1.6: Regulation of the Transcriptome Flashcards

1
Q

what composes the c terminal domain in humans

A

7aa repeated 52x in humans

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2
Q

the binding of rna processing proteins is regulated by ______ of rnap (of the ctd)

A

phosphorylation

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3
Q

list the 3 markers of mature mRNA, which must be acquired for export from the nucleus

A
  1. cap binding complex (CBC)
  2. exon junction complexes (EJC)
  3. poly a binding proteins
    these travel w the mRNA to the cytosol
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4
Q

what is the marker of immature mRNA that must be lost for export (must lose them before rna is considered as mature)

A

proteins involved in rna splicing (eg snRNPs)

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5
Q

what vesicle degrades improperly processed mRNAs in the nucleus

A

exosome

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6
Q

what is the probability that rna leaves the nucleus

A

1/20

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7
Q

why should the prevention of aberrant proteins be maintained

A

bc aberrant proteins can be toxic to cells

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8
Q

mRNA message is decoded in ________ that are resource intensive, aa’s are added to the _________ end of the growing polypeptide chain

A

ribosomes, c-terminal

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9
Q

what is the direction of protein synthesis

A

n to c terminus

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10
Q

what features do translation initiation machinery recognize

A

the 5’cap and poly a tail

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11
Q

which eukaryotic initiation factors are bound to 5’ cap and poly a tail

A

5’ cap bound by eIF4E
poly a binding protein bound by eIF4G

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12
Q

what do eukaryotic initiation factors do

A
  • recruit small ribosomal complex which will initiate translation at first AUG downstream of 5’ cap (some exceptions)
  • ensure both ends of mRNA are intact
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13
Q

how can the ejc stimulate translation

A

ensuring proper splicing

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14
Q

what is the prominent mRNA surveillance system and how does it work

A

it is nonsense mediated mRNA decay, it surveys for nonsense (STOP) codons in the wrong place which is an indicator of improper splicing

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15
Q

regarding nonsense mediated mRNA decay, describe the normal splicing pathway

A

the ribosome binds mRNA as it emerges from the nuclear pore to the cytosol, EJCs are displaced by the first moving ribosome, the stop codon is in the last exon. no ejcs remain bound when the ribosome reaches the stop codon, and mRNA is released in the cytosol bc it passed quality control

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16
Q

regarding nonsense mediated mRNA decay, describe the abnormal splicing pathway

A

the ribosome binds mRNA as it emerges from the nuclear pore, ejcs are displaced by the moving ribosome, the stop codon is premature, the ejcs remain on the mRNA when the ribosome reaches the stop codon, the remaining ejcs signal for Upf proteins to degrade the mRNA

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17
Q

where in the cell does nonsense mediated mRNA decay occur and is it pre/post transcriptional regulation

A

it occurs in the cytosol, and it is post transcriptional gene regulation

18
Q

is the nonsense mediated mRNA decay pathway for eukaryotes or prokaryotes

A

eukaryotes

19
Q

describe mRNA quality control in prokaryotes

A

ribosomes stall on broken or incomplete mRNAs and don’t release it, a tmRNA is recruited to the A site (it carries an alanine amino acid and acts as both tRNA (without anticodon-codon binding) and mRNA), broken mRNA is released, alanine is added onto the polypetide by the tmRNA, the ribosome translates 10 codons from tmRNA (alanine (not always but common) x10 + stop), the 11th aa tag is recognized by proteases that degrade the entire protein

20
Q

in prokaryotes, what enzyme rapidly degrade most mRNAs

A

exonucleases

21
Q

what is the critical length of poly a tails in humans

A

25 nucleotides

22
Q

what acts a timer of mRNA lifetime

A

exonucleases (deadenylase) when mRNA reaches the cytoplasm

23
Q

what are the (2) processes that are involved in mRNA stability, after the gradual shortening of the poly a tail

A
  1. decapping followed by rapid 5’ to 3’ degradation
  2. no decapping with continued 3’ to 5’ degradation
24
Q

t/f can cytoplasmic poly a ELONGATION occur to stabilize mRNA

A

true - as in if the tail gets too short, just make it longer again if you really wanna keep the protein

25
Q

what can aconitase do

A

interfere w poly a shortening

26
Q

what is the stimulus for the transferrin receptor

A

cellular iron is low - it imports iron into the cell

27
Q

describe the mrna stabilizing with transferrin

A

it imports iron into the cell when cellular iron is low == transferrin receptor is made. mRNA is stabilized by cytosolic aconitase and binds to 3’UTR.
when there is excess iron, aconitase binds iron and undergoes a conformational change, mRNA is released, and it exposes 3’ UTR endonucleolytic cleavage site (poly a removed)=mRNA is degraded

28
Q

describe the mrna stabilizing with deadenylase

A

there is competition between mRNA translation and mRNA degradation, deadenylase shortens the poly A tail binds the 5’ cap (like eIFs) = degradation. the process can also occur in reverse

29
Q

are miRNAs (microRNAs) coding

A

no

30
Q

how can miRNAs regulate mRNA stability

A

miRNAs base pair with specific mRNAs, it’s synthesized rnapII and get a 5’ cap and poly a tail. after special processing, the miRNA associates with a protein complex called a RNA induced silencing complex (RISC) –> RISC seeks mRNA with complementary nucleotide seq and a protein of RISC called argonaute plays a critical role in bp miRNA with mRNA

31
Q

what does RISC seek

A

mRNA with complementary nucleotide sequences - RISC is like a seq used as a targeting mech

32
Q

state the role of argonaute

A

base pairing miRNA with mRNA

33
Q

describe the 2 outcomes of argonaute and RISC

A
  1. extensive match: of miRNA to mRNA. splicing occurs, atp required. rapid mRNA degradation of the entire strand leading to no more protein
  2. less extensive match: the miRNA is not completely paired with mrna seq which leads to rapid translational repression, deadenylation and in most cases the eventual degradation of mRNA
34
Q

can RISC be reused

A

yes

35
Q

what is rna interference (RNAi)

A

they destroy double stranded rnas. double stranded rnas that end up suppressing the gene expression of other RNAs in a seq specific manner

36
Q

the proteins used in the miRNA regulatory mechanisms also serve as?

A

defense mechanisms against foreign rna molecules

37
Q

a scientist places high levels of a mirna targetting sxl rna into all cells of a developing drosophila embryo. thhis results in sxl rna being specifically and completely destroyed. no other RNAs are destroyed. which of the following will be observed?
a. the drophila will develop into a male
b. the drophila will develop into a female
c. the drophila will develop into a male only if the x:a ratio is 0.5
d. the drophila will develop into a female only if the x:a ratio is 1

A

a

38
Q

can you describe prokaryotic immunity relating to crispr-cas immunity

A

short fragments of viral dna integrate into the crispr region of the genome = templates = crrnas (crispr rnas). the viral dna complementary to crispr regions are directed for degradation by cas (crispr associated) proteins

(uses rna to cut dna) == the crRNAs are like a targetting mech to cut double stranded viral dna nad they can remember it

39
Q

which 4 types of rna are present in prokaryotes

A

trna, mrna, tmrna, crrna

40
Q

highlight the role of siRNAs in regulating transcription

A

siRNAs not only can interact w argonaute and risc proteins and follow the mirna route to destroy double stranded rna, they can also interact w argonaute and the rna induced transcriptional silencing (rits) complex.

one option is that they degrade dsRNA (double stranded), specifically only one of the 2 strands, by using viral rna as the targeting mech. this uses argonaute and risc.

another option is they induce transcriptional silencing by using rits. rits interacts w newly transcribed rna (recognizes it’s a viral dna) and recruits chromatin modifying enzymes (histone or dna methylation) to make the dna compact = cannot be read.

41
Q

describe how rnai can destroy double stranded rna as post transcriptional gene regulation

A

it’s initiated by dicer protein complex. some viruses have dsRNA which gets cut by the dicer leading to siRNAs (small interfering RNAs).