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Frequent replication, however, may point toward lead genes.
Whereas a severe limitation in dNTPs leads to frequent replication fork stalling (and probably reversal) and dependence on recombination enzymes, the mild limitation studied here, led to a controlled slowing of replication forks.
The increased C period obtained after HU-treatment could be explained by a reduced rate of fork movement in general or by frequent replication fork stalling causing an extended replication period due to repair of stalled forks.
The same mutant was also found to generate stalled replication forks at the permissive temperature that was not due to the limited supply of dNTPs, but rather assumed to be due to the presence of a less efficient replication hyperstructure causing frequent replication pauses [13].
In addition to frequent replication pauses at the 5′ and 3′ ends, Koike and Wolstenholme [ 36] point out that mtDNA replication is a discontinuous process.
Their heterochromatic nature and the interference of DNA-protein complexes and higher-order DNA secondary structures can induce frequent replication pausing.
Similar(51)
We also detected a large number of amino acid mutations (n = 35) that arose during recent dispersion of modern-lineage (subclade 1E) in Brazil and Venezuela, which could reflect more frequent viral replication cycles in large susceptible populations of primates from non-endemic regions and/or selective pressures for new viral variants with specific phenotypic characteristics.
Consequently, less frequent genome replication and reduced efficiency of purifying selection may contribute to the slower pace of nucleotide substitutions and higher dN/dS ratios of subterranean rodent genomes.
The defining aspect of DPP, the long repeating phosphorylation domain, apparently undergoes frequent slip replication and recombination events that rapidly change specific patterns but not its overall biochemical character in toothed animals.
The evidence available suggests a model whereby increased S-phase entry and more frequent DNA replication would be permissive for the maintenance of epigenetic marks already present, but would prohibit the stable loading of histone H1 and interaction with epigenetic regulator complexes.
As telomerase, the reverse transcriptase that adds telomere repeats to the ends of chromosomes, is largely repressed in somatic cells, including HSCs (Broccoli et al., 1995; Chiu et al., 1996; Yui et al., 1998), more frequent HSC replication would augment the rate of LTL shortening.
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