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Nucleic Acids Research Advance Access originally published online on February 20, 2009
Nucleic Acids Research 2009 37(7):2204-2210; doi:10.1093/nar/gkp086
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Nucleic Acids Research, 2009, Vol. 37, No. 7 2204-2210
© 2009 The Author(s)
This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License (http://creativecommons.org/licenses/by-nc/2.0/uk/) which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited.

Gene Regulation, Chromatin and Epigenetics

Methylation-state-specific recognition of histones by the MBT repeat protein L3MBTL2

Yahong Guo1, Nataliya Nady2, Chao Qi1,3, Abdellah Allali-Hassani1, Haizhong Zhu1, Patricia Pan1, Melanie A. Adams-Cioaba1, Maria F. Amaya1, Aiping Dong1, Masoud Vedadi1, Matthieu Schapira1, Randy J. Read4, Cheryl H. Arrowsmith1,2 and Jinrong Min1,3,5,*

1Structural Genomics Consortium, University of Toronto, Toronto, Ontario, M5G 1L6, 2Ontario Cancer Institute and Department of Medical Biophysics, University of Toronto, Toronto, Ontario, M5G 1L7, Canada, 3Hubei Key Laboratory of Genetic Regulation and Integrative Biology, College of Life Science, Huazhong Normal University, Wuhan 430079, People's Republic of China, 4Department of Haematology, Cambridge Institute for Medical Research, University of Cambridge, Cambridge, CB2 0XY, UK and 5Department of Physiology, University of Toronto, Toronto, Ontario, M5S 1A8, Canada

*To whom correspondence should be addressed. Tel: +1 416 946 3868; Fax: +1 416 946 0588; Email: jr.min{at}utoronto.ca

Received December 2, 2008. Revised January 9, 2009. Accepted January 30, 2009.

The MBT repeat has been recently identified as a key domain capable of methyl–lysine histone recognition. Functional work has pointed to a role for MBT domain-containing proteins in transcriptional repression of developmental control genes such as Hox genes. In this study, L3MBTL2, a human homolog of Drosophila Sfmbt critical for Hox gene silencing, is demonstrated to preferentially recognize lower methylation states of several histone-derived peptides through its fourth MBT repeat. High-resolution crystallographic analysis of the four MBT repeats of this protein reveals its unique asymmetric rhomboid architecture, as well as binding mechanism, which preclude the interaction of the first three MBT repeats with methylated peptides. Structural elucidation of an L3MBTL2–H4K20me1 complex and comparison with other MBT-histone peptide complexes also suggests that an absence of distinct surface contours surrounding the methyl–lysine-binding pocket may underlie the lack of sequence specificity observed for members of this protein family.

The authors wish it to be known that, in their opinion, the first four authors should be regarded as joint First Authors.


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