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In synchronous or eager replication, changes are propagated to replicas before the success of the write operation is acknowledged to the client.
This timing pattern of DNA replication changes throughout development as cells differentiate and is intimately linked to the chromatin state.
In transcription and replication, changes in the chromatin structure are required in order to allow binding of the factors involved [ 4, 5].
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We next investigated how the inhibition of DNA replication changed the chromatin proteome.
Recently, several studies have established a functional link between DNA repair and A-type lamin-associated syndromes, which are associated with transcriptional alterations, abnormal DNA replication, changed organization of higher order chromatin structure, and genomic instability (Serrano and Blasco 2007), suggesting a link between these syndromes and physiological aging (as seen in HGPS).
To be sure of the meaning of a positive DNA result, we have to assess either the total viral load (a higher viral load is typically associated with active viral replication) or changes in value over time (at least a 3-fold change in value is necessary to confirm significant changes in viral replication) [ 17].
Some replication timing changes can directly provoke overt genomic instability and induce dramatic mutational changes, such as chromothripsis and kataegis [149,150].
Furthermore, certain replication timing changes can directly lead to overt genomic instability and may explain unique mutational signatures that are present in cells that have undergone the recently described processes of "chromothripsis" and "kataegis".
Additionally, the results of the current study reveal that the anti-hypertrophic effects of MEF2C depletion may be related to a defective mobilization of mTOR/S6K by pressure overload, which may be associated with an intricate mechanism that involves negative modulation of the mtDNA replication and changes in myocardial energy metabolism caused by defective activation of PGC-1α.
To examine the statistical significance of replication timing changes, we first converted data sets to numeric vectors of 9,612 average replication-timing ratios of nonoverlapping 100 kb windows.
It is largely unknown what mechanism drives replication timing changes during loss of pluripotency and exactly what forces the pluripotency "indicator" domains to replicate early in ESCs.
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