inflammatory disorder mimicking congenital viral infection. He demonstrated that this enzyme's substrate, ribonucleotides embedded within DNA, to be the most common error in the mammalian genome. He has also linked genome instability to inflammation, showing that ruptured micronuclei trigger an innate immune response within the cell.
Andrew trained in Medicine in Newcastle, and obtained his PhD in molecular genetics from Leeds University. He leads a research programme at the MRC Human Genetics Unit, University of Edinburgh, where he is also a Consultant in Clinical Genetics. He is an EMBO member, a Fellow of the Royal Society of Edinburgh, and of the Academy of Medical Sciences.
Professor of Human Genetics, MRC Human Genetics Unit, University of Edinburgh
Interest and expertise
- Biochemistry and molecular cell biology
- Biochemistry and molecular biology, Cell biology (incl molecular cell biology), Molecular immunology
- Microbiology, immunology and developmental biology
- Developmental biology, Genetics (excluding population genetics)
- Health and human sciences
Human genetics, Monogenic disorders, Human genomics, Nucleic acid biochemistry, Innate Immunity, Nucleic acid sensing, Genome instability, DNA replication, Mitosis, Neurodevelopment