Final: Sem. 1 Essentials, Oncogenes + Signal Trans (Incomplete, Ben) Flashcards Preview

Y Biochem III > Final: Sem. 1 Essentials, Oncogenes + Signal Trans (Incomplete, Ben) > Flashcards

Flashcards in Final: Sem. 1 Essentials, Oncogenes + Signal Trans (Incomplete, Ben) Deck (11)
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1
Q

What kind of bond do DNA polymerases form and between which atoms?

A

Phosphodiester between ribose C3 and P grp on next nucleotide

2
Q

What are the prokaryotic DNA polymerases and their actions?

(as in polymerase… exonuclease… repair…gap filling etc.)

A
  • Polymerase I
    • 3>5, 5>3 exonuclease + 5>3 polymerase
    • low proc., gap filling, Okazaki primer removal and repair
  • Polymerase II
    • 3>5 exonuclease (proofread/repair only)
  • Polymerase III
    • main prokaryotic 5>3 polymerase, also 3>5 exonuclease
    • highly processive leading/lagging strand synth + proofread
  • “DnaG”
    • primase only (so not really a polymerase)
3
Q

What are the eukaryotic DNA polymerases and their actions?

A
  • Polymerase α
    • primase, gap filling + lagging strand synth (low processivity)
  • Polymerase β
    • 3>5 exonuclease
    • main eukaryotic repair polymerase, base excision
  • Polymerase γ
    • mitochondrial DNA synth + repair
  • Polymerase δ
    • main eukaryotic 5>3 polymerase, 3>5 exonuclease
    • leading/lagging synth, gap filling + proofreading
  • Polymerase Ɛ
    • can correct delta’s errors, minor role in synth
4
Q

Describe some important components / co-factors for DNA polymerase III and delta in their action of binding DNA.

A
  • DNA polymerase III
    • holoenzyme of many subunits, 2 β subunits = sliding DNA clamp
    • with primase + DNA proteins B/C = replisome
  • DNA polymerase delta
    • 4 subunits POLD1-4
    • uses separate protein PCNA as its sliding clamp
    • Replication Factor C“loads” PCNA onto the polymerase
5
Q

Where does replication initiate in prokaryotes + what characterizes the region?

What are the 7 components of the “replication bubble” there + their functions?

A

Starts at Ori C rich in A-T

  1. DNA A protein - binds origin + initiates replication
  2. DNA B protein - is helicase which unwinds DNA at origin using ATP
  3. DNA C protein - w/ helicase + primase, helps make primer
  4. SSBPs - bind single straded DNA to prevent re-annealing
  5. Primase - creates 4-10 bp RNA primer (+B+C = primosome)
  6. Topoisomerase II - w/ ATP creates negative supercoils, prevents tangle
  7. DNA polymerase III
6
Q

What histones make up the octamer?

What is the octamer plus DNA called?

And what is this unit plus the stretches of DNA between it?

A

Octamer = H2A, H2B, H3, and H4

Octamer + DNA = nucleosome

Nucleosome + DNA strand around H1 = Chromatosome

7
Q

How many DNA molecules are in a cell in G2 phase right before cell division?

A

92

the normal 46 chromosomes duplicated

8
Q

WHat is deaminated cytosine? adenine?

A

C is uracil, A is hypoxanthine

9
Q

What 3 enzymes perform depurination repair?

Which enzyme starts deamination repair followed by the action of the 3 just mentioned?

A
  • Depurination - endonuclease, polymerase I/Beta,Ligase
  • Deamination - starts with an DNA Glycosylase
10
Q

How are “transformed”/cancerous cells different from normal cells?

A
  1. No growth factor requirement
  2. No anchorage requirement
  3. Telomerase re-activated (“immortal”)
  4. No contact inhibition
  5. Increased glucose uptake
  6. Increased ability to trigger vascular growth
  7. Morphology changes (recepters, surface proteins, etc.)
11
Q

What is the most important tumor suppressor gene and what does it do?

Regulation?

A

P53

  • is a transcription factor for genes that encode cell cycle-inhibiting / apoptosis-promoting proteins such as cyclin dependent kinase inhibitors and BAX (respectively)
  • P53 is active when phosphorylated by DNA dependent kinases which bind to breaks in DNA, enhance P53 activity and thus arrest cell cycle
  • mutations of P53 are very common in tumors + can be caused by viruses