C57BL/6-Relb^{Tg(H2-K1/GH1)106Bri}/J

Stock number: 002835
Product name: line 272-4

Description

These mice carry a mutation resulting from the chance integration of a transgene that disrupted the Relb gene, causing immune system defects.

Detailed description

Mice homozygous for this mutation are viable but not fertile. This mutation was caused by the chance integration of a class I MHC clone resulting in the disruption of Relb. Homozygous mutant mice display numerous immune system defects. There is a complete absence of lymphocytes in peripheral lymph nodes and Peyer's patches. The thymic medulla fails to form fully. Splenomegaly is observed along with and severe inflammatory syndrome with mixed granulocyte/monocyte infiltrates in lung, liver, and other tissues. A loss of dendritic cell function and regulation of chemokine expression by nonlymphoid cells (such as fibroblasts) is also observed. Symptoms become apparent at three weeks to several months after birth.

Development

Line 272-4 was generated by microinjection of a construct containing a 7.8 kb fragment containing the complete mouse H2-K<k> structural locus and 2 kb of 5' flanking sequence, as well as a nonfunctional 2.1 kb portion of the human growth hormone gene (hGH1), which serves as a marker gene. Transgene insertion interrupted the Relb locus, resulting in inactivation of Relb. Line 272-4 is referred to as Tg(H2-K + GH1)Bri106 in the primary reference.

Allele

Symbol: Relb^{Tg(H2-K1/GH1)106Bri}
Name: transgene insertion 106, Ralph L Brinster
MGI accession ID: MGI:2179544
Generation method: Transgenic
Attributes: Null/Knockout; Inserted expressed sequence
Marker symbol: Relb
Marker name: avian reticuloendotheliosis viral (v-rel) oncogene related B
Chromosome: 7
Strain of origin: C57BL/6
Molecular note: The mutation was generated by microinjection of a construct containing a 7.8 kb fragment that includes the complete mouse H2-K structural locus and 2 kb of 5' flanking sequence, as well as a nonfunctional 2.1 kb portion of the human growth hormone gene (hGH1), which serves as a marker gene. The random insertion of this transgene just downstream of the exon encoding the Rel domain disrupted the gene. RT-PCR analysis of RNA derived from slpeen and thymus of homozygous mice demonstrated that no detectable transcript was expressed from this allele. Immunohistochemistry experiments on sections of thymus and spleen of homozygous mice confirmed that no detectable encoded protein was present.