CORSO- powerpoint 5 - EXAM 1

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57 Terms

1
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What is the difference between a pyrimidine and purine?

pyrimidine- 1 ring

purine- 2 rings

<p>pyrimidine- 1 ring</p><p>purine- 2 rings</p>
2
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What’s the difference between names like adenine and adenosine? Cytosine and Cytidine? Guanine and Guanosine? Thymine and Thymidine? Uracil and Uridine

the difference is that adenine, cytosine, guanine, thymine, and uracil are THE BASE ONLY, when you ADD RIBOSE THEY turn into adenosine, cytidine, guanosine, thymidine, and uridine

3
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What’s the difference between a nucleoside and a nucleotide?

A nucleoside doesn’t have a phosphate. (nucleotide= phosphate + nuceloside)

4
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What’s the difference between DNA and RNA?

DNA uses deoxyribose, RNA uses Ribose—> there is a 1 oxygen difference

5
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In addition to DNA and RNA, what else are nucleic acids used for?

  • cAMP

  • CoA

  • ATP

  • FAD

  • NAD+

6
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DNA is how many strands? What bases pair with each other?

  • DNA is 2 strands

  • A pairs with T

  • C pairs with G

7
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DNA and RNA is synthesized in the___’—>___’ direction

5’—> 3’

8
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Where is the phosphate attached to on the bases of DNA and RNA?

Since DNA and RNA goes in the 5’—>3’ direction, The phosphate is attached to the 5’ OH group on the ribose before and the 3’ OH group on the ribose after it

<p>Since DNA and RNA goes in the 5’—&gt;3’ direction, The phosphate is attached to the 5’ OH group on the ribose before and the 3’ OH group on the ribose after it</p>
9
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What is the primary and secondary structure of DNA?

primary- amino acid sequence

secondary- double helix

10
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What is the tertiary and quaternary structure of DNA?

tertiary- the double helix that is SUPERCOILED

quaternary- DNA wrapped around histone proteins/ thickness of the chromosome

<p>tertiary- the double helix that is SUPERCOILED</p><p>quaternary- DNA wrapped around histone proteins/ thickness of the chromosome</p>
11
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What are histone proteins? Why are they attracted to DNA?

proteins that are HIGHLY positively charged (bc of lysine and arginine), attracted to DNA because DNA is negatively charged

12
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What are centromeres and telomeres?

centromeres- point of attachment between two chromosomes after DNA duplication

telomeres- protective caps on linear chromosomes (protect chromosome from degredation)

<p>centromeres- point of attachment between two chromosomes after DNA duplication</p><p>telomeres- protective caps on linear chromosomes (protect chromosome from degredation)</p>
13
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What are the stages of the cell cycle? When does the cell divide? When is DNA synthesized?

  1. M- MITOSIS aka CELL DIVIDES

  2. G1

  3. S- DNA SYNTHESIS OCCURS

  4. G2

  5. repeat steps

14
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How do G0 and GTD interact with the cell cycle?

G0- contact inhibition? basically a nondividing state

GTD- terminally differentiated aka no more cell cycle

15
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What is the importance of the restriction point in the cell cycle?

to avoid mitotic catastophe

16
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What does semiconservative replication mean?

when we replicate 1 strand of DNA is new and 1 is old

<p>when we replicate 1 strand of DNA is new and 1 is old</p>
17
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What is the OriC site? What is the OriC site high in?

aka the origin of DNA replication or where DNA replication starts—— high in A-T pairs to make it easier to unzip

18
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How many replication forks does the OriC site have?

2

19
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What is a replisome?

collection of enzymes at the replication fork

20
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How does the OriC site on eukaryotic DNA compare to prokaryotic DNA?

in prokaryotes- one OriC site

in eukaryotes- multiple OriC sites

<p>in prokaryotes- one OriC site</p><p>in eukaryotes- multiple OriC sites</p>
21
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What are topoisomerases and what is the difference between type 1 and type 2?

  • they are needed to uncoil DNA before replication and then recoil after

  • difference between type 1 and type 2

    • type 1- break one strand and change linking number by 1

    • type II- break both strands and change linking number by 2

<ul><li><p>they are needed to uncoil DNA before replication and then recoil after</p></li><li><p>difference between type 1 and type 2</p><ul><li><p>type 1- break one strand and change linking number by 1</p></li><li><p>type II- break both strands and change linking number by 2</p></li></ul></li></ul><p></p>
22
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IN CANCER—→ WHY DO WE WANT TO INHIBIT TOPERISOMERASES?

  • said “possible exam question”

they can function to suppress rapidly dividing cells

23
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What is a replication fork?

where we separate DNA in order to synthesize new DNA

24
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Since DNA is ONLY synthesized in the 5’ to 3’ direction, what problem does this create?

creates a problem for the lagging strand that is anti parallel so it has to be synthesized in fragments

25
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What is a primer? What is a primer made of?

  • MADE OF RNA

  • used to START DNA synthesis

  • basically these RNA primers about 10-60 are put on the unzipped DNA before DNA polymerase comes in and puts down new DNA bases

26
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What is an Okazaki fragment?

  • basically how we synthesize the lagging strand

  • we make short fragments of DNA aka OKAZAKI FRAGMENTS and they are later joined together to make the new DNA strand <3

27
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How are primers removed?

DNA polymerase I

28
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How does the cell know which strand of DNA was the original strand?

once in awhile we add an extra methyl on DNA, when DNA replication occurs the new strand is not methylated

29
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What is methyl directed mismatch repair? What is the only sequence methyl’s are found on? Is the new strand or old strand methylated?

(i’m very sorry my explanation is long I just want to explain it well)

  • BASICALLY the problem is that we have a mismatched base (ex: A—> G). This methyl mismatch repair process will FIX the “mismatched” bases. We assume that the old strand has the correct base (A), and the new strand has the wrong base (G, when it should be T). However, we need to be able to tell which is the old and which is the new strand in order to fix the problem and that’s where the methyl on the old strand comes in. The NEW strand does NOT have this. Therefore, once we can tell which strand is which we can go in, form a loop around the wrong base, nick it, and replace it with the right base!!!!!!!!!!!

  • only sequence—> GATC//// methyl is attached to the adenosine (A) of this

  • OLD STRAND IS METHYLATED

30
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How does the cell know if DNA is paired correctly?

Only A=T and C=G have the correct distance between them. Other combos can hydrogen bond but the distance is different and recognized as incorrect

31
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When does methyl mismatch repair take place during the cell cycle?

S phase or DNA synthesis

32
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Mismatch repair defects are most associated WITH WHAT CANCER???

  • said “TEST QUESTION”

colorectal

33
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All repairs in DNA must be made before the…

restriction point (right before S phase)

34
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What is deamination and how does it cause mutations? What are some agents that promote deamination?

  • said “possible test question”

  • what is it? removal of nitrogen from a base

  • how does it cause mutations? turns it into the wrong base

  • agents- NITROSAMINES

35
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What are alkylations?

  • add a extra methyl (CH3) group

36
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What is depurinations?

  • basically we remove the purine group (which we know has 2 rings)

37
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Depurinations, dealkylations, and deamination’s are all examples of _____________ mutations.

chemical

38
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What type of repair is for right after DNA replication?

methyl mismatch repair

39
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What type of repair is to correct chemical mutations (smaller mutation)?

base-excision repair

40
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What type of repair is to correct larger mutations?

nucleotide-excision repair

41
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What type of repair is used to reverse mutations?

direct repair

42
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Explain how base excision repair works:

  1. we have a chemical mutation to one of the bases (depurination, alkylation, etc.)

  2. we remove the base

  3. we remove the DNA backbone

  4. DNA polymerase I comes in and adds new DNA to repair

  5. seal the nick

43
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The biggest mutation that deals with nucleotide excision repair is pyrimidines like thymine being mutated into _____________.

dimers

44
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What disease can be caused by a defect in nucleotide excision repair and causes EXTREME sun sensitivity, leading to high skin cancer risk and other problems?

Xeroderma Pigmentosum

45
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Direct repair is simpler than other types of repair but requires more ___________.

UV light

46
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explain direct repair:

  • Purpose: Reverses specific types of DNA damage directly, without excision

  • examples: repairs thymine dimers using UV light and alkylation’s using ENZYMES

47
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What is cross over repair? What is another name for crossover repair?

  • also known as “recombinational repair”

  • we have 2 chromosomes—> if one is damaged beyond repair, we can use the code from the good chromosome, cross it over, and duplicate it

48
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What genes are associated with cross-over repair? If defective what cancers are associated with each?

  • BRCA 1

    • breast cancer, cervical

  • BRCA 2

49
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What gene prevents the cell cycle from going into the S phase when elevated?

p53 gene (a tumor suppressor gene)

50
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What are the role of cyclins?

proteins necessary to pass restriction points

51
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What’s the difference between necrosis and apoptosis?

necrosis- “crush/break/damage”—> exposure to toxin or physical damage—> membrane damage, cell swelling and lysis

apoptosis- programmed cell death—> cell is not needed—> usually no lysis

52
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What factors can trigger apoptosis?

  • TNF

  • growth factors

  • radiation/toxins

53
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What is the Ames Test? What does it correlate?

  • said test question

  • TEST FOR MUTANOGENECITY

  • Correlation with cancer is 90%

54
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What is an allele?

different variations of the same gene found in different individuals

<p>different variations of the same gene found in different individuals</p>
55
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What is the difference between polymorphism and mutations?

polymorphism- variations that occur in more >1% of the population

mutation- variations that occur in <1% of the population

56
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What is an SNP?

single nucleotide polymorphism

57
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the most common DNA sequence within a population is called the ___________.

wild type