A novel Fanconi anaemia subtype associated with a dominant-negative mutation in RAD51
- Nat Commun. 2015 Dec 18;6:8829. doi: 10.1038/ncomms9829.
- 1. Department of Clinical Genetics, VU University Medical Center, Van der Boechorststraat 7, Amsterdam 1081 BT, The Netherlands.
- 2. Luxembourg Centre for Systems Biomedicine, House of Biomedicine, 7 Avenue des Hauts-Fourneaux, Esch/Alzette L-4362, Luxembourg.
- 3. Institute for Systems Biology, 401 Terry Avenue North, Seattle, Washington 98109-5234, USA.
- 4. Division of Biological Stress Response, The Netherlands Cancer Institute, Plesmanlaan 121, Amsterdam 1066 CX, The Netherlands.
- 5. Department of Genetics, Cancer Genomics Center, PO Box 2040, Rotterdam 3000 CA, The Netherlands.
- 6. Department of Radiation Oncology, Erasmus Medical Center, PO Box 2040, Rotterdam 3000 CA, The Netherlands.
- 7. Lawrence Berkeley National Laboratory, 1 Cyclotron Road, Berkeley, California 94720, USA.
- 8. Department of Paediatric Oncology, Hematology and Clinical Immunology, Center for Child and Adolescent Health, Medical Faculty, Heinrich Heine University, Moorenstrasse 5, 40225 Du¨sseldorf, Germany.
- 9. Deutsche Fanconi-Anämie-Hilfe e.V., Böckenweg 4, 59427 Unna, Germany.
- 10. Mass Spectrometry and Proteomics Facility, The Netherlands Cancer Institute, Plesmanlaan 121, Amsterdam 1066 CX, The Netherlands.
- 11. Pacific Northwest Diabetes Research Institute, 720 Broadway, Seattle, Washington 98122, USA.
- 12. Department of Human and Clinical Genetics, Leiden University Medical Center, Albinusdreef 2, Leiden 2333ZA, The Netherlands.
Fanconi anaemia (FA) is a hereditary disease featuring hypersensitivity to DNA cross-linker-induced chromosomal instability in association with developmental abnormalities, bone marrow failure and a strong predisposition to Cancer. A total of 17 FA disease genes have been reported, all of which act in a recessive mode of inheritance. Here we report on a de novo g.41022153G>A; p.Ala293Thr (NM_002875) missense mutation in one allele of the homologous recombination DNA repair gene RAD51 in an FA-like patient. This heterozygous mutation causes a novel FA subtype, 'FA-R', which appears to be the first subtype of FA caused by a dominant-negative mutation. The patient, who features microcephaly and mental retardation, has reached adulthood without the typical bone marrow failure and paediatric cancers. Together with the recent reports on RAD51-associated congenital mirror movement disorders, our results point to an important role for RAD51-mediated homologous recombination in neurodevelopment, in addition to DNA repair and Cancer susceptibility.