DNA methylation and late replication probably aid cell memory, and type I DNA reeling could aid chromosome folding and enhancer function

1990 ◽  
Vol 326 (1235) ◽  
pp. 285-297 ◽  
Keyword(s):  
Dna Methylation ◽  
X Chromosome ◽  
Replication Timing ◽  
X Chromosome Inactivation ◽  
Chromosome Inactivation ◽  
Type I ◽  
Late Replication ◽  
Cell Memory ◽  
Strong Candidate

DNA methylation in mammals is reviewed, and it is concluded that one role of methylation is to aid cell memory, which is defined as the ability of mitotically derived progeny cells to remember and re-establish their proper cellular identity. Methylation of X-linked CpG-rich islands probably stabilizes X-chromosome inactivation, but other mechanisms appear to be involved. Late replication is discussed as a key ancestral mechanism for X inactivation, and it is emphasized that early and late replication domains may each be self perpetuating. Therefore, early-late replication timing becomes another strong candidate mechanism for cell memory. A chromosome-loop folding enigma is discussed, and it is concluded that special mechanisms are needed to explain the formation and maintenance of specific looped domains. DNA reeling, such as done by type I restriction-modification enzymes, is proposed to provide this special mechanism for folding. DNA reeling mechanisms can help to explain the cis -spreading of X-chromosome inactivation as well as long-range action by enhancers.

scholarly journals DNA metylation as one of the main mechanisms of gene activity regulation

2004 ◽  
Vol 2 (1) ◽  
pp. 27-37
Author(s):  
Anna A Pendina ◽  
Vera V Grinkevich ◽  
Tatyana V Kuznetsova ◽  
Vladislav S Baranov
Keyword(s):  
Dna Methylation ◽  
Genomic Imprinting ◽  
X Chromosome ◽  
Epigenetic Inheritance ◽  
X Chromosome Inactivation ◽  
Chromosome Inactivation ◽  
Gene Repression ◽  
Activity Regulation ◽  
Inherited Diseases

 DNA methylation is one of the main mechanisms of epigenetic inheritance in eukaryotes. In this review we looked through the ways of 5-methylcytosin origin, it's distribution in genome, the mechanism of gene repression via hypermetilation, the role of metylation in genomic imprinting and in X-chromosome inactivation, in embryogenesis of mammals, in the processes of oncogenesis and in etiology of some common human inherited diseases

scholarly journals Do LINEs Have a Role in X-Chromosome Inactivation?

2006 ◽  
Vol 2006 ◽  
pp. 1-6 ◽  
Author(s):  
Mary F. Lyon
Keyword(s):  
X Chromosome ◽  
X Chromosome Inactivation ◽  
Chromosome Inactivation ◽  
Current Evidence ◽  
X Chromosomes ◽  
Repeat Elements ◽  
Sequencing Project ◽  
Human Genome Sequencing ◽  
Human And Mouse

There is longstanding evidence that X-chromosome inactivation (XCI) travels less successfully in autosomal than in X-chromosomal chromatin. The interspersed repeat elements LINE1s (L1s) have been suggested as candidates for “boosters” which promote the spread of XCI in the X-chromosome. The present paper reviews the current evidence concerning the possible role of L1s in XCI. Recent evidence, accruing from the human genome sequencing project and other sources, confirms that mammalian X-chromosomes are indeed rich in L1s, except in regions where there are many genes escaping XCI. The density of L1s is the highest in the evolutionarily oldest regions. Recent work on X; autosome translocations in human and mouse suggested failure of stabilization of XCI in autosomal material, so that genes are reactivated, but resistance of autosomal genes to the original silencing is not excluded. The accumulation of L1s on the X-chromosome may have resulted from reduced recombination or late replication. Whether L1s are part of the mechanism of XCI or a result of it remains enigmatic.

Changes in DNA methylation during mouse embryonic development in relation to X-chromosome activity and imprinting

1990 ◽  
Vol 326 (1235) ◽  
pp. 299-312 ◽  
Keyword(s):  
Gene Expression ◽  
Dna Methylation ◽  
Embryonic Development ◽  
X Chromosome ◽  
De Novo ◽  
Germ Line ◽  
X Chromosome Inactivation ◽  
Chromosome Inactivation ◽  
Chromatin Configuration ◽  
Methylation Patterns

Changing DNA methylation patterns during embryonic development are discussed in relation to differential gene expression, changes in X-chromosome activity and genomic imprinting. Sperm DNA is more methylated than oocyte DNA, both overall and for specific sequences. The methylation difference between the gametes could be one of the mechanisms (along with chromatin structure) regulating initial differences in expression of parental alleles in early development. There is a loss of methylation during development from the morula to the blastocyst and a marked decrease in methylase activity. De novo methylation becomes apparent around the time of implantation and occurs to a lesser extent in extra-embryonic tissue DNA. In embryonic DNA, de novo methylation begins at the time of random X-chromosome inactivation but it continues to occur after X-chromosome inactivation and may be a mechanism that irreversibly fixes specific patterns of gene expression and X-chromosome inactivity in the female. The germ line is probably delineated before extensive de novo methylation and hence escapes this process. The marked undermethylation of the germ line DNA may be a prerequisite for X-chromosome reactivation. The process underlying reactivation and removal of parent-specific patterns of gene expression may be changes in chromatin configuration associated with meiosis and a general reprogramming of the germ line to developmental totipotency.

scholarly journals Stochastic epigenetic mutations (DNA methylation) increase exponentially in human aging and correlate with X chromosome inactivation skewing in females

Aging ◽  
2015 ◽  
Vol 7 (8) ◽  
pp. 568-578 ◽  
Author(s):  
Davide Gentilini ◽  
Paolo Garagnani ◽  
Serena Pisoni ◽  
Maria Giulia Bacalini ◽  
Luciano Calzari ◽  
...  
Keyword(s):  
Dna Methylation ◽  
X Chromosome ◽  
X Chromosome Inactivation ◽  
Chromosome Inactivation ◽  
Human Aging
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