Mutation frequencies and AID activation state in B-cell lymphomas from Ung-deficient mice.
B-cell lymphomas arising in lymph nodes and spleen of aging mice deficient in the Ung DNA glycosylase were recovered, dispersed, grown in short-term culture, and CD19-positive B-cells retrieved and analysed. Several tumors as well as controls only expressed detectable amounts of the Aid deaminase after mitogenic stimulation, as estimated by real-time PCR of transcripts. However, one unusually large lymph node tumor expressed a high level of Aid constitutively. This particular tumor also showed a substantially increased mutation frequency in the Aid gene itself as well as in the bcl-6 and c-myc genes, but not in the p53 gene, consistent with aberrant somatic hypermutation. Other B-cell lymphomas from Ung(-/-) mice exhibited a modest increase in mutation frequency.
Nilsen
Hilde
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Clare Hall Laboratories, CR-UK London Research Institute, South Mimms, Hertfordshire EN6 3LD, UK.
An
Qian
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Lindahl
Tomas
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D000818:Animals; D003564:Cytidine Deaminase / Q000235:genetics / Q000378:metabolism*; D016393:Lymphoma, B-Cell / Q000235:genetics* / Q000378:metabolism; D051379:Mice; D012333:RNA, Messenger / Q000378:metabolism; D000098830:AICDA (Activation-Induced Cytidine Deaminase)
D012333:RNA, Messenger; D000098830:AICDA (Activation-Induced Cytidine Deaminase); D003564:Cytidine Deaminase