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J. Cell Biol.,
Volume 141, Number 2, April 20, 1998 309-319
* The Murdoch Institute for Research into Birth Defects, Royal Children's Hospital, Parkville 3052, Australia; and 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.
Institute of
Reproduction and Development, Monash University, Clayton 3168, Australia
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