C57BL/6J-Clock^m1Jt/J

Stock number: 002923
Product name: Clock
Research areas: Neurobiology Research, Reproductive Biology Research

Description

These mice carry an ENU-induced mutation characterized by a lengthening of their circadian period.

Detailed description

Mice heterozygous for this Clock^delta19 mutation (also called Clock^mut or Clock^m1Jt) show a lengthening of their circadian period by about 1 hour. Homozygous mice show a lengthening of 4 hours followed by a loss of circadian rhythm. Homozygous mice are viable. Male homozygotes are fertile, but female homozygotes appear to have reduced fertility.

Development

ENU-mutagenesis of male C57BL/6J mice created an A to T transversion at the third base position of the 5' splice donor site of intron 19. Exon 19 is missing from Clock mRNA, causing a 51 amino acid deletion within the glutamine-rich region of the protein's C terminus (amino acids 514-564). Mice with this Clock^delta19 mutation (also called Clock^mut or Clock^m1Jt) maintained on the C57BL/6J genetic background prior to sending to The Jackson Laboratory Repository.

Allele

Symbol: Clock^m1Jt
Name: Clock
MGI accession ID: MGI:1861634
Generation method: Chemically induced (ENU)
Marker symbol: Clock
Marker name: circadian locomotor output cycles kaput
Chromosome: 5
Strain of origin: C57BL/6J
Molecular note: ENU mutagenesis caused an A to T transversion at the third base position of the 5' splice donor site of intron 19. RT-PCR using primers for exon 15 and exon 21 detected shorter transcripts and no wild-type transcript in hypothalamus of homozygous mutant mice. Sequence analysis revealed that these shorter transcripts are missing exon 19. The authors predict the protein will be missing a 51 amino acid region within the carboxy terminus.