module 5 Flashcards
parent strand/ template
Provide a platform for complementary base pairing to form a new duplex
daughter strand
newly synthesized strand of DNA 5>3; made by the addition of a nucleotide that is complementary to the parent strand of DNA
DNA polymerase I
Prokaryotic removed and replaced the primer
DNA polymerase III
Prokaryotic major replication polymerase
DNA polymerase alpha
Initiates replication by synthesizing primer
DNA polymerase beta
Replaces nucleotide in DNA repair
DNA polymerase epsilon
Major replication polymerase leading strand
DNA polymerase delta
Major replication polymerase lagging strand
primer
Short sequence of RNA that stabilizes the initial nascent daughter strand to parent strand
helicase
Separated duplex
RPA
Replication protein A
Single strand binding protein
Protect ssDNA
Prevent complementary base pairing
ssDNA BP
Used in bacteria
Protect ssDNA
prevent complementary base pairing
RFC
Replication factor c
Loads PCNA clamp
Used in eukaryotes
PCNA
Proliferating cell nuclear antigen
DNA clamp loading structure
Works with RFC in eukaryotes
primase
Used in bacteria
Add __NTP primer
topoisomerase
Enzyme that breaks binds of double stranded DNA to unwind and release supercoiling and synthesize starts
flap endonuclease/ FEn
In eukaryotes
Works with RNAse to remove primers
lagging strand
synthetic direction away from the growing fork
leading strand
can be replicated continuously and polymerization of the new strand moves with the fork
okazaki fragment
Lagging strand synthesized in short units (prokaryotic)
beta clamp
Used in bacteria
Clamp loaders
telomerase
Enzyme that elongates telomeres at lagging strand to provide a template
Has TERT, TERC
Adds repeating sequence
After extension, recruits DNA pol alpha
reverse transcriptase
extends the telomere lagging strand; enzyme used to generate complementary DNA from an RNA template
methyguanine methyltransferase
MGMT
Corrects alkylated guanine
Uses cystine residue to catalyze the reaction to methylate guanine
thymine dimer
Covalent bonding of adjacent thymines in DNA
caused by UV radiation
XPC
Functions to build scaffold that would have helicase and endonuclease activity
CSB
Works with XPC to recognize and repair DNA
Recognition protein
nucleotide excision repair
Fixes Large modifications covalently bonded to base intra cross link/ diners
base excision repair
Corrects small changes to DNA base
-Glycosylase recognize mismatch and flip it out, APE nicks one side of sugar and recruits phosphodiesterase to remove DNA sugar
-DNA pol beta adds new nucleotide
-last phosphodiester bond made by ligase
deamination
Loss of amine group
Replaced by oxygen to create free radical which is highly reactive
thymine glycol
when thymine is oxygenated twice and releases free radical oxygen which can impact the genome
thymine glycosylase
enzyme that targets and removes only thymine from sugar
uracil glycosylase
Flips incorrect uracil out to be cleaved
a-basic
When removal of base sugar creates apyrimidic or apurinic site
a-puranic
When purine is missing during BET process
(G and a)
a-pyrimidimic
When pyrimidine is missing during BET process (T and C)
endonuclease
enzymes that cleave the phosphodiester bond within a polynucleotide chain; create nicks
exonuclease
enzymes that work by cleaving nucleotides one at a time from the end of a chain
ligase
Completes last phosphodiester bond
MMR
mismatch repair
-done for mispairs and loops from insertion/ deletion events
repair system to correct mispaired bases in double stranded DNA from replication
MutS
Complex that checks for base stacking
-won’t stack if bases mismatched
MutL
Coordinate between mutS and mutH to put Nick where mismatch occurred
MutH
Recognize heavy methylated site for bacteria
MSH2
in eukaryotes
do recognition in MMR (G) for small loops and mistmatches
recognize on large loops
MSH3
recognize on large loops
MSH6
in eukaryotes
do recognition in MMR for mismatched pairs
MLH1
forms dimer during MMR
PMS2
forms dimer during MMR
endonuclease activity
Nicks the strand where the mis match occurred
IDL
insertion daughter strand
candidates for what causes DNA mismatches that need repaired
Ku 70/80
Proteins that interact w DNA protein kinase C
Used in NHEJ
MRE11-NBS1-Rad50 (trimer)
coordinates with pyH2AX
interacts with phosphorylated yH2X
NHEJ repair
always will result in deletion mutation
rare in bacteria, yeast, and Drosophilia
NonHomologous end joining repair
Used when double strand break occurs
holliday junction
occurs after DNA synthesis
homologous or nonhomologous repairs of a strand
Formed after rad 51 causes strand invasion
strand invasion
done by RAD51
one strand goes in and uses other strand as a template
forms loop in uncut duplex
TERT
Telomerase Reverse Transcriptase
protein enzyme that can extend the telomeres
TERC
Telomerase RNA
recruits DNA Pol alpha. DNA Pol alpha has a platform to
create the last Okazaki fragment
Rad51
Used in homologous recombination
Coordinates strand invasion process
Aneuploidy
Aberrant chromosome complements
benign tumor
Confined to local site or origin
malignant tumor
Faster rate of growth, rate may be same and apoptosis decreased so appears to grow faster
-poorly demarcated borders, invasive growth
5-fluro uracil
topical drug that halts DNA synthesis and that can be used to treat basal cell carcinoma
temozolamide
adds methyl groups to guanine during MGMT
iomeguatrib
cancer therapeutic; drug that targets MGMT so DNA repair is inhibited killing the cells much the same way as temozolamide
PAHs
Polycyclic Aromatic Hydrocarbons
DNA damaging agent
loss of heterozygosity
Happens in mitosis from chromosome non disjunction
Extra copies of chromosomes, degrades good chromosome
Homozygous mutant results
heterogenetic
produced by infection outside the body
hyperchromatic
malignant cells become this
nucleus that looks darker than normal when examined under the microscope
protooncogene
Cyclin
Growth factor
Receptor
Produce proteins which function to enhance cell growth/division
tumor suppressor gene
Regulate cell growth
Make sure stop correctly
P21 inhibits cell cycle
2 hits required
metastasis
Spread of cancer behind the primary tumor
-invasion into the extra cellular matrix
-vascular dissemination
anaplasia
lack of differentiation or poorly differentiated
differentation
extent to which parenchymal cells resemble normal cells
Benign- well differentiated
Malignant- less differentiated/ undifferentiated
contact inhibition
arresting cell growth when cells come in contact with each other
epigenetic mechanisms
Promotion of cancer by gene expression or misregulation rather than mutations
initiation
Works with promotor to induce tumor, will not cause by itself
promotion
Have to have enough promoter to induce tumor with initation
If enough spacing between promoters, won’t cause tumor
-chemical irritant, dietary fat etc
mutator phenotype
characteristic behavior of a cell that has lost DNA repair ability
non-disjunction
describes incorrect chromosome separation during M phase
angiogenesis
Formation of new blood vessels into the tumor
-supplies nutrients and oxygen and route for metastasis
hypo methylation
Loss inhibition
Genes that should be silenced are expressed
hyper methylation
Silence gene activity
ROSs
oxidative chemicals that can be initiators of cancer; can damage cellular proteins, lipids and DNA