Lecture 5 Flashcards
(17 cards)
The Ames test uses bacteria without the capability of producing _____. They are plated on agar lacking ______ and grow colonies only if there is a ____ mutation to allow the bacteria to produce _____.
Histidine
Histidine
Reversion
Histidine
One common example of DNA lesions that occurs as a result of chemotherapy is the ________ of guanine.
Methylation
In nucleotide excision repair (NER), XPC-R23 scans DNA for damage. When it recognizes damage, it recruits ________ which nicks the DNA on either side of the damage, leaving a gap of about 12-30 NTs, which is filled in by polymerase.
Exonucleases
Base excision repair, unlike NER, initially cleaves only the _____ bond of a DNA base (the enzyme that carries this out is specific to the base for which the bond is being cleaved), and this leaves an _____ site. Then, ____ endonuclease and ___________ remove the sugar phosphate (essentially cleave the strand, leaving a gap where the base was removed from). Same as with NER, polymerase and ligase fill and seal the deal.
Glycosyl bond
AP endonuclease
Phosphodiesterase
Ribonucleotide Excision Repair (RER) initiates when _____ H2 (only active on RNA-DNA hybridization) nicks the DNA strand on the _____ side of the RNA that was incorporated. Then, DNA polymerase dispaces the side where the nick was made, leaving behind a flap of DNA that is cleaved by _____ endonuclease.
RNase H2
5’ side
FLAP endonuclease (FEN1)
________ pigmentosum is a disease in which patients suffer from hypermutagenisis bc of a defect in which one of the following?
NER
BER
RER
Xeroderma pigmentosum (XP)
NER
Why is it that loss of NER functionality is more severe than loss of the other excision repair pathways?
NER is a generalist pathway. It can recognize more types of DNA damage than the other excision pathways, which are more specific.
Why are actively transcribed genes given “priority” with excision repair pathways? That is, what might act to signal the repair pathways?
RNA Pol stalling at the damage site acts as a signal to recruit repair complexes.
______ syndrome (autosomal ________) is caused by the loss of CS-A or CS-B, or certain partial defects in _____, 3’ to 5’ helicase in DNA repair mech, ______, 5’ to 3’ helicase in DNA repair mech, or XPG. Symptoms include _______sensitivity, growth and mental retardation, premature ______, but LITTLE skin cancer.
Recessive
XPB
XPD
Photosensitivity
Aging
____________ (TTD - autosomal _______) is a progeroid syndrome characterized by growth and mental retardation, brittle _____ and _____ due to _____ deficiency, UV sensitivity; half of these patients are also partially defective for DNA repair helicases ______ (3’ to 5’) and ______ (5’ to 3’), as well as transcription/repair factor ______. These patients, like CS patients, show LITTLE skin cancer.
Recessive
Hair
Nails
Sulfur
XPB
XPD
TFIIH
Different defects in _____ (5’ to 3’ helicase) can lead to different phenotypes (XP, CS, or TTD). CS and TTD arise from defects affecting the _______ aspect, while XP arise from a defect affecting the NER aspect. Keep in mind all three phenotypes can be present at the same time, but the severity of XP supersedes CS and TTD.
XPD
Transcriptional
There are a few types of non-excision DNA repair pathways. Photoreactivation involves the enzyme ______, which uses energy from visible light to correct _____ dimers.
O6-_______ DNA methyl transferase is an enzyme involved in repair of alkylating mutagenisis. It transfers the methyl group onto itself. Once the enzyme acquires the methyl group, it becomes inactivated, so a cell’s capacity to repair these lesions depends on what?
Photolyase
TT dimers
O6-methylguanine DNA methyltransferase
The amount of the enzyme present.
DNA double strand break can be repaired via non-______ recombination or ______ recombination. Two proteins bind the ends of the breaks in non-______ recomb:
- ______
- ______
These proteins also recruit other proteins to bring the ends together and rejoin them.
non-homologous
homologous
non-homologous
Ku70
Ku80
_______ syndrome is autosomal _____ and is characterized by growth defects and cancer predisposition. Patients also show _____ sensitivity, skin pigmentation, Chromosomal instability, male _____, and female sub-_____. These patients show characteristic ______ chromosomes (due to a defect in ______.) This syndrome arises from a defect in BLM, a gene coding for a _____-like helicase.
Bloom Syndrome
Recessive
Sun-sensitivity
Infertility
sub-Fertility
Harlequin chromosomes
Recombination
RecQ-like helicase
_____ Syndrome is a progeroid syndrome characterized by high levels of chromosomal instability. It is caused by a defect in the WRN protein, a _____-family helicase, a unique helicase with both helicase and _____ activity.
Werner Syndrome
RecQ-family helicase
Nuclease
p___ is a protein whose major function is as a _____ factor. It recognizes DNA damage and causes cell cycle arrest to allow the cell to repair the DNA damage. If the damage is irreparable, the cell enters _____ (programmed cell death.)
p53
Transcription factor
Apoptosis
Pol-____ acts only in when DNA Pol stops bc of a TT dimer. Pol-____ adds AA across from the dimer and allows DNA Pol to continue. _____ ______ Variant (XPV) patients suffer from hypermutagenisis bc they lack Pol-____.
Pol-Eta
Pol-Eta
Xeroderma Pigmentosum Variant (XPV)
Pol-Eta
