D. Increase the transcription of target genes.
Rnase H and FEN1.
D. DNA helicase
1. Ribonucleotides (NTPs) 2. Deoxyribonucleotides (dNTPs) 3. Dideoxyribonucleotides (ddNTPs)
1. Pentose sugar (varies between NTPs, dNTPs, and ddNTPs) 2. Nitrogenous base 3. Phosphate group
DNA polymerase may skip some sequence, causing deletion mutations.
By the kinases that normally phosphorylate nucleosides and nucleotides.
At 42°C.
DNA polymerase.
D. Nuclear DNA associates with histone proteins to form chromatin.
Dideoxynucleoside triphosphates.
Cyclin dependent kinases (CDKs), cyclins, p53, RB, Ras, c-myc, and E2F.
E. Topoisomerase II
Twins with the shortest telomeres had a three times greater risk of death during the follow-up period than their co-twins with the longest telomere measurements.
It terminates the chain elongation of the DNA.
Continuously in the direction of replication fork movement.
Stabilize single-stranded DNA in the region of the replication fork.
It prevents hairpins from forming and also prevents re-annealing of the parental strands.
Growth factor signaling cascade.
DNA replication.
To covalently join DNA fragments together by forming phosphodiester bonds.
By joining one chain with a free 3'-OH group and one chain with a free 5'-phosphate group.
The two strands of parental DNA separate, and each serves as a template for synthesis of a new daughter strand by complementary base pairing.
Helicase, primase, and two molecules of DNA Polymerase III.
Both molecules of DNA polymerase.
To unwind DNA.
S-Cdk.
Ligase.
A repeating unit of chromatin.
Repetitive DNA sequences found at the ends of chromosomes.
To facilitate the attachment of chromosomes to kinetochore during cell division.
To enable the drug to target viral replication more specifically than cellular replication.
By the addition of nucleotides to its 3' end.
Ribose and deoxyribose.
In small pieces (Okazaki fragments) backward from the overall direction of replication.
Only at licensed origins.
DNA Pol I.
<p>Before the joining of Okozaki fragments. </p>
Stress, including psychological stress, has been shown to increase the rate of loss of telomeric DNA.
Shorter telomeric DNA is associated with an increased risk of aging-related diseases.
It terminates the chain elongation of viral DNA by lacking a 3'-OH group, preventing additional nucleotides from being attached.
Cut and reseal DNA in advance of the replication fork to eliminate supercoiling.
Cutting and resealing DNA in advance of the replication fork.
Therapeutic agents or in laboratory techniques such as DNA sequencing.
Both daughter cells will have one copy of mutated TP53.
DNA can't be religated.
The supercoiling of DNA ahead of the replication fork causing torsional stress.
Telomerase maintains telomere length.
5' to 3' only.
DNA Replication: Part I and DNA Replication: Part II.
Topoisomerase.
They do not have a hydroxyl group on either the 2- or 3-carbon.
Telomere length at advanced age is a biomarker that predicts survival beyond the impact of early familial environment and genetic factors.
RNA primers are used to initiate the synthesis of Okazaki fragments during DNA replication.
S phase.
It prevents further addition of nucleotides and terminates DNA synthesis.
Single-strand nicks.
Fluoroquinolone antibiotics like ciprofloxacin.
<p>bacteria pol III, mammals pol beta. </p>
Telomerase.
Preserve the 3’ overhang at the ends of chromosomes during replication.
It has 5 carbon atoms.
Double-strand breaks.
It can lead to a double-strand break.
They shorten.
<p>Gyrase is a bacterial Type II topoisomerase, so it makes double-strand breaks..</p>
https://drawittoknowit.com/course/ap-biology/prokaryotes/bacteria/1484/bacterial-genetics/video?autoplay=true&curriculum=ap-biology
Option C: TAACCTTGGACA
By causing chain termination due to the absence of a hydroxyl group on the 3-carbon.
During the S phase of the cell cycle.
It causes cell death.
Dideoxynucleotides lack a 3'-hydroxyl group.
It involves retaining half of the parent molecule in each daughter molecule.
Leading strand and lagging strand.
Removing RNA primers, proofreading, DNA repair, and filling in gaps left by DNA pol III.
They recruit Mcm helicase in G1.
They include a topoisomerase inhibitor.
I, II, III, IV & V.
It must have a 3’-OH on the target in order to add a nucleotide.
Cytoplasm.
To perform proofreading.
It folds back and provides structure for shelterin proteins to bind.
ATP.
DNA polymerase and other replication proteins bind within the bubble and begin DNA replication.
Helicase.
Polymerase d.
Preventing hairpins and keeping parental strands from reannealing.
Using FEN1 and RNaseH.
Binding to template DNA and the sliding clamp, synthesizing DNA 5’ to 3’.
DNA replication.
Telomeres.
Prokaryotic DNA replication.
Synthesizing most of the DNA and has proofreading activity.
They generate progressively shorter telomeres and are likely to reach senescence.
<p>Telomeres and they consist of many tandem copies of a 6 bp DNA sequence, plus proteins that bind.</p>
To bind to exposed single strands and stabilize the DNA for replication.
To decrease supercoiling caused by unwinding.
In germline cells, stem cells, and over 85% of cancer cells examined.
They can be activated.
The pre-replication complex is disassembled, and multiple redundant mechanisms ensure that it can't form again until the next G1, preventing re-replication of DNA.
It is a type II topoisomerase used by bacteria.
High degree of genomic instability due to increased recombination.
It acts as a reverse transcriptase.
It hydrolyzes ATP as it loads the clamp onto a primer-template junction.
It stabilizes the telomeres, allowing the cells to proliferate indefinitely, making them immortal.
Numerous origins.
S phase.
Okazaki fragments.
Initiator proteins.
It synthesizes RNA fragments about 10 base pairs long using DNA as a template.
It is removed when the neighboring growing strand reaches the primer stretch.
They undergo chromosome shortening every time they divide.
Unwinding the helix.
PCNA (proliferating cell nuclear antigen).
S phase.
Genomic rearrangements.
Bi-directional replication.
To replicate all base-pairs within the 6-8 hours of S phase of the cell cycle.
Telomerase.
It binds to the origin throughout the cell cycle.
Genetic and environmental factors.
Ribonucleotides have OH, while deoxyribonucleotides have just H.
Only in mitochondria.
It is temporarily displaced but quickly rebinds to the replicated DNA, preventing the other components of the pre-replicative complex from binding to the phosphorylated form of ORC.
Disruption of the cell cycle or cell aging (senescence).
Senescence.
It chews away misincorporated nucleotides.
Sealing the nicks.
Helicases.
Approximately 1,000 nucleotides long.
Primers cannot be placed at the very end of the parental linear DNA.
DNA ligase.
It can cause decreased capacity for repair due to depletion of stem cell populations.
Eukaryotes have multiple origins, while prokaryotes have a single origin.
Protect ends of chromosomes from degradation and fusion, and distinguish ends of intact chromosomes from broken ones.
To correct misincorporated nucleotides.
DNA repair and replicative polymerase that may substitute for d in certain cases.
Origins of replication.
Bi-directional from each origin.
By making reversible nicks in the DNA.
It acts as a swivel ahead of the fork.
Most somatic cells.
It acts as an active helicase, separating the strands to create the replication bubble and moving away from the origin with the replication forks.
It holds DNA polymerase to the template DNA as long as it's moving, but releases it when double-stranded DNA is reached.
MCM.
It can be a cause and/or an effect of disease.
A ring-like structure.
Making RNA primer.
To remove RNA primers.
Removing RNA primers, gaps filled by DNA pol.
A single origin.
Approximately 220 origins.
Topoisomerases.
To release the tension and prevent double-strand breaks.
RNA primers are removed by DNA polymerase I and Okazaki fragments are joined by DNA ligase.
Pre-RC (pre-replicative complex) which 'licenses' the origin at the end of G1.
No, telomeric DNA doesn’t encode any proteins.
They increase the rate of telomere attrition.
Cell cycle checkpoint mechanisms.
Semi-conservative replication.
Primase activity of DNA pol α can use it as a template to synthesize an RNA primer.
DNA polymerases.
Unwinds strands of DNA at the replication forks.
A sliding clamp.
Circular.
It is involved with the initial synthesis of DNA strands off RNA primers.
To synthesize new DNA strands.
Short stature, photosensitivity, multiple health problems, and increased risk of cancer.
Cells continue to proliferate without telomeres, leading to genomic instability and crisis.
It acts as a template for reverse transcriptase activity.
Displace and reassemble nucleosomes.
Transcriptionally active DNA (euchromatin).
By DNA polymerase using adjacent newly synthesized DNA to provide the 3’OH.
About 1 in 100,000 nucleotides.
Loss of telomeric DNA.
A rare disorder caused by mutation of a helicase.
A clamp loader.
Loading sliding clamp around 3’ end of the primer.
It base-pairs with the G-rich, single-stranded 3′-end of telomeric DNA.
In the usual 5′→3′ direction.
Circular and do not have telomeres.
It is extended by DNA pol α and then removed by nucleases.
Licensing of origins in G1, and removal of the license from origins already used.
Constitutive heterochromatin.
<p>Phosphodiester bond between the phosphate group on its 5' carbon and the hydroxyl group on the 3' carbon of the nucleotide added in the previous step (5'-> 3').</p>
<p>Dideoxyribonucleotides have just H, while deoxyribose has OH. </p>
<p>alpha, beta, delta, gamma, epsilon</p>
<p>patients with AIDS. </p>
<p>high accuracy, high speed and processivity. </p>
<p>proofreading. </p>
<p>cell death by apoptosis.</p>
<p>They initiate DNA replication. </p>
<p>RNA polymerases. </p>
<p>primosome. </p>
<p>in the DNA Polymerase alpha complex. it initiates DNA replication. </p>
