Transcription Flashcards

1
Q

RNA polymerase

A
  • -doesnt use a primer!

- -much more error prone than DNA pol., not a big deal since mRNA’s dont stick around forever like DNA

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2
Q

RNA Pol. I

A
  • -synthesizes 28S, 18S, and 5.8S rRNA (5S done by Pol. III)

- -

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3
Q

Each Ribosomes contains

A

–one copy of each rRNA: 28S, 18S, 5.8S, 5S

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4
Q

RNA Pol. III

A
  • -5S rRNA

- -systhesis of tRNA molecules

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5
Q

Cells have multiple copies of which genes?

A

rRNA and tRNA to produce adequate quantities to support ribosome/protein synthesis

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6
Q

Pol. II

A

mRNA

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7
Q

Promoters of RNA synthesis

A
  • -TATA, CAAT boxes or GC rich region

- -A/T rich regions are easier to pull apart

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8
Q

Enhancers of RNA synthesis

A

–enhance transcription but can be found many hundreds of BPs away from gene that is enhanced

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9
Q

TFIID

A
  • -made up of many proteins
  • -has TBP (TATA box binding protein)
  • -binds to DNA and causes distortion
  • -signpost for other GTF’s and Pol II
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10
Q

Death Cap Mushroom

A
  • -amanita phalloides
  • -90% of deaths from mushrooms worldwide
  • -alpha-amantin toxin which inhibits Pol. II
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11
Q

Rifampicin

A
  • -antibiotic
  • -inhibitor of RNA pol
  • -Euk. Pol II unaffected by it
  • -can selectively kill bacteria
  • -good against mycobaterium tuberculosis
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12
Q

5’ capping

A

modifies mRNA and helps cell distinguish mRNA from other types of RNA

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13
Q

Spliceosome

A
  • -made up of snRNA and protein

- -protein = scaffold and snRNA = catalytic unit used to splice out introns

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14
Q

Export of mRNA from nucleus

A
  • -doesnt occur w/o capping, splicing and polyadenylation
  • -nuclear pore recognizes if these modifications have/have not been made and will not export any unmodified mRNA which will be degraded in nucleus
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15
Q

Degradation of mRNA

A

removal of 5’ cap and some of poly-A tail and then ribonucleases degraded mRNA from both ends

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16
Q

Beta-Thalassemia

A
  • -incorrect splicing of mRNA
  • -mutations that result in reduced synthesis of the Beta-chain of hemoglobin
  • -mutation around splice site recognized so another splice site is used
17
Q

PKU

A
  • -cannot convert Phe to Tyr

- -common mutation in PKU Pts. single base change in the 5’ splice donor site of one particular intron

18
Q

HAT vs HDAC

A
  • -HAT’s acetylate histones reducing their negative charge to loosen interactions w/ DNA and promote transcrition
  • -HDAC’s de-acetylate histones to condense DNA more around histones
  • -lysine residues ususally acetylated
19
Q

DNA methylation

A

–occurs on cytosine residues and recruits HDACs to de acetylate the DNA

20
Q

3 Types of Gene regulatory proteins and where do they bind?

A
  • -helix turn helix: side chains of AA bind to DNA
  • -zinc finger: zinc coordinated to histidine and cysteine
  • -leucine zipper: dimer of two alpha-helix form coiled coil, every seventh AA is hydrophobic leucine
  • -all bind in major groove!
21
Q

Rubenstein-Taybi Syndrome

A

–point mutations, small deletions or rearrangements in genes encoding CBP or EP3000

22
Q

Tamoxifen

A
  • -competitive inhibitor of estrogen receptor
  • -estrogen receptor when bound w/ estrogen and activate transcription
  • -inhibits tumor growth in breast cancer
  • -Tamoxifen/receptor complexes still bind to DNA but fail to recruit additional proteins needed to transcribe