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Biochemistry > Molecular Biochemistry > Flashcards

Molecular Biochemistry Flashcards

1
Q

DNA is condensed, it loops twice around a histone octamer to form…

A

Nucleosome. “Beads on a string”.

H1 binds to nucleosome and linker DNA = stabilizes.

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2
Q

Phosphate gives a _____ charge.

Arginine and lysine give a ______ charge.

A

Negative.

Positive.

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3
Q

During which cell cycle phase occurs histone and DNA synthesis?

A

During S phase.

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4
Q

Mithochondrial DNA characteristics

A

Circular with no histones.

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5
Q

Condensed chromatin, transcriptionally inactive and inaccessible.

A

HeteroChromatin.
HighlyCondensed.

Barr bodies can be seen in the periphery of nucleus.

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6
Q

Less condensed chromatin, lighter on microscope, active and accessible.

A

Euchromatine, Expressed.

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7
Q

Changes a DNA segment, doesn’t change the sequence.

Involved in genomic imprinting, X-chrom inactivation, repression of elements, carcinogenesis and aging.

Occurs in promoter (CpG islands).

A

DNA methylation.

It silences gene transcription.

Mute.

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8
Q

Reversible transcriptional suppression but can cause activation depending on location of methyl group.

A

Histone Methylation.

Mute.

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9
Q

Removes histone + charge. Relaxes DNA coiling and promotes transcription.

A

Histone Acetylation.

Active.

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10
Q

Removes acetyl groups, tights DNA coil, reduces transcription.

A

DNA deacetylation.

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11
Q

Base + Deoxyribose.

A

NucleoSide.

Sugar.

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12
Q

Base + deoxyribose + phosphate.

A

NucleoTide.

phosphaTe.

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13
Q

Which bases are purines?

A

A & G.

PURe As Gold.

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14
Q

Which bases are pyrimidines?

A

C, U & T.

CUT the PY.

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15
Q

Deamination reactions:

Cytosine -
Adenine -
Guanine -
5-methylcytosine -

A

Cytosine - uracil
Adenine - hypoxanthine
Guanine - xanthine
5-methylcytosine - thymine

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16
Q

Thymine is in _____

Uracil is in _____

A

Thymine: DNA
Uracil: RNA

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17
Q

Amino acids needed for purine synthesis

A

Glycine, Aspartate and Glutamine.

cats PURr until they GAG.

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18
Q

Drugs interfering with pyrimidine synthesis

A

Leflunomide: inhibits dihydroorotate dehydrogenase.

MTX, TMP and pyrimethamine: inhibit dihydrofolate reductase.

5-FU and its prodrug capecitabine: form 5-F-dUMP which inhibits thymidylate synthase.

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19
Q

Inhibitors of purines:

A

6-MP and its prodrug AZA: inhibit de novo purine synthesis.

Mycophenolate and ribavirin: inhibit inosine monophosphate dehydrogenase.

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20
Q

Inhibit both purine and pyrimidine:

A

Hydroxyurea: inhibit ribonucleotide reductase.

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21
Q

CPS 1 & 2 (carbamoyl phosphate synthetase) are found in:

A

CPS1: m1tochondria (urea cycle)

CPS2: cyTWOsol

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22
Q

Cause of autosomal recessive SCID, its deficency causes accumulation of dATP and lymphotoxicity.

A

Adenosine deaminase deficency. ADA.

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23
Q

Absent HGPRT causes defective purine salvage.

Impaired hypoxantine to IMP and guanine to GMP.

Excessive uric acid, de novo purine synthesis.

X-linked recessive.

A

Lesch-Nyhan syndrome.

HGPRT
Hyperuricemia
Gout
Pissed off (aggression, self-mutilation)
Retardation
dysTonia
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24
Q

The genetic code feature Unambiguous means

A

That each codon specifies only one amino acid.

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25
Q

The genetic code feature Degenerate/Redundant means

A

Most amino acids are coded by more than one codon.

Except for Methionine (AUG) and Tryptophan (UGG) encoded only by one codon.

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26
Q

What are Wooble-codons?

A

They differ in the third position and may code for the same tRNA/aa. Specific base pairing is only needed in the first two nucleotide positions of mRNA codon.

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27
Q

The genetic code feature Commaless/Overlapping means

A

Read from a fixed starting point as a continuos sequence of bases, some viruses don’t.

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28
Q

The genetic code feature Universal means

A

The genetic code is conserved throughout evolution, except for the mitochondria.

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29
Q

DNA replication features:

A

Semiconservative, both continuos and discontinuos (Okazaki fragments) synthesis and 5’ -> 3’.

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30
Q

Where is the origin of replication?

A

In AT rich sequences (TATA box). Those are in promoters and origins of replication.

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31
Q

What is the replication fork?

A

A Y-shaped region where the leading and lagging strands are synthesized.

32
Q

What does an helicase do?

A

It unwinds DNA template at the replication fork, it Halves DNA and it is deficient in Bloom syndrome.

33
Q

What is the single stranding binding proteins function?

A

Preventing the strands from reannealing.

34
Q

What do DNA topoisomerases do?

A

They create breaks to add or remove supercoils.

In eukaryotes Irinotecan/Topotecan inhibit TOP I, while Etoposide/Teniposide inhibit TOP II.

In prokaryotes, Fluoroquinolones inhibit TOP II (DNA gyrase) and TOP IV.

35
Q

What does a primase do?

A

It makes RNA primers so DNA polymerase III can begin replication.

36
Q

What is polymerase III function?

A

It elongates the leading strand by adding deoxynucleotides to the 3’ and elongates the lagging until it reaches the primer of the preceding fragment.

Its synthesis goes 5 to 3, it proofreads 3 to 5.

Only in prokaryotes.

37
Q

What does polymerase I do?

A

In prokaryotes, it degrades the RNA primer and replaces it with DNA.

38
Q

What do DNA ligase do?

A

Catalyzes phosphodiester bond in a double strand DNA.
It joins Okazaki fragments.
Ligase Links DNA.

39
Q

What’s the function of telomerases?

A

It adds DNA (TTAGGG) to 3’ ends so there won’t be a loss of genetic material in duplications
Only in eukaryotes.
Might be dysregulated in cancer.
Telomerase TAGs for Greatness and Glory.

40
Q

Which of the DNA mutations is the least severe?

Which is the most?

A

Silent < Missense < Nonsense < Frameshift

41
Q

What is a base transition and what is a transversion?

A

Transition: purine to purine or pyrimidine to pyrimidine.

Transversion: purine to pyrimidine or the other way around.

42
Q

What is a silent mutation?

A

A substitution in nucleotides but coding for the same amino acid. It often changes in the 3rd position (tRNA wooble).

43
Q

What is a missense mutation?

A

The nucleotide substitution that results in a change of amino acids such as in Sickle cell disease where there is a change of glutamic acid with valine.

Sometimes the new a.a. is similar in chemical structure, this is called a Conservative missense mutation.

44
Q

What is a nonsense mutation?

A

A nucleotide substitution that results in a premature stop codon (UAG, UAA, UGA). It results in nonfunctional proteins.
Stop the nonsense!

45
Q

What is a frameshift mutation?

A

An insertion or deletion of nucleotides that are not divisible by three, so the whole sequence will be misread.
Might result in shorter/longer, disrupted or altered function.

e.g. Duchenne, Tay-Sachs.

46
Q

What is a mutation at the split site?

A

A mutation at the split site causes retained intron in the rNA, which results in proteins with impaired function.
Some are found in cancer, dementia, epilepsy and some types of ß-thalassemia.

47
Q

What does a lac operon do?

A

It is activated when there is not enough glucose but lactose is available, so there is a switch to lactose metabolism. It is a genetic response to environmental change.

Low glucose augments adenylate cyclase activity which augments cAMP from ATP and it activates the catabolite activator protein (CAP) increasing transcription.
When there is high lactose the repressor protein from the repressor/operator site is unbound to increase transcription.

48
Q

Which are the mechanisms for single strand DNA repair?

A

Nucleotide excision repair, base excision repair and mismatch repair.

49
Q

Which are the mechanisms for double strand DNA repair?

A

Non-homologous end joining and homologous recombination.

50
Q

What is base excision repair?

A

The removal of an altered base by a base-specific Glicosylase, it creates an AP site (apurinic/apyrimidinic); nucleotides are removed by AP-Endonuclease, which cleaves at the 5’ end. Lyase cleaves at the 3’.
DNA Polymerase-ß fills the gap and the DNA Ligase seals it.
It occurs during the whole cycle.

Repair for spontaneous/toxic deamination.

“GEL PLease”

51
Q

What is base mismatch repair?

A

The mismatched nucleotides are removed and the gap filled in newly synthesized strands. Occurs during S phase, mostly.

Defective mechanism in Lynch syndrome.

52
Q

What is the non-homologous end joining?

A

When there is a defect, two cells of DNA fragments are brought together to repair the double-stranded breaks it doesn’t need homology and some ADN can be lost.

It is defective in ataxia-telangiectasia.

53
Q

What is the homologous recombination?

A

It requieres two homologous DNA duplexes and a strand from the altered dsDNA is repaired with a complimentary strand of the intact dsDNA as template. Accurate restore with no loss of nucleotides.

Defective in breast/ovarian ca with BRCA1 mutation and in Fanconi anemia.

54
Q

Which are mRNA start codons?

A

AUG or GUG.

AUG inauGUGates protein synthesis.

55
Q

Start mRNA codons in eukaryotes code for:

A

Methionine, it might be removed before the translation is completed.

56
Q

Start mRNA codons in prokaryotes code for:

A

N-formylmethionine (fMet).

57
Q

Which are mRNA stop codons?

A 
UGA = U Go Away
UAA = U Are Away
UAG = U Are Gone
58
Q

What is a promoter?

A

It is the site where the RNA polymerase II and other transcription factors bind to DNA, AT-rich upstream sequences like the TATA and CAAT boxes).

When there is a mutation in promoters it results in a great diminution of the gene transcription.

59
Q

What is an enhancer?

A

The DNA locus where the regulatory (activator) proteins bind to increase the expression of a gene in the same chromosome.

It may be close, far or within (intron) the gene whose expression they regulate.

60
Q

How is the RNA processing in eukaryotes?

A

The inicial transcript (heterogenous nuclear RNA [hnRNA]) suffers capping of the 5’ end by addition of 7-methylguanosine cap, then polyadenylation of the 3’ (about 200 A’s) and spplicing of the introns, all in the nucleous.

Then this hnRNA is called mRNA which goes to the cytosol to be translated.

The quality control occurs at the P-bodies (cytoplasmic processing bodies that contain exonucleases, decapping enzymes and miRNAs.
The mRNA can be degraded or stored in those bodies for future translation.

The Poly-A polymerase doesn’t requiere templates.

AAUAAA = polyadenylation signal.

61
Q

Which are the eukaryote RNA polymerases?

A

RNA polymerase I > rRNA (Rampant, the most common), only in nucleolus.

RNA polymerase II > mRNA (largest one, Massive) and small nuclear (snRNA).
Read 5’ to 3’.
alpha-amanitin (Amanita phalloides, death cap mushroom) inhibits it, severe hepatotoxicity if ingested.

RNA polymerase III > 5S mRNA, tRNA
(smalles, Tiny).

No proofreading but can initiate chains. RNA polym II opens at promoter site.

62
Q

What are microRNAs?

A

Small, noncoding RNA that posttranscriptionally regulate gene expression, targeting the 3’ untranslated region of specific mRNA for degradation or translational repression. Its abnormal expression contributes to malignancies.

63
Q

What is the tRNA charging?

A

Aminoacyl-tRNA synthetase uses ATP, together with the binding of charged tRNA to the codon are in charge of the accuracy of aa selection.

If incorrect aa is attached, the bond gets hydrolyzed.

Mischarged tRNA reads the usual codon, but will insert the wrong aa.

64
Q

How is the protein synthesis elongation?

A

Aminoacyl-tRNA binds to the A-site (the initiator methionine binds to the P) needs elongation factor and GTP.

rRNA (ribozyme) catalyzes the peptide bond formation, transfers growing polypeptide to aa A-site.

ribosome advances 3 nucleotides towards 3’ end of mRNA, moving peptidyl tRNA to P site (translocation).

“going APE”
A site: incoming Aminoacyl-tRNA
P site: accomodates growing Peptide
E site: holds Empty tRNA as it Exits.

65
Q

How is the protein synthesis termination?

A

Eukaryotic release factors (eRF)recognize the stop codon and halt translation, the completed polypeptide is then released from the ribosome, requieres GTP.

66
Q

Whats is Trimming?

A

The removal of the N or C terminal propetides from the zymogen, to generate a mature protein.
(trypsinogen to trypsin)

67
Q

What is a chaperone protein?

A

An intracellular protein that facilitates or mantains the protein folding.

An example are heat shock proteinf that express at high temperatures to prevent the protein from misfolding.

68
Q

What is a covalent alteration?

A

Phosphorylation, glycosylation, hydroxylation, methylation, acetylation, ubiquitination.

69
Q

What are the posttranslational modifications?

A

Trimming and covalent alterations.

70
Q

How is the protein synthesis initiation?

A

The eukaryotic initiation factor (eIF) identifies 5’ cap.
eIF help assemble 40S ribosomal subunit with the initiator tRNA.
When 60S assembles with complex, the eIF is released, it requieres GTP.

Euka: 40S + 60S - 80S (Even)
Proka: 30S + 50S - 70S (Prime)

Synthesis goes N-terminus to C-terminus.

ATP: tRNA Activation
GTP: tRNA Gripping and Going (translocation).

71
Q

What is the tRNA structure?

A

Secondary structure, with 75-90 nucleotides, cloverleaf-like, anticodon end is opposite 3’ aminoacyl end. The 3’ end is CCA.

T-arm: T†C (ribothymidine, pseudouridine, cytidine) sequence necessary for tRNA-ribosome binding.
T-arm Tethers tRNA to ribosome.

D-arm: Dihydrouridine residues for tRNA recognition by aminoacyl-tRNA synthetase.
D-arm Detects tRNA by aminoacyl-tRNA synthetase.

72
Q

What is alternative splicing?

A

Exons may be combined to produce more unique proteins by alternative splicing, which produces them from a single hnRNA sequence.

The variants of abnormal splicing are involved in oncogenesis, ß-thalassemia, Gaucher,
Tay-Sachs, Marfan.

73
Q

Differences between introns and exons

A

Introns are INtervening sequences of DNA that stay IN the nucleous.

Exons have the genetic information coding for proteins, they EXit and are EXpressed.

74
Q

What is a silencer?

A

The locus DNA where the repressors bind decreasing the expression of a gene in the chromosome. As the enhancer, it can be close, far or within the gene.

75
Q

What is the prokaryote RNA polymerase?

A

There is one, a multisubunit complex that makes the three kinds of RNA.

Rifampin inhibits DNA-dependent RNA polymerase in prokaryotes.

Actinomycin D (dactinomycin) inhibits RNA polymerase in both euka and prokaryotes.

76
Q

What’s Bloom syndrome?

A

Short stature, predisposed to cancer, genomic instability. Autosomal recessive. Mutations in BLM gene, member of the RecQ DNA helicase family.

Biochemistry (6 decks)

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