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© The Rockefeller University Press, 0021-9525/1998//309 $5.00
The Journal of Cell Biology, Volume 141, Number 2, , 1998 309-319

Articles

Centromere Protein B Null Mice are Mitotically and Meiotically Normal but Have Lower Body and Testis Weights



Damien F. Hudson*, Kerry J. Fowler*, Elizabeth Earle*, Richard Saffery*, Paul Kalitsis*, Helen Trowell*, Joanne Hill*, Nigel G. Wreford{ddagger}, David M. de Kretser{ddagger}, Michael R. Cancilla*, Emily Howman*, Linda Hii*, Suzanne M. Cutts*, Danielle V. Irvine*, and K.H.A. Choo*

* The Murdoch Institute for Research into Birth Defects, Royal Children's Hospital, Parkville 3052, Australia; and {ddagger} Institute of Reproduction and Development, Monash University, Clayton 3168, Australia

CENP-B is a constitutive centromere DNA-binding protein that is conserved in a number of mammalian species and in yeast. Despite this conservation, earlier cytological and indirect experimental studies have provided conflicting evidence concerning the role of this protein in mitosis. The requirement of this protein in meiosis has also not previously been described. To resolve these uncertainties, we used targeted disruption of the Cenpb gene in mouse to study the functional significance of this protein in mitosis and meiosis. Male and female Cenpb null mice have normal body weights at birth and at weaning, but these subsequently lag behind those of the heterozygous and wild-type animals. The weight and sperm content of the testes of Cenpb null mice are also significantly decreased. Otherwise, the animals appear developmentally and reproductively normal. Cytogenetic fluorescence-activated cell sorting and histological analyses of somatic and germline tissues revealed no abnormality. These results indicate that Cenpb is not essential for mitosis or meiosis, although the observed weight reduction raises the possibility that Cenpb deficiency may subtly affect some aspects of centromere assembly and function, and result in reduced rate of cell cycle progression, efficiency of microtubule capture, and/or chromosome movement. A model for a functional redundancy of this protein is presented.

Abbreviations used in this paper: ASC, advanced sperm count; ES, embryonic stem; RT, reverse transcription.

Address all correspondence to Dr. Andy Choo, The Murdoch Institute for Research into Birth Defects, Royal Children's Hospital, Flemington Road, Parkville 3052, Australia. Phone: 61-3-9345-5045; FAX: 61-3-9348-1391; E-mail: choo{at}cryptic.rch.unimelb.edu.au


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