Mice homozygous for the little spontaneous mutation (Ghrhrlit) are characterized by a deficiency in pituitary growth hormone along with prolactin and growth retardation.Read More +
Mice homozygous for the little spontaneous mutation (Ghrhrlit) are characterized by a deficiency in pituitary growth hormone (GH) along with prolactin and growth retardation. Because GH in the circulation regulates IGF-1, homozygotes have about one-tenth the normal level of IGF-1. Male mice have reduced fertility and female mice show a delay in lactation.
The little (Ghrhrlit) mutation arose spontaneously in C57BL/6J at The Jackson Laboratory in 1970. It has been maintained on this background through sibling matings with occasional backcrosses to C57BL/6J. In 1983 C57BL/6J females were bred to heterozygous males to generate embryos for cryopreservation.
A 32 SNP (single nucleotide polymorphism) panel analysis, with 27 markers covering all 19 chromosomes and the X chromosome, as well as 5 markers that distinguish between the C57BL/6J and C57BL/6N substrains, was performed on the rederived living colony at The Jackson Laboratory Repository. While the 27 markers throughout the genome suggested a C57BL/6 genetic background, 2 of 5 markers that determine C57BL/6J from C57BL/6N were found to be segregating. These data suggest the mice may have been crossed to C57BL/6N or C57BL/10J in the past.
|Allele Synonym(s)||lit; litm|
|Gene Symbol and Name||Ghrhr, growth hormone releasing hormone receptor|
|Strain of Origin||C57BL/6J|
|Molecular Note||The mutation in little mice is a A-to-G transition in codon 60 that alters this residue from a aspartate to a glycine in the encoded protein (p.D60G). Reduced levels of mRNA were noted in total RNA derived from pituitary of homozygous mice, and in vitro assays demonstrated that no functional protein is made from this allele.|
When using the B6-little mouse strain in a publication, please cite the originating article(s) and include JAX stock #000533 in your Materials and Methods section.