Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

CAN > Maintenance of genome > Flashcards

Maintenance of genome Flashcards

1
Q

How does damage to the DNA occur?

A

Copying errors during DNA replication
* Spontaneous depurination
* Exposure to different agents
e.g. background ionising radiation, UV light, tobacco

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What are the five different ways to repair DNA

A
  • Direct reversal of damage
  • Base excision
  • Nucleotide excision repair
  • Homologous recombination repair and non homologous end joining
  • DNA mismatch repair

DR: occurs mainly in prokaryotes

BE: corrects DNA damage caused by reactive oxygen species deamination, hydroxylation, spontaneous depurination

NER: - removes adducts that
produce large distortions in DNA

homologous: repairs DNA double strand
breaks

DMR: repairs copy errors made
during replication

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

How does guanine being methylated become problmatic

A
  1. Guanaine binds to cytosine
  2. but because its been methylated guanine
  3. O 6 alkyl guanine pairs with thymine.
  4. on next replication of strand thymine will pair with adenine instead
  5. this causes a kink in DNA
  6. causes problems during replication,
  7. DNA polymerase cant synthesise DNA becasue of kink so cell dies
  8. if methyl guanine does not cause cell death, it can cause mutageninis, (e.g O-6 alkyl)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

How can UV damage DNA

A
  1. can cause thymine dimers (two adjacent thymine bases become covalently crossed linked)
  2. causes a disotrion in DNA
  3. creates problems when replicating

Way 2
1. Can create 6-4 photoproducts

UV damage can be mutagenic

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

How does the cell solve UV induced dimmers

in bacteria

A

can be removed by photolipase
humans dont do this

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

How do we remove methylated bases

A

use alkyl tranferase to remove alkyl group

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

How do we fix strand breaks in sugar phosphate backbone

A

ligate them back together

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

In what situations would a cell do base exicision repair

A
  1. Spontaneous hydrolytic depurination of DNA.
  2. Deamination of cytosine (changes into uracil)
  3. Exposure to reactive small
    metabolites (causes DNA adducts)

class switchig is the only time cytsoime is converted into uracil

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

How does BER work

A
  • remove base using glycoslayes
  • this site is now abasic (theres the S-P backbone)
  • apuric endonuclease releases that there is a base missing, it removes the site (removal of sugar and base)
  • DNA polymerase comes along fills in gap
  • ligase and then good to go
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

How does Nucleotide excision repair work

A
  • works on double stranded not single stranded (not useful in DNA replication)
  • Non specfic -> recgonises disortions, not specific adducts
  • removes large adducts
  • effiecent and error free

how does it work
1. XPC gene recgonises 6, 4 proudct (specfic example)
2. endonueclase cut the distortion (e.g XPB, + D) -> use single stranded binding protein is present to stop DNA being cut up since its vulnerable
2. exonuecluses remove damged bit of DNA (e.g XPF AND G)
3. DNA polymerase fills in Gap
4. then ligase pulls it back together

we use this process usually for UV light

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What is XERODERMA PIGMENTOSUM

epidemology, what is it,

A
  • Autosomal recessive disorder
  • happens to 1,4 per million
  • exteremly sensitive to sun
  • develop tumors
  • can have neurological abnormalities due to lack of NER
  • cells have defect in DNA nucleotide excision repair
  • XP cells show a high mutation rate (may be due to unexcised dimers, so incorrect bases are incorporated to oppose damage)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What can mutations in the PTCH 1 gene cause

A

can cause basal cell carcionmas

patients with XP that also had BCC had problems with PTCH1

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

DNA replication doesnt stop in XP, so it uses daughter strand gap repair

how does that work

A

1.DNA polymerase hits thymine dimmer cant get passed it
2.DNA polymerase goes passed it somehow
3.and this leads to daughter strand gaps
4. the thymine dimer is still present + XP variants come in here

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What happens in XP variants

A
  • in XP there is a defect in repliation of DNA after UV exposure
    • the enxyme DNA polymerase n, is defeinct in this disorder, which makes it unable to replicate DNA past UV photoproducts
  • in the absence of the proper DNA polymerase, so XP variants come along
  • but these arent great at their job, and can cause muataions to happen
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

How does DNA double strand break happen

A
  • Caused by errors in replication
  • Reactive oxygen species (cellular metabolism) -> hair dying, teeth whitening
    exposure to ionising radiation (x rays, cosmic rays, chemo)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

BRCA 1 structure

A

has two critical domains
means its a E3 ubiquntine ligase
- likes putting ubiquitin on other proteins

17
Q

BRCA 2 structure

A

-has BCR repeats
-need this to bind to Rad51
-twice as big as BRCA 1

18
Q

what is the role of BRCA 1 and 2

A

allow for repair for double strand breaks via

1.Non-homologous end joining
2.Homologous recombination repair

19
Q

How does homologous recomboination repair work

A

1.detect break, by MRe11/Rad50/NBs1
2.this cuts DNA and leaves a small amount of single stranded DNA
3.single stranded DNA binds to Rad51
4. Rad51 then looks at undamaged strand, to find exact sequence
5. BRCA1 and 2 load Rad51 onto DNA
6. so you form interlinked DNA
7. the cell does DNA synthesise across the break, a loop forms
8. and tnen the cell can synthesise new strand across this using the undamaged dna strand template
9. problem the two strands connect
9. then you unconnect the two strands
10. ligase and then dip

problem: two strands end up together idk dk what he said

for this process you need to exact temeplate so happens in s phase and stuff

20
Q

What is the difference between BRCA 1 and 2

A

BRCA 2 involved in controlling Rad51

BRCA 1 has roles in Rad51 but also functions like checking cell cycle check points

Cells deficient in BRCA1/2 are unusually sensitive to PARP inhibitors

21
Q

What are PARP inhibitors

A

PARP is an enzyme that make chains of ADP ribose
the inhibitor prevents this
if you inhibit PARP, it gets trapped in DNA so you get double strand break with protein stuck on end
you need homologous recombination to repair this

if you dont have this the cell can die (double strand breaks are BAD)

22
Q

when does a cell induce double strand breaks

A

when making immune cells b and t lymphocytes
during meiosis -> swapping of genes

23
Q

How does Non homologus end joining work

A
  1. Break in DNA is sensed by Ku70/86 heterodimmer
  2. binds to end of DNA
  3. recurits kinase called DNA PKcs
  4. this becomes active kinase, phosphyrlates proteins
  5. can trigger artemis (trims back DNA to reveal some single stranded DNA)
  6. single strand DNA undergoes microhomology base pairings
  7. Flap gets removed

no idea how this works

24
Q

How does DNA mistmacth repair work

A
  1. repairs base mistmatches
  2. can repair insertion deletion loops due to polymerase slippage -> microsatalite instablity -> important in huntingtons

Can get microstalitie instability, even though you fixed DNA more likely to get mutations

25
Q

What is the mutator phenotype hypothesis

A

-if you have base mismacthes and repeated sequences
-if you cannot repair this using DNA mismatch repair,
-then more mutations can happen
-can lead to adenoma to become carcinoma
-you need to get additional mutations

CAN (10 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions