Control of UVB immunosuppression in the mouse by autosomal and sex-linked genes View Full Text


Ontology type: schema:ScholarlyArticle     


Article Info

DATE

1994-08

AUTHORS

F. P. Noonan, H. A. Hoffman

ABSTRACT

Irradiation with UVB (290–320 nm) initiates a systemic immunosuppression detectable as suppression of contact hypersensitivity (CHS). We investigated susceptibility to UV suppression in reciprocal F1-hybrid and backcross mice derived from BALB/c (low susceptibility) and C57BL/6 (high susceptibility) inbred strains. CB6F1 male mice exhibited high susceptibility and B6CF1 male mice exhibited low susceptibility, indicating a major X-linked effect in the genetic control of UV immune suppression. Females of either F1 hybrid showed intermediate suppression, consistent with random X-inactivation. A model of monogenic X-linked control was not sufficient, and evidence for the action of two genetically unlinked autosomal genes was found in parental backcross animals. Both sexes of (BALB/c × CB6F1) mice showed a 1 high: 1 low ratio of phenotypes, indicating control by a major autosomal locus, Uvs1, confirmed by propagation of the high phenotype through selective backcrossing for nine generations to BALB/c. Uvs1 was not genetically linked to 12 chromosomal markers including the pigment genes b (brown) and c (albino). Backcross animals (C57BL/6 × CB6F1) showed a significant sex difference, male mice giving a 3 high: 1 low ratio of phenotypes, compatible with the action of a second autosomal locus, Uvs2, in this hybrid. The findings are compatible with a model in which high phenotype (Uvs1b/Uvs1b) is dominant when subjected to recessive epistatis by the X-chromosome locus Uvs3, or by the autosomal locus Uvs2. The finding of genetic control by interacting autosomal and X-linked genes is unique. Genetically determined high susceptibility to UV immunosuppression may be an important risk factor for UV-related human diseases. More... »

PAGES

247-256

Identifiers

URI

http://scigraph.springernature.com/pub.10.1007/bf00189969

DOI

http://dx.doi.org/10.1007/bf00189969

DIMENSIONS

https://app.dimensions.ai/details/publication/pub.1036051567

PUBMED

https://www.ncbi.nlm.nih.gov/pubmed/8082890


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