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

Michael Brandeis, Ian Rosewell, Mark Carrington, Tessa Crompton, Mary Ann Jacobs, Jane Kirk, Julian Gannon, Tim Hunt*

*Corresponding author for this work

Research output: Contribution to journalArticlepeer-review

257 Scopus citations

Abstract

Two B-type cyclins, B1 and B2, have been identified in mammals. Proliferating cells express both cyclins, which bind to and activate p34cdc2. To test whether the two B-type cyclins have distinct roles, we generated lines of transgenic mice, one lacking cyclin B1 and the other lacking cyclin B2. Cyclin B1 proved to be an essential gene; no homozygous B1-null pups were born. In contrast, nullizygous B2 mice developed normally and did not display any obvious abnormalities. Both male and female cyclin B2-null mice were fertile, which was unexpected in view of the high levels and distinct patterns of expression of cyclin B2 during spermatogenesis. We show that the expression of cyclin B1 overlaps the expression of cyclin B2 in the mature testis, but not vice versa. Cyclin B1 can be found both on intracellular membranes and free in the cytoplasm, in contrast to cyclin B2, which is membrane-associated. These observations suggest that cyclin B1 may compensate for the loss of cyclin B2 in the mutant mice, and implies that cyclin B1 is capable of targeting the p34cdc2 kinase to the essential substrates of cyclin B2.

Original languageAmerican English
Pages (from-to)4344-4349
Number of pages6
JournalProceedings of the National Academy of Sciences of the United States of America
Volume95
Issue number8
DOIs
StatePublished - 14 Apr 1998

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