A mechanism for preventing asymmetric histone segregation onto replicating DNA strands

Author:

Yu Chuanhe1,Gan Haiyun2ORCID,Serra-Cardona Albert2ORCID,Zhang Lin34ORCID,Gan Songlin34ORCID,Sharma Sushma5ORCID,Johansson Erik5ORCID,Chabes Andrei5ORCID,Xu Rui-Ming34,Zhang Zhiguo2

Affiliation:

1. Department of Biochemistry and Molecular Biology, Mayo Clinic, Rochester, MN 55905, USA.

2. Institute for Cancer Genetics, Department of Pediatrics and Genetics and Development, Columbia University, New York, NY 10032, USA.

3. National Laboratory of Biomacromolecules, CAS Center for Excellence in Biomacromolecules, Institute of Biophysics, Chinese Academy of Sciences, Beijing 100101, China.

4. University of Chinese Academy of Sciences, Beijing 100049, China.

5. Department of Medical Biochemistry and Biophysics, Umeå University, SE 90187 Umeå, Sweden.

Abstract

How cells ensure symmetric inheritance Parental histones with modifications are recycled to newly replicated DNA strands during genome replication, but do the two sister chromatids inherit modified histones equally? Yu et al. and Petryk et al. found in mouse and yeast, respectively, that modified histones are segregated to both DNA daughter strands in a largely symmetric manner (see the Perspective by Ahmad and Henikoff). However, the mechanisms ensuring this symmetric inheritance in yeast and mouse were different. Yeasts use subunits of DNA polymerase to prevent the lagging-strand bias of parental histones, whereas in mouse cells, the replicative helicase MCM2 counters the leading-strand bias. Science , this issue p. 1386 , p. 1389 ; see also p. 1311

Funder

National Institutes of Health

National Science Foundation of China

the Strategic Priority Research Program of Chinese Academy of Sciences

the Ministry of Science and Technology grant

Swedish Cancer foundation and the Swedish Research Council

Publisher

American Association for the Advancement of Science (AAAS)

Subject

Multidisciplinary

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