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White-bellied agouti A W mice have agouti coloration, with hairs that are black at the tips, then yellow, then black again, and white to tan bellies. [4] Agouti A looks like A W but the belly is dark like the back. [4] Black and tan a t causes a black back with a tan belly. A/a t heterozygotes look like A W mice. [4]
By crossing SCID mice with these other mice, more severely immunocompromised strains can be created to further aid research (e.g. by being less likely to reject transplants). The degree to which the various components of the immune system are compromised varies according to what other mutations the mice carry along with the SCID mutation.
The mutation causing SCIDs in mice was discovered by Melvin and Gayle Bosma in 1983 [1] in the CB/17 mouse line. [2] SCIDs occurs in these mice due to a mutation in the gene for protein kinase, DNA activated, catalytic polypeptide (PRKDC), which plays a role in repairing double-stranded DNA breaks .
This indicated that the yellow mutation is dominant, and all the parental yellow mice were heterozygotes for the mutant allele. By mating two yellow mice, Cuénot expected to observe a usual 1:2:1 Mendelian ratio of homozygous agouti to heterozygous yellow to homozygous yellow. Instead, he always observed a 1:2 ratio of agouti to yellow mice.
In 2003, Jirtle provided molecular evidence that maternal dietary supplementation of Agouti viable yellow (A vy) mice with methyl donors (i.e. folic acid, choline, vitamin B 12, and betaine) altered the coat color distribution and disease susceptibility in genetically identical offspring by increasing DNA methylation at the A vy locus.
Agouti-signaling protein is a protein that in humans is encoded by the ASIP gene. [5] [6] It is responsible for the distribution of melanin pigment in mammals.[7] [8] Agouti interacts with the melanocortin 1 receptor to determine whether the melanocyte (pigment cell) produces phaeomelanin (a red to yellow pigment), or eumelanin (a brown to black pigment). [9]
The NSG mouse (NOD scid gamma mouse) is a brand of immunodeficient laboratory mice, developed and marketed by Jackson Laboratory, which carries the strain NOD.Cg-Prkdc scid Il2rg tm1Wjl /SzJ. NSG branded mice are among the most immunodeficient described to date. [1] NSG branded mice lack mature T cells, B cells, and natural killer (NK) cells. [2]
Indeed, gene targeting has been widely used to study human genetic diseases by removing ("knocking out"), or adding ("knocking in"), specific mutations of interest. [ 28 ] [ 29 ] Previously used to engineer rat cell models, [ 30 ] [ 31 ] advances in gene targeting technologies enable a new wave of isogenic human disease models .