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Article: Gene silencing as a threat to the success of gene therapy.

Bestor, T H

2000 Volume 105, Issue 4, Page(s) 409–411

MeSH term(s)	Animals ; DNA, Viral/genetics ; Gene Silencing ; Genetic Therapy/methods ; Repetitive Sequences, Nucleic Acid ; Retroviridae/genetics ; Transcription, Genetic ; Transgenes
Chemical Substances	DNA, Viral
Language	English
Publishing date	2000-02
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Research Support, U.S. Gov't, P.H.S. ; Review
ZDB-ID	3067-3
ISSN	1558-8238 ; 0021-9738
ISSN (online)	1558-8238
ISSN	0021-9738
DOI	10.1172/JCI9459
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Article: The DNA methyltransferases of mammals.

Bestor, T H

Human molecular genetics

2000 Volume 9, Issue 16, Page(s) 2395–2402

Abstract: The biological significance of 5-methylcytosine was in doubt for many years, but is no longer. Through targeted mutagenesis in mice it has been learnt that every protein shown by biochemical tests to be involved in the establishment, maintenance or ... ...

Abstract	The biological significance of 5-methylcytosine was in doubt for many years, but is no longer. Through targeted mutagenesis in mice it has been learnt that every protein shown by biochemical tests to be involved in the establishment, maintenance or interpretation of genomic methylation patterns is encoded by an essential gene. A human genetic disorder (ICF syndrome) has recently been shown to be caused by mutations in the DNA methyltransferase 3B (DNMT3B) gene. A second human disorder (Rett syndrome) has been found to result from mutations in the MECP2 gene, which encodes a protein that binds to methylated DNA. Global genome demethylation caused by targeted mutations in the DNA methyltransferase-1 (Dnmt1) gene has shown that cytosine methylation plays essential roles in X-inactivation, genomic imprinting and genome stabilization. The majority of genomic 5-methylcytosine is now known to enforce the transcriptional silence of the enormous burden of transposons and retroviruses that have accumulated in the mammalian genome. It has also become clear that programmed changes in methylation patterns are less important in the regulation of mammalian development than was previously believed. Although a number of outstanding questions have yet to be answered (one of these questions involves the nature of the cues that designate sites for methylation at particular stages of gametogenesis and early development), studies of DNA methyltransferases are likely to provide further insights into the biological functions of genomic methylation patterns.
MeSH term(s)	Animals ; Catalysis ; DNA (Cytosine-5-)-Methyltransferase 1 ; DNA (Cytosine-5-)-Methyltransferases/genetics ; DNA (Cytosine-5-)-Methyltransferases/metabolism ; DNA Methylation ; DNA Methyltransferase 3A ; DNA Modification Methylases ; Female ; Humans ; Male ; Mammals ; Oocytes/enzymology ; Spermatocytes/enzymology ; DNA Methyltransferase 3B
Chemical Substances	DNMT3A protein, human ; DNA Modification Methylases (EC 2.1.1.-) ; Dnmt2 protein, mouse (EC 2.1.1.-) ; DNA (Cytosine-5-)-Methyltransferase 1 (EC 2.1.1.37) ; DNA (Cytosine-5-)-Methyltransferases (EC 2.1.1.37) ; DNA Methyltransferase 3A (EC 2.1.1.37) ; DNMT1 protein, human (EC 2.1.1.37) ; Dnmt1 protein, mouse (EC 2.1.1.37) ; TRDMT1 protein, human (EC 2.1.1.37)
Language	English
Publishing date	2000-10
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Research Support, U.S. Gov't, P.H.S. ; Review
ZDB-ID	1108742-0
ISSN	1460-2083 ; 0964-6906
ISSN (online)	1460-2083
ISSN	0964-6906
DOI	10.1093/hmg/9.16.2395
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Article: Gene regulation: stochastic and deterministic effects in gene regulation.

Edwards, J R / Bestor, T H

Heredity

2007 Volume 99, Issue 3, Page(s) 243–244

MeSH term(s)	Animals ; DNA Methylation ; Drosophila melanogaster ; Escherichia coli ; Genomic Imprinting/genetics ; Models, Genetic ; X Chromosome Inactivation/genetics
Language	English
Publishing date	2007-09
Publishing country	England
Document type	Journal Article ; Review
ZDB-ID	2423-5
ISSN	1365-2540 ; 0018-067X
ISSN (online)	1365-2540
ISSN	0018-067X
DOI	10.1038/sj.hdy.6801028
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Article: Sex brings transposons and genomes into conflict.

Bestor, T H

Genetica

1999 Volume 107, Issue 1-3, Page(s) 289–295

Abstract: ... Methylation also causes permanent inactivation in the germline by driving C-->T transition mutations ...

Abstract	Given that transposons are so abundant in mammalian genomes, it is natural to assume that through their maintenance the host gains some net benefit. This need not be true; sexual reproduction allows a transposon to go to fixation if the reduction in fitness of the host is anything less than two-fold. Obligate outcrossing sexual reproduction therefore favors the evolution of aggressive transposons, which in turn select for the evolution of host mechanisms that suppress transposon activity. Hosts that have asexual or self-fertilizing generations will select for transposons that are more benign and self-limiting than those of obligate sexuals, and obligate asexuals and uniparental organelle genomes will be free of active transposons if these impose any fitness penalty. We are interested in host mechanisms that suppress transposons in sexuals and have found that mammals (all of which are obligate sexuals) control their large populations of potentially active retroposons by methylating the five position of cytosine residues within promoter elements. This causes strong transcriptional repression and assembly of the affected sequences into the condensed state. Methylation also causes permanent inactivation in the germline by driving C-->T transition mutations at methylated sites. It is now known that methylation remains in place for the large majority of the life of germ cells and is essential for control of the very large transposon burden. There is pressure on transposons to evolve mechanisms that overcome host suppression, and over evolutionary time, the balance swings back and forth between parasite and host. The ability of the mammalian genome to absorb and accumulate additional transposons has caused the amount of reverse transcriptase coding sequence in the human genome to far exceed the sum total of all cellular coding sequence. While transposons could, in principle, contribute functions useful to the host, the fact that asexual species and uniparental organelle genomes lack transposons is strong evidence that transposons have a net deleterious effect even in genomes that might be thought to require an additional source of plasticity. The abundance of transposons in many genomes cannot be taken as evidence of a mutualistic relationship, and the conflict between transposons and genomes may have actually retarded rather than accelerated evolution. It is suggested that the relationship between sex and transposons is as follows: (i) Obligate sexuals will tend to harbor aggressive transposons limited largely by host suppressive mechanisms, which in mammals involve methylation of transposon promoters. (ii) The aggressiveness of transposons in facultative sexuals and self-fertilizing sexuals will be in part self-limited and will be proportional to the relative frequency of asexual and outcrossing sexual generations. (iii) Obligate asexuals arid organelles transmitted in a uniparental manner will have no active transposons if these have a net negative effect on host fitness.
MeSH term(s)	Animals ; Cytosine/metabolism ; DNA Methylation ; DNA Transposable Elements ; Genome, Human ; Germ Cells/metabolism ; Humans
Chemical Substances	DNA Transposable Elements ; Cytosine (8J337D1HZY)
Language	English
Publishing date	1999
Publishing country	Netherlands
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Research Support, U.S. Gov't, P.H.S.
ZDB-ID	2165-9
ISSN	0016-6707
ISSN	0016-6707
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Article: Cytosine methylation and the unequal developmental potentials of the oocyte and sperm genomes.

Bestor, T H

American journal of human genetics

1998 Volume 62, Issue 6, Page(s) 1269–1273

MeSH term(s)	Animals ; Cloning, Organism ; Cytosine/metabolism ; DNA Methylation ; Female ; Gene Expression Regulation, Developmental ; Genome ; Humans ; Male ; Oogenesis/genetics ; Spermatogenesis/genetics
Chemical Substances	Cytosine (8J337D1HZY)
Language	English
Publishing date	1998-06
Publishing country	United States
Document type	Journal Article ; Research Support, U.S. Gov't, P.H.S. ; Review
ZDB-ID	219384-x
ISSN	1537-6605 ; 0002-9297
ISSN (online)	1537-6605
ISSN	0002-9297
DOI	10.1086/301891
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Article: The decatenation checkpoint.

Damelin, M / Bestor, T H

British journal of cancer

2007 Volume 96, Issue 2, Page(s) 201–205

Abstract: The decatenation checkpoint delays entry into mitosis until the chromosomes have been disentangled. Deficiency in or bypass of the decatenation checkpoint can cause chromosome breakage and nondisjunction during mitosis, which results in aneuploidy and ... ...

Abstract	The decatenation checkpoint delays entry into mitosis until the chromosomes have been disentangled. Deficiency in or bypass of the decatenation checkpoint can cause chromosome breakage and nondisjunction during mitosis, which results in aneuploidy and chromosome rearrangements in the daughter cells. A deficiency in the decatenation checkpoint has been reported in lung and bladder cancer cell lines and may contribute to the accumulation of chromosome aberrations that commonly occur during tumour progression. A checkpoint deficiency has also been documented in cultured stem and progenitor cells, and cancer stem cells are likely to be derived from stem and progenitor cells that lack an effective decatenation checkpoint. An inefficient decatenation checkpoint is likely to be a source of the chromosome aberrations that are common features of most tumours, but an inefficient decatenation checkpoint in cancer stem cells could also provide a potential target for chemotherapy.
MeSH term(s)	Cell Line, Tumor ; Chromosomal Instability ; G2 Phase ; Humans ; Loss of Heterozygosity ; Neoplasms/genetics ; Neoplasms/pathology ; Stem Cells/cytology
Language	English
Publishing date	2007-01-29
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	80075-2
ISSN	1532-1827 ; 0007-0920
ISSN (online)	1532-1827
ISSN	0007-0920
DOI	10.1038/sj.bjc.6603537
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Article: Gene silencing. Methylation meets acetylation.

Bestor, T H

Nature

1998 Volume 393, Issue 6683, Page(s) 311–312

MeSH term(s)	Acetylation ; Animals ; Chromatin/metabolism ; Chromosomal Proteins, Non-Histone ; Cytosine/metabolism ; DNA/metabolism ; DNA Methylation ; DNA-Binding Proteins/metabolism ; Gene Expression Regulation ; Histone Deacetylases/metabolism ; Histones/metabolism ; Methyl-CpG-Binding Protein 2 ; Repressor Proteins/metabolism ; Transcription, Genetic
Chemical Substances	Chromatin ; Chromosomal Proteins, Non-Histone ; DNA-Binding Proteins ; Histones ; Methyl-CpG-Binding Protein 2 ; Repressor Proteins ; SIN3A transcription factor ; Cytosine (8J337D1HZY) ; DNA (9007-49-2) ; Histone Deacetylases (EC 3.5.1.98)
Language	English
Publishing date	1998-05-28
Publishing country	England
Document type	Comment ; News
ZDB-ID	120714-3
ISSN	1476-4687 ; 0028-0836
ISSN (online)	1476-4687
ISSN	0028-0836
DOI	10.1038/30613
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Article: The host defence function of genomic methylation patterns.

Bestor, T H

Novartis Foundation symposium

1998 Volume 214, Page(s) 187–95; discussion 195–9, 228–32

Abstract: It has long been held that reversible promoter methylation allows genes to be expressed in the appropriate cell types during development. However, no endogenous gene has been proven to be regulated in this way, and it does not appear that significant ... ...

Abstract	It has long been held that reversible promoter methylation allows genes to be expressed in the appropriate cell types during development. However, no endogenous gene has been proven to be regulated in this way, and it does not appear that significant numbers of promoters are methylated in non-expressing tissues. It has recently become clear that the large majority of genomic 5-methylcytosine is actually in parasitic sequence elements (transposons and endogenous retroviruses), and the primary function of DNA methylation now appears to be defence against the large burden of parasitic sequence elements, which constitute more than 35% of the human genome. Direct transcriptional repression provides short-term control, and the tendency of 5-methylcytosine to deaminate to thymidine drives irreversible inactivation. It is suggested that intragenomic parasites are recognized by virtue of their high copy number, and that the disturbances of methylation patterns commonly seen in human cancer cells activate a host of parasitic sequence elements, which destabilize the genome and tip the cell towards the transformed state.
MeSH term(s)	Animals ; Cytosine/metabolism ; DNA Methylation ; DNA Transposable Elements/immunology ; DNA, Neoplasm/metabolism ; Dosage Compensation, Genetic ; Genomic Imprinting ; Humans
Chemical Substances	DNA Transposable Elements ; DNA, Neoplasm ; Cytosine (8J337D1HZY)
Language	English
Publishing date	1998
Publishing country	England
Document type	Journal Article ; Research Support, U.S. Gov't, P.H.S. ; Review
ISSN	1528-2511
ISSN	1528-2511
DOI	10.1002/9780470515501.ch11
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Article ; Online: Photochemical conversion of a cytidine derivative to a thymidine analog via [2+2]-cycloaddition.

Li, Xiaoxu / Erturk, Ece / Chen, Xin / Kumar, Shiv / Guo, Cheng / Jockusch, Steffen / Russo, James J / Bestor, Timothy H / Ju, Jingyue

Photochemical & photobiological sciences : Official journal of the European Photochemistry Association and the European Society for Photobiology

2018 Volume 17, Issue 8, Page(s) 1049–1055

Abstract: ... intramolecular reactions that convert modified C to T analogues. We synthesized a model compound, a cinnamyl ...

Abstract	Epigenetic information is encoded in the mammalian genome in the form of cytosines methylated at the 5 position. Cytosine methylation has multiple biological effects, but our understanding of these effects has lagged because extant methods for mapping methylation sites genome-wide have severe shortcomings. For instance, the gold standard bisulfite sequencing approach suffers from the use of harsh reaction conditions resulting in DNA cleavage and incomplete conversion of unmethylated cytosine to uracil. We report here on a new photochemical method in which a DNA (cytosine-5)-methyltransferase can be used to covalently attach reactive functionalities which upon irradiation at ∼350 nm initiate photoinduced intramolecular reactions that convert modified C to T analogues. We synthesized a model compound, a cinnamyl ether-containing cytidine derivative, and demonstrated its conversion to a thymidine analogue using mild conditions and a DNA-compatible wavelength (∼350 nm), enabled by the use of a triplet sensitizer, thioxanthone. Transfer of a cinnamyl ether or comparable reactive functionality from an AdoMet analog to cytosine followed by the use of this photoconversion method would require only small amounts of DNA and allow complete methylation profiling on both long and short read sequencing platforms.
MeSH term(s)	CpG Islands ; Cycloaddition Reaction ; Cytidine/chemical synthesis ; Cytidine/chemistry ; DNA/chemistry ; DNA/metabolism ; DNA Methylation ; Lasers ; Magnetic Resonance Spectroscopy ; Photolysis ; Spectrophotometry, Ultraviolet ; Thioxanthenes/chemistry ; Thymidine/chemistry ; Xanthones/chemistry
Chemical Substances	Thioxanthenes ; Xanthones ; Cytidine (5CSZ8459RP) ; DNA (9007-49-2) ; thioxanthone (EOK1SAC304) ; Thymidine (VC2W18DGKR)
Language	English
Publishing date	2018-08-06
Publishing country	England
Document type	Journal Article
ZDB-ID	2072584-X
ISSN	1474-9092 ; 1474-905X
ISSN (online)	1474-9092
ISSN	1474-905X
DOI	10.1039/c8pp00161h
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Article ; Online: The colorful history of active DNA demethylation.

Ooi, Steen K T / Bestor, Timothy H

Cell

2008 Volume 133, Issue 7, Page(s) 1145–1148

Abstract: Patterns of DNA cytosine methylation are subject to mitotic inheritance in both plants and vertebrates. Plants use 5-methylcytosine glycosylases and the base excision repair pathway to remove excess cytosine methylation. In mammals, active demethylation ... ...

Abstract	Patterns of DNA cytosine methylation are subject to mitotic inheritance in both plants and vertebrates. Plants use 5-methylcytosine glycosylases and the base excision repair pathway to remove excess cytosine methylation. In mammals, active demethylation has been proposed to operate via several very different mechanisms. Two recent reports in Nature now claim that the demethylation process is initiated by the same enzymes that establish the methylation mark, the DNA methyltransferases DNMT3A and DNMT3B (Kangaspeska et al., 2008; Métivier et al., 2008).
MeSH term(s)	Animals ; DNA/metabolism ; DNA Methylation ; DNA Modification Methylases/metabolism ; Mammals/genetics ; Mammals/metabolism ; Plants/genetics ; Plants/metabolism
Chemical Substances	DNA (9007-49-2) ; DNA Modification Methylases (EC 2.1.1.-)
Language	English
Publishing date	2008-06-27
Publishing country	United States
Document type	Journal Article ; Review
ZDB-ID	187009-9
ISSN	1097-4172 ; 0092-8674
ISSN (online)	1097-4172
ISSN	0092-8674
DOI	10.1016/j.cell.2008.06.009
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Zs.MG 58: Show issues

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