Dr. Tomas Lindahl is noted for his contributions to the comprehension of DNA repair at the molecular level in bacterial and mammalian cells. He was the first to isolate a mammalian DNA ligase and to describe a totally unanticipated novel group of DNA glycosylases as mediators of DNA excision repair. He has also discovered a unique class of enzymes in mammalian cells, namely the methyltransferases, which mediate the adaptive response to alkylation of DNA and has shown that the expression of these enzymes is regulated by the ada gene. More recently he has elucidated the molecular defect in Blooms syndrome [sic] to be the lack of DNA ligase I. Apart from providing profound insights into the nature of the DNA repair process his very important contributions promise to facilitate the design of more selective chemotherapeutic drugs for the treatment of cancer. Lindahl has also made a number of significant contributions to understanding at the DNA level the mechanism of transformation of B-lymphocytes by the Epstein-Barr virus. The most notable of these was the first description of the occurrence in lymphoid cells of closed circular duplex viral DNA.
He shared the Nobel Prize in Chemistry in 2015. The Swedish Academy noted that "The Nobel Prize in Chemistry 2015 was awarded jointly to Tomas Lindahl, Paul Modrich and Aziz Sancar 'for mechanistic studies of DNA repair'."
^Yang, Y. G.; Lindahl, T; Barnes, D. E. (2007). "Trex1 exonuclease degrades ssDNA to prevent chronic checkpoint activation and autoimmune disease". Cell. 131 (5): 873–86. doi:10.1016/j.cell.2007.10.017. PMID18045533.
^Crow, Y. J.; Hayward, B. E.; Parmar, R; Robins, P; Leitch, A; Ali, M; Black, D. N.; Van Bokhoven, H; Brunner, H. G.; Hamel, B. C.; Corry, P. C.; Cowan, F. M.; Frints, S. G.; Klepper, J; Livingston, J. H.; Lynch, S. A.; Massey, R. F.; Meritet, J. F.; Michaud, J. L.; Ponsot, G; Voit, T; Lebon, P; Bonthron, D. T.; Jackson, A. P.; Barnes, D. E.; Lindahl, T (2006). "Mutations in the gene encoding the 3'-5' DNA exonuclease TREX1 cause Aicardi-Goutières syndrome at the AGS1 locus". Nature Genetics. 38 (8): 917–20. doi:10.1038/ng1845. PMID16845398.