Final Exam Lec16-19 Flashcards Preview

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Flashcards in Final Exam Lec16-19 Deck (97)
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1
Q

What is the role of Edeine

A

Binds to small ribosomal unit to block P site

2
Q

How does in vitro transcription and translation work

A

all necessary RNA polymerase, ribosomes, tRNAs, translation factors are isolated in a tube, just add DNA and protein is produced

3
Q

in bacterial mrnas, degradation is initiated by what?

A

an endonuclease, usually RNase E

4
Q

What inhibits RNase E activity

A

a 5’ triphosphate

5
Q

What do stem-loop structures do

A

inhibit exonucleases

6
Q

what helps degradation as bacterial mrnas are deconstructued

A

3’ poly(A) tract

7
Q

can endonuclease activity initiate degredation in eukaryotes?

A

yes

8
Q

what is the first step in RNA degredation in eukaryotes

A

poly(a) tail shortening by a deadenylase

9
Q

do 3’ poly(A) tails hinder or aid degredation in eukaryotes

A

hinder

10
Q

what do decapping enzymes do

A

remove the 5’cap

11
Q

What is viral ‘highjacking’ of translation

A

viral mrnas develop ways to compete for translation

12
Q

how do mrnas hijack translation

A

shut down translation of host mRNAs to hoard resources

13
Q

what is an example of viral hijacking

A

piconaviruses that cleave translation factors, flu viruses remove the 5’ xcap

14
Q

what is the role of picornavirsues

A

inhibit cap-dependent tranlsation, so themselves use cap-independant tranlsation by isng EREs within the 5’ UTR to directly recruit ribosomes

15
Q

what to rotaviruses lack

A

a 3’ poly(A) tail

16
Q

What do Viral mRNAs do to elimate the need to use hostprotein factors

A

make a closed loop complex via RNA-RNA interactions

17
Q

what are the three main principles of regulatory RNAs

A
  1. to yield the molecule
  2. employ complementary base pairing wtih DNA/RNA targets
  3. interact with other components (like proteins) to carry out their functions
18
Q

how do regulatory RNAs identify their targets

A

through base pairing

19
Q

what are the three ways regulatory RNAs can be encoded

A
  1. on the dna strand antisense to the target
  2. in a separate DNA region (trans)
  3. as part of the target (cis)
20
Q

how long are sRNAs usually

A

100-300 nt

21
Q

how are most sRNAs encoded

A

most encoded in trans

22
Q

where to sRNAs usually bind

A

close to the Shine-Delgarno motif

23
Q

how do some sRNAs affect degredation

A

by recruiting ribonucleases to the target

24
Q

What happens to RyhB when iron levels are low

A

ribosomes are prevented from binding, RyhB recruits Rnase E and the mRNA is degraded

25
Q

T or F: sRNAs can interact with multiple targets

A

T

26
Q

What kind of protein is Hfq

A

chaperone protein

27
Q

What is the role of the chaperone protein Hfq

A

a hexameric protein that helps sRNAs find their targets

28
Q

Wha thappens when Hfq levels in a cell are low

A

sRNAs compete for Hfq and it becomes part of the regulatory system

29
Q

High chitosugar levels induce what

A

transcription of a ‘decoy mRNA’

30
Q

T or F: regulatory RNAs are the same in eukaryotes vs bacteria

A

true

31
Q

are eukaryotic sRNAs longer or shorter than bacterial sRNAs

A

shorter

32
Q

what are the three classes of eukaryotic sRNAs

A

microRNAs (miRNAs)
Small interfering RNAs (siRNAs)
Repeat-associated small interfering RNAs (rasiRNAs)

33
Q

What is argonaute

A

binds to sRNAs and facilitates their interactions with complementary molecules

34
Q

T or F; All eukaryotic sRNAs carry out their functions in association with Arg

A

T

35
Q

What are the four Argnaute domains

A

N, PAZ, Mid and PIWI

36
Q

What does PAZ do

A

binds the 3’ end of bound RNA

37
Q

what does Mid do

A

interacts with the 5’ end of RNA

38
Q

What does PIWI do

A

related to RNase H and interacts wtih the whole RNA

39
Q

Where are sRNAs dervied from

A

from different types of long percursor molecules

40
Q

Where are miRNAs derived from

A

primary transcripts of genes

41
Q

where are si RNAs derived from

A

double stranded RNAs

42
Q

where are rasiRNAs derived from

A

repetitive regions of the genome

43
Q

what do processing cuts do

A

cut precursor RNAs to correct sRNA size

44
Q

What is drosha

A

relies on accessory protein for positioning and determination of fragment length

45
Q

what is dicer

A

determines the length of cleaved fragments by securing the 3’of the RNA with the PAZ domain and cutting it

46
Q

what are dicer and drosha

A

cutting enzymes

47
Q

T or F: several miRNAs can be produced from the same pri-miRNA

A

True

48
Q

what happens in the microprocessor complex

A

produces a 60-70 nt hairpin with 3’ OH and 5’ monophosphate, hairpin exported from the nucleus

49
Q

where are siRNAs derived from

A

double stranded RNAs from various endo or exogenous sources

50
Q

T are F: siRNAS are involved in clelular defense against exogenous RNAS

A

true

51
Q

how are MiR:miR* and siR:siR* similar

A

both have 3’OH and 5’ monophosphates

both undergo post-transcriptional modifications such as methylation

52
Q

what is the RISC complex

A

the guide RNA-Argonaute complex,

53
Q

what does miRISC do

A

usually pairs initially via 2-8 nucleotide seed sequence, 3’ end remains tightly bound by the PAZ domain

54
Q

what doe sthe siRISC do

A

an bind along its full length, releases PAZ domain and induces conformational change that activates PIWI domain

55
Q

where are miRNA binding sites usually found

A

in the 3’ UTR of the target sequence

56
Q

where does rasiRISCs do

A

can cleave target RNA, also have epigenetic effects

57
Q

how are foreign nucleic acids removed in eukaryotes

A

by RNA interference (RNAi)

58
Q

how is viral defence mediated in bacteria

A

CRISPR

59
Q

how does CRISPR work

A

contains 20-50 nucleotieds, cleaved foreign DNA cleaved, transcribed by Cas proteins to give short crRNAs

60
Q

What does dicer do

A

cleaves long dsRNA into short siRNA

61
Q

what does RISC do

A

RNA-induced silencing complex (includes argonaute)

62
Q

What is the purpose of CRISPR/Cas9

A

modification of HBB gene, rsponsible for Beta-thalassemia in embryos

63
Q

t or f: sRNAS are larger and more complex than regulatory RNAs

A

Fals

64
Q

What can riboswitches control

A

transcription, translation and RNA splicing

65
Q

T or F: riboswitches adopt complex 3D configuration

A

T

66
Q

Protein binding RNAs can act as _____ to bring proteins into close proximity with one another

A

tethers

67
Q

What are the three things that regulatory RNAs can bind to in order to exert effects

A

Other RNAs, Metabolites (Riboswitches), and Proteins (Chaperones, Endonucleases)

68
Q

What is PKU?

A

phenylketonuria, cannot metabolize phenylalanine and if consumed, mental retardation and ill helath results, genetic disorder, normally Phe converted to Tyr

69
Q

what are SNPs and what do they do

A

single nucleotide polymorphisms, used as markers for genomic analysis of human diseases

70
Q

what are microsattelites

A

can be used as genetic markers

71
Q

what is classic mapping

A

identifies marker all over a genome correlates marker with trait of interest

72
Q

T or F: SNPs and microsattelites are usually the cause of the rare disease under investigation

A

F

73
Q

What are SNP chips

A

used to detect SNPs at specific genomic loci

74
Q

recombination tends to take place in “___ ____”

A

“hot spots”

75
Q

What are the two ways of finding the cause of disease

A

linkage analysis and association studies

76
Q

What is linkage anaysis

A

Traces specific disease alleles within families

77
Q

what are association studies

A

identify disease genes by studying large groups of unrelated individuals,

78
Q

what is the common disease-common variant hypothesis

A

if a disease is common in a population, there will be a small number of allele for the gene that causes the disease

79
Q

T or F; whole genome sequencing is initally focused on the exome

A

true

80
Q

What is Pharmacogenomics

A

uses information from individual genomes to identify treatments that are more likely to be effective on certain individuals

81
Q

what is the difference between gain of function and loss of function genetic causes

A

Loss of function is a lack of gene expression, while gain of function causes an expression of a gene that causes a disease phenotype

82
Q

What are some of the pros and cons of chain termination dedeoxynucleotide sequencing

A
Pros:
-Highly accurate
-Widely avaliable
-Short time
-Cost manageable
Cons:
-expensive for fluorescent ddNTPS
-requires a primer
83
Q

What is Illumina dye sequencing

A

technique used to determine the series of base pairs in DNA , slide flooded with florescently labeled nucleotides

84
Q

what are some of the pros and cosn of Illumina sequencing

A
Pros:
-Highly accurate
-lower cost
Cons:
-short sequences obtained that must be analyzed computationally
85
Q

whats the difference ebtween a transition and transversion mutatoion

A

transition occurs if a purine is replaced by other purine or vice versa, whereas a transversion is a purine to a pyrimidine

86
Q

what is dna damage often caused by

A

cell metabolites

87
Q

T or F; DNA damage can occur from intra and extracellular agents

A

true

88
Q

UV light promotes what?

A

pyrimidine dimers

89
Q

what is an example of single point damage

A

depurination/depyrimidation

90
Q

What is a mismatch repair

A

fixes mistakes made during replication, using the other strand as a template

91
Q

what are the steps in a mismatch repairq

A
  1. mismatch recognized by MutH
  2. MutSLH complex assembles
  3. MutH nicks the new strand
  4. Nicked strand is digested by exonuclease
  5. DNA resynthesized
92
Q

what can repetitive regions of DNA form

A

hairpins, and can be skipped during replication

93
Q

what protein orchestrates apoptosis (cell death)

A

protein p53

94
Q

how does protein p53 control cell death

A

by binding at promoters of target genes to increase proteins that inhibit the cell cycle or stimulate apoptosis

95
Q

T or F: p53 is highly regulated

A

T

96
Q

how does p53 function when no DNA damage is present

A

Whne no DNA damage is present, MDM2 ubiquitinates lysines in p53 C-terminal domain, targeting it for degredation

97
Q

how does p53 function when DNA damage is present

A

kinase activity stimulated and results in phosphoyrilation of p53 and MDM2 so they no longer interact, p53 tetramerizes and interacts with transcription proteins, which acetylates histones and p53