| Primary Identifier | MGI:1856580 | Allele Type | Radiation induced |
| Gene | Tyr | Inheritance Mode | Recessive |
| Strain of Origin | (101 x C3H)F1 | Is Recombinase | false |
| Is Wild Type | false |
| description | Tyrc-14CoS. This induced mutation was found at Oak Ridge National Laboratory. Homozygotes die neonatally (J:5063), and have deficiencies in activity of at least five liver enzymes, glucose-6-phosphatase, tyrosine aminotransferase, serine dehydratase, glutamine synthetase, and UDP-glucuronyltransferase, as well as low levels of liver microsomal cytochrome P-450 and the plasma proteins, albumin, a-fetoprotein, and transferrin (J:5715, J:5588, J:5730). Control of the level of two enzymes occurs at the transcriptional level; control of the level of the three plasma proteins occurs posttranscriptionally (J:7838, J:7840). There is a marked decrease in the number of receptors for insulin and glucocorticoids (J:6996) and for epidermal growth factor and glucagon (J:12047). Two specific liver polypeptides recognizable in two-dimensional gels are lacking (J:7420). The rough endoplasmic reticulum of the liver, and to a lesser extent of the kidneys, is dilated and vesiculated (J:5386). Complementation studies with other alleles have shown that this is probably the shortest of the six deletions (J:5435). It is known not to include the Mod2 locus (J:5437). Compound heterozygotes carrying Tyrc-ch show dilution of the chinchilla pigmentation compared to homozygous chinchilla mice (Tyrc-ch/Tyrc-ch, J:5435). |
| molecularNote | Large intergenic deletion. |
