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Published Online November 22, 2001
Science DOI: 10.1126/science.1065848

Reports

Submitted on August 29, 2001
Accepted on November 7, 2001

Dnmt3L and the Establishment of Maternal Genomic Imprints

Déborah Bourc'his 1, Guo-Liang Xu 2, Chyuan-Sheng Lin 3, Brooke Bollman 4, Timothy H. Bestor 1*

1 Department of Genetics and Development, College of Physicians and Surgeons of Columbia University, New York, NY 10032, USA.
2 Institute of Biochemistry and Cell Biology, Chinese Academy of Sciences, Shanghai 200031, People's Republic of China; Department of Genetics and Development, College of Physicians and Surgeons of Columbia University, New York, NY 10032, USA.
3 Transgenic Animal Facility, Herbert Irving Comprehensive Cancer Center, College of Physicians and Surgeons of Columbia University, New York, NY 10032, USA.
4 Department of Biological Sciences, Dartmouth College, Hanover NH, USA; Department of Genetics and Development, College of Physicians and Surgeons of Columbia University, New York, NY 10032, USA.

* To whom correspondence should be addressed. E-mail: thb12{at}columbia.edu.

Complementary sets of genes are epigenetically silenced in male and female gametes in a process termed genomic imprinting. The Dnmt3L gene is expressed during gametogenesis at stages where genomic imprints are established. Targeted disruption of Dnmt3L caused azoospermia in homozygous males and heterozygous progeny of homozygous females died prior to midgestation. Bisulfite genomic sequencing of DNA from oocytes and embryos showed that removal of Dnmt3L prevented methylation of sequences that are normally maternally methylated. The defect was specific to imprinted regions and global genome methylation levels were not affected. Lack of maternal methylation imprints in heterozygous embryos derived from homozygous mutant oocytes caused biallelic expression of genes that are normally expressed only from the allele of paternal origin. The key catalytic motifs characteristic of DNA cytosine methyltransferases have been lost from Dnmt3L and the protein is more likely to act as a regulator of imprint establishment rather than as a DNA methyltransferase.


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