CyclinB2 Null Mouse

Although mutant mice lacking cyclin B2 proved to be viable, and both sexes were fertile, the sizes of the litters of homozygous mating pairs were consistently smaller than those of their heterozygous littermates.

Contributors

Inventor Institute
Tim Hunt Cancer Research UK, London Research Institute: Clare Hall Laboratories
Cat. #: 151845
Research Fields: Cell biology;Cell signaling and signal transduction;Genetics
Target: Cyclin B2
Model: Knock-Out
Product description: Cyclin B2 is a mitotic B-type cyclin that activates the p34 cdc2 protein kinase to form maturation promoting factor, which is required for cells to undergo mitosis. Cyclin B2 is expressed in majority of dividing cells and is usually associated with intracellular membranes. Nullizygous B2 mice developed normally and did not display any obvious abnormalities in adult life. Moreover, both male and female cyclin B2-null mice proved to be fertile. Although mutant mice lacking cyclin B2 proved to be viable, and both sexes were fertile, the sizes of the litters of homozygous mating pairs were consistently smaller than those of their heterozygous littermates.
Conditional: No
Genetic background: The targeting vectors (20 mg) for disruption of cyclins B1 or B2 were linearized with NotI and separately electroporated into GK129 ES cells from 129yOla mice and selected as described by Fantl et al. (see reference). G418-resistant colonies were picked and grown in duplicate 96 well plates. Genomic DNA for screening was prepared from one set of plates while the cells in the other set were stored as frozen stocks. DNA was prepared (see reference) and screened for homologous recombination as described in the publication. Cells from colonies that underwent homologous recombination were thawed, expanded and injected into blastocysts as described by Fantl et al.. The chimeras that developed from these blastocysts were mated to C57BLy6 mice and agouti offspring were screened by Southern blotting with the same intron 7 probe used for the screen of the neomycin-resistant colonies for the cyclin B2 gene.
Production details: The targeting vectors (20 mg) for disruption of cyclins B1 or B2 were linearized with NotI and separately electroporated into GK129 ES cells from 129yOla mice and selected as described by Fantl et al. (see reference). G418-resistant colonies were picked and grown in duplicate 96 well plates. Genomic DNA for screening was prepared from one set of plates while the cells in the other set were stored as frozen stocks. DNA was prepared (see reference) and screened for homologous recombination as described in the publication. Cells from colonies that underwent homologous recombination were thawed, expanded and injected into blastocysts as described by Fantl et al.. The chimeras that developed from these blastocysts were mated to C57BLy6 mice and agouti offspring were screened by Southern blotting with the same intron 7 probe used for the screen of the neomycin-resistant colonies for the cyclin B2 gene.
Shipping conditions: Embryo/Spermatoza- Dry Ice
References:

Brandeis et al. 1998. Proc Natl Acad Sci U S A. 95(8):4344-9. PMID: 9539739.

Cyclin B2-null mice develop normally and are fertile whereas cyclin B1-null mice die in utero.

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