Abstract:
:A spontaneous lymphoma was detected in mice, which was caused by a recessive autosomal mutation. The genetic basis was revealed to be a 5-bp deletion at the splicing donor site of the first intron of the FasL gene, resulting in aberrant transcripts coding for non-functional proteins. This mutation of the FasL gene caused development of lymphoma in all four mouse genetic backgrounds tested and the lymphoma was characterized by an expansion of leucocytes that were TCR+CD3+B220+CD19-CD4-CD8-. Accordingly, severe splenomegaly developed in the mutant mice. Interestingly, thymic hyperplasia was observed in mutant mice at later stages. These results underscore the functional importance of the splicing donor site in the function of the FasL gene and provide an independent evidence for a role of FasL in normal development of lymophocytes. The mutant mice offer another genetically defined mouse model for further studies of the role and mechanism of action of FasL.
journal_name
Biochem Biophys Res Communjournal_title
Biochemical and biophysical research communicationsauthors
Wang CC,Zeng Q,Hwang LA,Guo K,Li J,Liew HC,Hong Wdoi
10.1016/j.bbrc.2006.07.215subject
Has Abstractpub_date
2006-10-13 00:00:00pages
50-8issue
1eissn
0006-291Xissn
1090-2104pii
S0006-291X(06)01693-7journal_volume
349pub_type
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