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Biochemistry- First Aid > Biochemistry First Aid- Molecular > Flashcards

Biochemistry First Aid- Molecular Flashcards

1
Q

what is a nucleosome

A

a nucleosome consists of DNA wrapped twice around a histone octamer

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2
Q

histones are rich in what two amino acids

A

lysine and arginine

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3
Q

what type of histone molecule connects consecutive nucleosomes

A

H1

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4
Q

what’s the difference between heterochromatin and euchromatin

A

heterochromatin is “highly condensed” and inaccessible for transcription; euchromatin is “truly transcribed”

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5
Q

what does DNA methylation do for mismatch repair

A

DNA methylation (at adenine and cytosine) occurs in new DNA and is absent from old DNA; this allows DNA mismatch repair enzymes to differentiate old and new DNA

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6
Q

what does methylation of CpG islands do?

A

represses transcription

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7
Q

what does histone methylation do?

A

can activate or repress transcription depending on the context

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8
Q

what does histone acetylation do

A

relax DNA coiling allowing for transcription

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9
Q

which base has a methyl group

A

thymine

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10
Q

which base has a ketone

A

guanine

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11
Q

from which base is uracil made and how

A

uracil is made via deamination of cytosine

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12
Q

which base pair has 3 H-bonds

A

C and G

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13
Q

which base pair has 2 H-bonds

A

A and T

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14
Q

what does 6-MP do

A

6-mercaptopurine inhibits purine synthesis from PPRP (phospho-ribosyl pyrophosphate)

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15
Q

how are purines synthesized

A

PRPP (sugar + phosphate) is added to a base to make IMP which then becomes either AMP or GMP

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16
Q

how are pyrimidines synthesized

A

carbamoyl phosphate becomes orotic acid which joins PRPP to make UMP. UMP becomes UDP which becomes either CTP or dUDP. (deoxyUDP) dUDP becomes dUMP which becomes dTMP

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17
Q

what does nucleotide reductase do and what drug inhibits it

A

nucleotide reductase converts UDP to dUDP and it is inhibited by hydroxyurea

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18
Q

what does thymidylate synthase do and what is it inhibited by

A

thymidylate synthase converts dUMP to dTMP (deoxyuracil monophosphate to deoxythymine monophosphate) by converting THF to DHF; it is inhibited by 5-FU

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19
Q

what does dihydrofolate reductase do and what drug is it inhibited by

A

dihydrofolate reductase converts DHF to THF and it is blocked by methotrexate and trimethoprim

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20
Q

what does ornithine transcarbamoylase (OTC) do and what does its deficiency cause

A

OTC is a key enzyme in the urea cycle and its deficiency leads to accumulation of carbamoyl phosphate leading to orotic acid build up

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21
Q

what enzyme defect causes orotic aciduria

A

defect in UMP synthase which catalyzes conversion of orotic acid to UMP

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22
Q

how do you differentiate between orotic aciduria and OTC deficiency

A

hyperammonemia in OTC; no hyperammonemia in orotic aciduria

OTC doesn’t cause megaloblastic anemia while orotic aciduria does

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23
Q

name some findings for orotic aciduria

A

failure to thrive, megaloblastic anemia, high urinary orotic acid

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24
Q

how is orotic aciduria treated

A

oral uridine administration

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25
Q

what pattern of inheritance does orotic aciduria have

A

autosomal recessive inheritance

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26
Q

what does adenosine deaminase do and what does its insufficiency cause

A

adenosine deaminase converts adenosine to inosine;
deficiency of this enzyme leads to excess ATP and dATP causing feedback inhibition of ribonucleotide reductase leading to low lymphocyte count and SCID

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27
Q

what is the inheritance pattern of adenosine deaminase deficiency

A

autosomal recessive

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28
Q

what causes Lesch-Nyhan syndrome

A

absence of HGPRT (hypoxanthine guanine phosphoribosyltransferase, which converts hypoxanthine to IMP and guanine to GMP) leading to excess uric acid production and de novo purine synthesis

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29
Q

what is the inheritance pattern of Lesch-Nyhan syndrome

A

X-linked recessive

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30
Q

what are the clinical findings of Lesch-Nyhan syndrome

A 
H=hyperuricemia
G=gout
P=pissed off (aggression/ self-mutilation)
R=mental retardation
T=dystonia (choreoathetosis)
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31
Q

name four features of the genetic code

A

unambiguous, degenerate (redundant), commaless (nonoverlapping), universal

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32
Q

what does it mean that the genetic code is commaless or nonoverlapping and what kind of organism is an exception to this rule

A

the genetic code is read from a fixed starting point as a continuous sequence of bases; some viruses are an exception to this rule

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33
Q

what does it mean that the genetic code is degenerate or redundant

A

most amino acids are coded by multiple codons (except for methionine and tryptophan encoded by AUG and UGG, respectively)

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34
Q

name the four kinds of point mutations

A
  1. silent (same amino acid)
  2. missense (diff. amino acid)
  3. nonsense (stop codon)
  4. frameshift
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35
Q

what does helicase do

A

unwind DNA at the replication fork

36
Q

what do single-stranded binding proteins do

A

prevent strands from reannealing

37
Q

what do DNA topoisomerases do

A

unwind DNA supercoiling by creating nicks in the helix

38
Q

what drug inhibits DNA gyrase (prokaryotic topoisomerase II)

A

floroquinolones

39
Q

what does primase do

A

primase makes an RNA primer on which DNA polymerase III can initiate replication

40
Q

which organisms have DNA polymerase III

A

prokaryotes only

41
Q

what two activities does DNA polymerase III perform during replication

A

synthesis (in the 5’ to 3’ direction)

proofreading (in the 3’ to 5’ direction)

42
Q

which organisms have DNA polymerase I

A

prokaryotes only

43
Q

what does DNA polymerase I do

A

degrades RNA primer and replaces it with DNA (can excise in the 5’ to 3’ direction)

44
Q

what does DNA ligase do

A

catalyzes phosphodiester bonds to anneal fragments of DNA (i.e. joins Okazaki fragments)

45
Q

what does telomerase do

A

adds extra DNA to 3’ ends of chromosomes to protect the genetic material

46
Q

how does nucleotide excision repair work

A

specific endonucleases cleave oligonucleotides containing damaged bases, DNA polymerase and ligase replace and reseal the gap; this process repairs bulky helix-distorting lesions

47
Q

what disease is associated with defects in nucleotide excision repair

A

xeroderma pigmentosum (pyrimidine dimers due to UV persist)

48
Q

how does base excision repair work

A

Base-specific glycosylase recognizes altered base and creates AP site (apurinic/apyrimidinic). Nucleotide(s) are removed by AP-endonuclease, which cleaves the 5’ end. Lyase cleaves the 3’ end. Gap is filled by DNA polymerase beta and resealed by DNA ligase.

49
Q

what specific problem is base excision repair important for

A

repair of spontaneous/ toxic deamination

50
Q

how does mismatch repair work

A

a newly synthesized strand is recognized (via methylation), mismatched nucleotides are removed and the gaps are filled and resealed

51
Q

what disease is associated with defective mismatch repair

A

mutation in mismatch repair is associated with hereditary nonpolyposis colorectal cancer (HNPCC)

52
Q

what does nonhomologous end joining entail

A

bringing together two ends of double stranded DNA to fix double stranded breaks

53
Q

in what disease is nonhomologous end joining mutated

A

ataxia telangiectasia

54
Q

in what direction is protein synthesized

A

N to C

55
Q

in what direction along the DNA is the DNA proofread during DNA replication

A

3’ to 5’

56
Q

in what direction do the newly synthesized DNA and RNA strands grow during synthesis and trascription respectively

A

5’ to 3’

57
Q

which component of the nucleotide does the incoming nucleotide contribute to the phosphodiester bond

A

the incoming nucleotide binds with its triphosphate (“the nucleotide provides the energy for the bond”)
the 5’ triphosphate is attacked by 3’OH

58
Q

which type of RNA is most abundant

A

rRNA

59
Q

which type of RNA is the smallest

which is the longest

A

tRNA is smallest

mRNA is longest

60
Q

what is the start codon

A

AUG (rarely GUG)

61
Q

what are the stop codons

A

UGA, UAA and UAG

62
Q

where are enhancers located relative to the genes whose expression they alter

A

close to, far from or even within (in an intron) the gene

63
Q

what is a gene silencer

A

a site where repressors bind

64
Q

what does eukaryotic RNA polymerase I do

A

synthesize rRNA

65
Q

what does eukaryotic RNA polymerase II do

A

synthesize mRNA

66
Q

what does eukaryotic RNA polymerase III do

A

synthesize tRNA

67
Q

what is the mechanism of action for alpha-amanatin, found in Amanita phalloides (death cap mushrooms)

A

inhibits RNA polymerase II causing severe hepatotoxicity when ingested

68
Q

in prokaryotes which RNA polymerases make what

A

1 RNA polymerase makes all 3 kinds of RNA

69
Q

what is heterogenous nuclear RNA (hnRNA)

A

newly synthesized RNA in the nucleus that hasn’t yet been processed

70
Q

name three kinds of post-transcriptional processing that happens to pre-mRNA in the nucleus

A
  1. addition of 5’ 7-methylguanosine cap
  2. addition of poly A tail
  3. splicing out of introns
71
Q

what are the three main steps of pre-mRNA splicing

A
  1. primary transcript combines with snRNP’s to form splicesosome
  2. lariat-shaped intermediate is formed
  3. lariat intron is released and 2 exons are joined
72
Q

in what disease are antibodies against splicesosomal snRNPs formed?

A

Lupus

73
Q

what is the conserved final sequence of tRNAs

A

CCA

74
Q

to which end of the tRNA is the amino acid bound

A

3’ end

75
Q

how are tRNAs charged

A

aminoacyl-tRNA synthetase uses ATP to match an amino acid with its proper tRNA; this match is checked before and after charging and hydrolyzed if it is wrong

76
Q

how do tetracyclines work

A

they bind 30S subunit of ribosome preventing attachment of aminoacyl-tRNA

77
Q

what is tRNA wobble

A

degeneracy of the genetic code allows for the third base of the codon to be changed without altering the amino acid most of the time

78
Q

what are the two subunits of the eukaryotic ribosome

A

40S and 60S

79
Q

what is ATP used for in protein synthesis initiation and what is GTP used for during this process?

A

ATP is used for tRNA charging (“activation”)

GTP is used for binding tRNA and translocation (“gripping and going”)

80
Q

what are the three steps of elongation

A
  1. amino-acyl tRNA binds to A side
  2. ribosomal rRNA catalyze peptide bond between newly added amino acid and the growing polypeptide chain
  3. ribosome translocates 3 nucleotides toward 3’ end of mRNA and polypeptide is moved to P site
81
Q

what does the A site do?
what does the P site do?
what does the E site do?

A

A site is where the amino-acyl tRNA binds
P site is where the growing polypeptide sits
E site is where the empty tRNA exit

82
Q

how do aminoglycosides act?

A

they bind the 30S and inhibit initiation complex formation

83
Q

how do tetracyclines work?

A

tetracyclines bind the 30S subunit and block entry of aminoacyl tRNA

84
Q

how does chloramphenicol work

A

chloramphenicol blocks the 50S subunit and inhibits peptidyl transferase

85
Q

how do macrolides work?

A

macrolides bind 50S and prevent exit of uncharged tRNAs

86
Q

what are the three steps of protein synthesis

A

initiation, elongation, termination

87
Q

name three post-translational modifications

A
  1. trimming: removal of propeptide components of a zymogen to get mature protein
  2. covalent alterations: glycosylation, methylation, hydroxylation, acetylation, phosphorylation
  3. proteosomal degredation: ubiquitin tagging of defective protein

Biochemistry- First Aid (6 decks)

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