Examples of using Replication fork in English and their translations into Portuguese
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The assembly of two replisomes establishes two replication forks in opposite orientations.
The replication forks proceed bi-directionally until they meet at the opposite side of the chromosome the terminus region.
Once topoisomerase-I creates a single strand break,the DNA can rotate in front of the advancing replication fork.
The replication fork is a structure that forms within the long helical DNA during DNA replication. .
In replicating cells this leads to DNA double strand breaks(DSBs)when replication forks meet the PARP-DNA adduct.
Since the two strands of DNA molecule are antiparallel and replication fork separates the two strands at the same site, strand in the 5'→ 3' direction is easily replicated towards the opening of replication fork.
PCNA is required for the coordinated synthesis of both leading and lagging strands at the replication fork during DNA replication. .
Injuries that occur during dna replication, holds the replication fork lock, leading to overall response(sos) which will induce translesion synthesis tls.
Pol IV is a Family Y polymerase expressed by the dinB gene that is switched on via SOS induction caused by stalled polymerases at the replication fork.
Separation of DNA single strands leads to formation of replication fork, where the replication machinery(protein and enzyme complex) will bind.
Ligases are particularly important in lagging strand DNA replication, as they join together the short segments of DNA produced at the replication fork into a complete copy of the DNA template.
Depending on the type of lesion, this encounter result in replication fork collapse and consequently mechanisms able to circumvent these obstacles are activated.
The anti-tumour activity of topotecan involves the inhibition of topoisomerase-I,an enzyme intimately involved in DNA replication as it relieves the torsional strain introduced ahead of the moving replication fork.
In this process, several small fragments of the delayed chain are replicated as replication fork advances(5'→ 3') and further separates the double helix from DNA molecule.
The problem lies in the other strand, which is oriented in 3'← 5' direction, in which DNA polymerase cannot bind andperform its function because the opening of replication fork occurs in the opposite direction to replication. .
Another function of Pol IV is to perform translesion synthesis at the stalled replication fork like, for example, bypassing N2-deoxyguanine adducts at a faster rate than transversing undamaged DNA.
Studies in yeast have shown that telomeres are replicated from internal replication origins with replication forks moving toward the ends of chromosomes.
Deficient SMARCAL 1 cells show collapsed replication forks, cell cycle arrest in S phase, chromosomal instability and genomic hypersensitivity to toxic agents, changing cellular sensitivity to the replication infecting agents.
The main role of Pol II is thought to be the ability to direct polymerase activity at the replication fork and helped stalled Pol III bypass terminal mismatches.
Camptothecin forms a stable ternary complex, preventing normal DNA re-ligation, andcauses the complex to collide with the replication fork, leading to a DNA double-strand break and cytotoxicity.
In E. coli, a polymerase“tool belt” model for switching pol III with pol IV at a stalled replication fork, where both polymerases bind simultaneously to the β-clamp, has been proposed.