The cenpB gene is not essential in mice

Mini Kapoor, Roberto Montes De Oca Luna, Gen Liu, Guillermina Lozano, Chris Cummings, Michael Mancini, Ilia Ouspenski, B. R. Brinkley, Gregory S. May

Research output: Contribution to journalArticlepeer-review

115 Scopus citations

Abstract

Centromere protein B (CENP-B) is a centromeric DNA-binding protein that binds to α-satellite DNA at the 17 bp CENP-B box sequence. The binding of CENP-B, along with other proteins, to α-satellite DNA sequences at the centromere, is thought to package the DNA into heterochromatin subjacent to the kinetochore of mitotic chromosomes. To determine the importance of CENP-B to kinetochore assembly and function, we generated a mouse null for the cenpB gene. The deletion removed part of the promoter and the entire coding sequence except for the carboxyl-terminal 35 amino acids of the CENP-B polypeptide. Mice heterozygous or homozygous for the cenpB null mutation are viable and healthy, with no apparent defect in growth and morphology. We have established mouse embryo fibroblasts from heterozygous and homozygous cenpB null littermates. Microscopic analysis, using immunofluorescence and electron microscopy of the cultured cells, indicated that the centromere-kinetochore complex was intact and identical to control cells. Mitosis was identical in fibroblasts derived from cenpB wild-type, heterozygous and null animals. Our studies demonstrate that CENP-B is not required for the assembly of heterochromatin or the kinetochore, or for completion of mitosis.

Original languageEnglish (US)
Pages (from-to)570-576
Number of pages7
JournalChromosoma
Volume107
Issue number8
DOIs
StatePublished - 1998

ASJC Scopus subject areas

  • Genetics
  • Genetics(clinical)

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