Congenic NOD mice homozygous for the Faslgld mutation develop lymphadenopathy and systemic autoimmunity. It has been reported that this model displays an accelerated Lupus phenotype compared to the C57BL/6 congenic background. This model is useful for studying apoptosis of lymphocytes, particularly T cells, and Lupus.
Li Wen, Yale School of Medicine
NOD congenic mice homozygous for the Faslgld spontaneous mutation are viable and fertile. The donating investigator reports that homozygous males and females develop lymphadenopathy and systemic autoimmunity beginning at 8 weeks of age, but do not develop diabetes. The Lupus phenotype is accelerated in this strain when compared to the B6-Faslgldstrain. This mutant strain may be useful in the studies of apoptosis of lymphocytes, particularly T cells, and in studies of Lupus.
In an attempt to offer alleles on well-characterized or multiple genetic backgrounds, alleles are frequently moved to a genetic background different from that on which an allele was first characterized.. It should be noted that the phenotype could vary from that originally described. We will modify the strain description if necessary as published results become available.
The spontaneous mutation Faslgld, Fas ligand (TNF superfamily, member 6); generalized lymphoproliferative disease found on Chr 1, was transferred from a C57BL/6 congenic background (Stock No. 001021) to the NOD/Caj (substrain maintained at Yale) background through 12 generations of backcrossing prior to making homozygous for the mutation. In 2008, the T1DR received this strain at N12F20.
|Allele Name||generalized lymphoproliferative disease|
|Allele Synonym(s)||CD95-; FasL-; gld; Tnfsf6gld|
|Gene Symbol and Name||Fasl, Fas ligand (TNF superfamily, member 6)|
|Strain of Origin||C3H/HeJ|
|Molecular Note||A T-to-C transition point mutation near the 3' end of the coding sequence causes a replacement of a highly conserved phenylalanine with a leucine at position 273 (p.F273L) in the extracellular region of the encoded protein.|