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USMLE Step 1 Biochemistry > Biochemistry-Molecular > Flashcards

Biochemistry-Molecular Flashcards

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USMLE® Step 1 flashcards
1
Q

DNA methylation:
When does it occur?
What bases can be methylated?
How does methylation affect transcription?

A

Template strand cytosine and adenine are methylated in DNA replication, which allows mismatch repair enzymes to distinguish between old and new strands in prokaryotes.
DNA methylation at CpG islands represses transcription.

*I believe all base pairs can be methylated.

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2
Q

Histone Methylation: What is its affect on DNA transcription?

A

Histone methylation usually reversibly represses DNA transcription, but can activate it in some cases depending on methylation location.

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3
Q

Histone acetylation: how does it affect transcription?

A

Relaxes DNA coiling, allowing for transcription.

Think, Acetylation makes DNA Active

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4
Q

Name the two classes of nucleotides and the which nucleotides belong to which class. How many rings does each class have?

A

PYrimidines = C,U,T (think, CUT the Py)
-pyRIMidines have 1 ring (like a b-ball rim)

PURines = A, G (think, PURe As Gold)
-purines have 2 rings

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5
Q

Which nucleotide has a methyl?

A

THYmine has a meTHYl

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6
Q

Deamination of ______ makes uracil.

A

cytosine

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7
Q

Is uracil found in DNA?

A

No. Uracil is only in RNA. Thymine is only in DNA.

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8
Q

Which bond is stronger?

C-G or A-T

A

C-G has three H-bonds, making it stronger than A-T which only has two H-bonds.

Therefore, C-G rich DNA has a higher melting point (the more bonds, the more energy required to break them)

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9
Q

What three amino acids are necessary for purine synthesis?

A

GAG

Glycine, Aspartate, Glutamine

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10
Q

What is the difference between a nucleoside and a nucleotide?

A 
nucleoSide = base + (deoxy)ribose (Sugar)
nucleoTide = base + (deoxy)ribose + phosphaTe
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11
Q

Describe purine synthesis in the body.

A

pg. 63

Start with sugar + phosphate (PRPP)
Add base

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12
Q

Describe Pyrimidine synthesis.

What amino acid is required?

A

pg. 63
Aspartate is required for pyrimidine synthesis

Make a temporary base (orotic acid)
Add sugar + phosphate (PRPP)
Modify base

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13
Q

During Pyrimidine and Purine synthesis, __________ are synthesized first and are converted to _________ by _______.

A

Ribonucleotides are synthesized first and are converted to deoxyribonucleotides by ribonucleotide reductase.

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14
Q

Carbamoyl phosphate is involved in 2 metabolic pathways:

A
  1. de novo pyrimidine synthesis

2. Urea cycle

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15
Q

Purine salvage deficiencies:

A

see pg. 64

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16
Q

Adenosine deaminase deficiency:

major disorder caused:

A

Excess ATP and dATP throw off/imbalance nucleotide pool via feedback inhibition of ribonucleotide reductase -> prevents DNA synthesis and thus decreases lymphocyte count.

This is one of the major causes of autosomal recessive SCID (Severe Combined Immunodeficiency)

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17
Q

What is the difference between heterochromatin and euchromatin?

A

Heterochromatin = Condensed, appears darker on EM. Transcriptionally inactive, sterically inaccessible. (think..HeteroChromatin = Highly Condensed)

Euchromatin = Less condensed, appears lighter on EM. Transcriptionally active, sterically accessible.

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18
Q

Lesch-Nyhan Syndrome

  1. It is caused by the absence of ________. This absence results in excess ________ production and __________ synthesis.
  2. How is this trait passed on genetically?
  3. Signs:
A
  1. Caused by defective purine salvage due to absent HGPRT. (HGPRT converts hypoxanthine to IMP and guanine to GMP). This absence of HGPRT results in excess uric acid production and de novo purine synthesis.
  2. X-linked recessive
  3. Signs: (can be remembered with the HGPRT nemonic)
    Hyperuricemia
    Gout
    Pissed off (aggression, self-mutilation)
    Retardation
    dysTonia (neurologic muscle disorder where sustained muscle contractions cause abnormal movements and postures)
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19
Q

GENETIC CODE FEATURES:

Describe how the genetic code is….

  1. unambiguous
  2. degenerate/redundant
  3. commaless, nonoverlapping
  4. universal
A
  1. Unambiguous = each codon specifies only 1 amino acid
  2. Degenerate/redundant = most amino acids are coded by multiple codons (exceptions: methionine and tryptophan, AUG and UGG)
  3. Commaless, nonoverlapping: read from a fixed starting point as a continuous sequence of bases (exception: some viruses)
  4. Universal: genetic code is conserved throughout evolution (exception in humans: mitochondria)
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20
Q

What are Okazaki fragments?

A

In DNA replication, the lagging strand synthesizes DNA in small fragments termed Okazaki fragments. This is discontinuous synthesis.

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21
Q

DNA replication:

Origin of replication

A

Origin of Replication: Particular consensus sequence of base pairs in genome where DNA replication begins. May be single (prokaryotes) or multiple (eukaryotes)

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22
Q

DNA replication:

Replication Fork

A

Replication Fork: Y-shaped region along DNA template where leading and lagging strands are synthesized

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23
Q

DNA replication:

__________ is the enzyme that unwinds double stranded DNA template at replication fork.

A

Helicase (unzips DNA)

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24
Q

DNA replication:

___________ prevent strands from reannealing (coming back together) after helicase has unzipped them.

A

Single-stranded binding proteins

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25
Q

DNA replication:

DNA topoisomerases

A

DNA topoisomerases create a single- or double-stranded break in the helix to add or remove supercoils.

26
Q

DNA replication:

primase

A

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

27
Q

DNA replication:

DNA polymerase III

A

Prokaryotic only.

Elongates leading strand by adding deoxynucleotides to the 3’ end. Elongates lagging strand until it reaches primer of preceding fragment. 3’ -> 5’ exonuclease activity “proofreads” each added nucleotide.

DNA polymerase III has 5’->3’ synthesis and proofreads 3’ -> 5’ exonuclease

28
Q

DNA polymerase I

A

Prokaryotic only.

Degrades RNA primer (which was laid down by primase); replaces it with DNA

It has the same function as DNA polymerase III but also excises RNA primer with 5’ -> 3’ exonuclease.

29
Q

DNA replication:

DNA ligase

A

Catalyzes the formation of a phosphodiester bond within a strand of double-stranded DNA (i.e. joins Okazaki fragments)

30
Q

DNA replication:

Telomerase

A

Eukaryotes only.

An RNA-dependent DNA polymerase that adds DNA to 3’ ends of chromosomes to avoid loss of genetic material with every duplication.

31
Q

Mutations in DNA

Severity of damage (from least to most):
Silent mutations
Missense mut.
Nonsense mut.
Frameshift mut.

Define all four of these mutations. Silent, missense, and nonsense mutations are caused by ______ mutations.

A

Silent, missense, and nonsense mutations are all caused by point mutations.

Silent mutations: Nucleotide substitution occurs, but codon still codes for same amino acid; often base change in 3rd position of codon (tRNA wobble)
Missense Mutations: Nucleotide substitution resulting in changed amino acid (called conservative if new amino acid is similar in chemical structure).
Nonsense Mutations: Nucleotide substitution resulting in the coding of a stop codon (resulting in the stopping of translation prematurely); (think…STOP the NONSENSE)
Frameshift mutation: Deletion or insertion of a number of nucleotides not divisible by 3, resulting in misreading of all nucleotides downstream, usually resulting in a truncated, nonfunctional protein.

32
Q

What well known condition was originally caused by a missense (point) mutation?

A

Sickle cell disease (glutamic acid is substituted with valine) in protein of RBCs

33
Q

What condition was originally caused by a frameshift mutation?

A

Duchenne muscular distrophy

34
Q

Lac operon: A classic example of a genetic response to an environmental change. ________ is the preffered metabolic substrate in E. coli, but when ________ is absent and _________ is available, the lac operon is activated to switch to lactose metabolism.

A

GLUCOSE is the preffered metabolic substrate in E. coli, but when GLUCOSE is absent and LACTOSE is available, the lac operon is activated to switch to lactose metabolism.

35
Q

When glucose is absent and lactose is available, the lac operon turns on. Describe the mechanism of shift:

A

Low glucose -> increased adenylyl cyclase activity -> increased generation of cAMP from ATP -> activation of catabolite activator protein (CAP) -> increased transcription of lac operon

High lactose -> unbinds repressor protein from repressor/operator site -> increase transcription of lac operon

36
Q

In the scenario that there is low glucose but lactose is unavailable, will some lac gene still be expressed?

A

no because while the low glucose levels will cause CAP to bind to the CAP site near the promoter region (induces transcription), the repressor protein will still be bound to the operator site of the gene (because lactose is what removes the repressor protein, enabling transcription to occur)

Thus, you need both low glucose (to allow CAP to bind) and available lactose (to unbind repressor protein) in order for the lac gene to be expressed.

37
Q

DNA repair:

Nucleotide excision repair
What happens?
What phase of the cell cycle does this type of repair occur?

A

Specific endonucleases release the oligonucleotides containing damaged bases; DNA polymerase and ligase fiull and reseal the gap, respectively. Repairs bulky helix-distorting lesions. Occurs in G1 phase of cell cycle.

38
Q

Nucleotide excision repair is defective in what skin disorder?

A

xeroderma pigmentosum: a genetic disorder that prevents repair of pyrimidine dimers caused by UV light exposure (UV light always damages DNA to an extent causing pyrimidine dimers. In xeroderma pigmentosum, individuals are unable to excise these pyrimidine dimers.

39
Q

DNA repair:

Base excision repair
Describe it.
During what stage of the cell cycle does it occur?

A

Base-specific glycosylase removes altered base and creates AP site (apurinic/apyrimidinic). One or more nucleotides are removed by AP-endonuclease, which cleaves the 5’ end. Lyase cleaves the 3’ end. DNA ligase seals it. Occurs throughout cell cycle.

*Important in the repair of spontaneous/toxic deamination.

40
Q

DNA repair:

Mismatch repair
Describe it.
During what phase of cell cycle does it occur?

A

Newly synthesized strand is recognized, mismatched nucleotides are removed, and the gap is filled and resealed. Occurs predominantly in G2 phase of cell cycle.

41
Q

What hereditary cancer is caused by a defective mismatch repair system?

A

*Mismatch repair system is defective in hereditary nonpolyposis colorectal cancer (HNPCC)

42
Q

DNA repair:

Nonhomologous end joining
What happens in this type of repair?

A

Brings together 2 ends of DNA fragments to repair double-stranded breaks. No requirement for homology. Some DNA may be lost.

43
Q

Nonhomologous end joining (a DNA repair mechanism), is defective in what two disorders?

A

Ataxia telangiectasia

Fanconi anemia

44
Q

DNA/RNA/protein synthesis direction; In what direction does each process occur?

A

DNA and RNA both synthesized 5’ -> 3’. The 5’ end of the incoming nucleotide bears the triphosphate (E source for bond).

Protein synthesis is N-terminus to C-terminus.

45
Q

mRNA is read 5’ -> 3’.

T or F?

A

T

46
Q

The mRNA start codon(s):

What amino acid does it/they code for in Eukaryotes? Prokaryotes?

A

AUG (or rarely GUG)

(think.. AUG inAUGurates protein synthesis)

Eukaryotes: Codes for methionine, which may be removed before translation is completed.
Prokaryotes: Codes for N-formylmethionine (fMet). fMet stimulates neutrophil chemotaxis

47
Q

List the mRNA stop codons:

A

UGA, UAA, UAG

Memory tip:
UGA =U Go Away
UAA = U Are Away
UAG = U Are Gone

48
Q

Functional organization of a Eukaryotic gene:

A

See pg. 68

enhancer, promoter, Exons, Introns, Termination signals) (sensing/coding strand and the template strand

49
Q

_____________ inhibit prokaryotic enzymes topoisomerase II (DNA gyrase) and topoisomerase IV, making them effective antibiotics.

A

Fluoroquinolones

If prokaryotic topoisomerase II and topoisomerase IV can’t add or remove supercoils in DNA, the organism won’t be able to transcribe the necessary genes for survival and will eventually die

50
Q

Describe the significance of the Promoter site:

How would a mutation to the promoter region likely affect transcription rates?

A

Site where RNA polymerase II and multiple other transcription factors bind to DNA upstream from gene locus (AT-rich upstream sequence with TATA and CAAT boxes)

*Mutation of a promoter region commonly results in dramatic decrease in level of gene transcription

51
Q

Enhancer region:

A

Stretch of DNA that alters gene expression by binding transcription factors

52
Q

Silencer region

A

Site on DNA where negative regulators (repressors) bind

53
Q

Are silencer regions usually located before or after, close to or far from the gene of interest? Enhancers?

A

*Enhancers and silencers may be located close to, far from, or even within (in an intron) the gene whose expression it regulates

54
Q

RNA polymerases: Eukaryotes

  1. RNA polymerase I makes…
  2. RNA polymerase II makes….
  3. RNA polymerase III makes…
  4. RNA polymerase has a “proofreading” function to check for transcription mistakes. T or F?
A
  1. RNA polymerase I makes…rRNA (most numerous RNA, r=Rampant)
  2. RNA polymerase II makes….mRNA (largest RNA, m=Massive)
  3. RNA polymerase III makes…tRNA (smallest RNA, t=Tiny)
  4. RNA polymerase has a “proofreading” function to check for transcription mistakes. FALSE, No proofreading function, but can initiate chains. RNA polymerase II opens DNA at promoter site.

*I, II, and III are numbered as their products are used in protein synthesis!

55
Q

RNA polymerases: Eukaryotes + Prokaryotes

  1. __________, found in death cap mushrooms, inhibits RNA polymerase II and will cause severe hepatotoxicity if ingested.
  2. __________ inhibits RNA polymerase in prokaryotes.
  3. _________ inhibits RNA polymerase in both prokaryotes and eukaryotes.
A
  1. alpha-amanitin, found in Amanita phalloides (death cap mushrooms)
  2. Rifampin (just prokaryotes)
  3. Actinomycin D (both)
56
Q

RNA polymerases: Prokaryotes

How many types of RNA polymerase do prokaryotes have?

A

1 RNA polymerase (multisubunit complex) makes all 3 kinds of RNA in prokaryotes

57
Q

RNA processing: Eukaryotes

  1. The initial transcript is called __________ ________ RNA. It is then modified and becomes ________.
  2. Describe the process that occurs in the nucleus following transcription: (hint: what happens to the 5’ end? the 3’ end?)
A
  1. The initial transcript is called heterogeneous nuclear RNA (hnRNA). It is then modified and becomes mRNA.
  2. Following transcription in the nucleus:
    -capping of 5’ end (addition of 7-methylguanosine cap)
    -Polyadenylation of 3’ end (~200 A’s)
    -Splicing out of introns
    The final capped, tailed, and spliced transcript is called mRNA
58
Q

After its processed (capped, tailed, and spliced) in the _________, mRNA is transported to the ___________, where it is translated.

A

After its processed (capped, tailed, and spliced) in the NUCLEUS, mRNA is transported to the CYTOSOL, where it is translated.

59
Q

mRNA quality control occurs at cytoplasmic __________, which contain:

A 
Cytoplasmic P-bodies, which contain:
-exonucleases
-decapping enzymes
-microRNAs
(mRNA's may be stored in P-bodies for future translation)
60
Q

Poly-A polymerase:

What does it do?
Does it require a template?
What is the polyadenylation signal?

A

During RNA processing in the nucleus, Poly-A polymerase adds a poly-A tail (~200 A’s)
It does not require a template, AAUAAA = polyadenylation signal

USMLE Step 1 Biochemistry (1 decks)

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