Abstract
Random monoallelic expression and asynchronous replication define an unusual class of autosomal mammalian genes. We show that every cell has randomly chosen either the maternal or paternal copy of each given autosome pair, such that alleles of these genes scattered across the chosen chromosome replicate earlier than the alleles on the homologous chromosome. Thus, chromosome-pair non-equivalence, rather than being limited to X-chromosome inactivation, is a fundamental property of mouse chromosomes.
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Acknowledgements
We thank H. Cedar, G. Fink, D. Housman, R. Jaenisch, D. Page, C. Cowles and members of A.C.'s laboratory for discussions and comments on the manuscript; H. Higgins for manuscript preparation; G. Paradis for help with fluorescence-activated cell sorting analyses; J. Young for Chromosome 6 BACs, D. Littman for the Cd4 cosmid; R. Lane for the Olfr41 BAC; B. Holdener for the tyrosinase deletion mice; A. Dunn for the CSF2 knock-in mice; P. Soriano for the β-geo transgenic mice; N. Rosenberg for the Abelson leukemia virus–producing lines; D. MacAlpine for advice on immunoprecipitation; S. Gabriel, B. Blumenstiel, M. DeFelice and E. Winchester for help with MALDI-TOF genotyping; and S. Rozen for help with sequencing. This work was supported by grants from the U.S. National Institutes of Health (National Institute on Deafness and Other Communication Disorders) to A.C., F.A.W.E. and M.T. A. W.E. is a Howard Hughes Medical Institute Predoctoral Fellow.
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Singh, N., Ebrahimi, F., Gimelbrant, A. et al. Coordination of the random asynchronous replication of autosomal loci. Nat Genet 33, 339–341 (2003). https://doi.org/10.1038/ng1102
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DOI: https://doi.org/10.1038/ng1102
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