Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Board Review > BIOCHEM--Molecular > Flashcards

BIOCHEM--Molecular Flashcards

p 34-45 FA2018

1
Q

_____ give DNA a neg (-) charge

A

phosphate groups

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

_____ and _____ give histones a pos (+) charge

A

lysine and arginine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

DNA and histone synthesis occur during ___-Phase

A

S-phase

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

describe the structure of a nucleosome

A

DBA loops twice around a histone octamer forming “beads on a string”

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

____ binds to the nucleosome and ____ to stabilize the chromatin fiber

A

H1 binds to the nucleosome and linker DNA

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

what bits make up the histone octamer

A

two of each of the following: H2A, H2B, H3, and H4

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

describe heterochromatin

A

“HeteroChromatin = Highly Condensed”
transcriptionally inactive, sterically inaccessible
increased methylation, decreased acetylation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q
  1. how does heterochromatin appear on EM

2. how does euchromatin appear on EM

A
  1. dark

2. lighter

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What is a Barr body

A

inactive X chromosome made of heterochromatin

maybe visible on the periphery of nucleus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

describe Euchromatin

A

“Eu=true, truly transcribed”
“Euchromatin is Expressed”
Transcriptionally active, sterically accessible

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q
  1. what is DNA methylation

2. what is the result of DNA methylation

A
  1. direct methylation of DNA itself; does not change the sequence of DNA
  2. “CpG Methylation Makes DNA Mute.”
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

where are gene promoters located

A

CpG islands

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

examples of events in which DNA methylation takes place

A 
genomic imprinting
x-chromosome inactivation
repression of transposable elements
aging
carcinogenesis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q
  1. what is histone methylation

2. what is the result of histone methylation

A
  1. methyl groups attached to histones, NOT DNA
  2. usually causes reversible transcriptional suppression, but can also cause activation depending on location of methyl groups
    “Histone Methylation Mostly Makes DNA Mute”
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Histone Acetylation causes what…

A

relaxation of DNA coiling»>allow for DNA transcription

“histone Acetylation make DNA Active”

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

what is a nucleoSide

A

base + deoxyribose (Sugar)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

what is a nucleoTide

A

base deoxyribose + phosphaTe

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

what kind of bond links a phosphate to deoxyribose?

A

3’-5’ phosphodiester bond

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

which end of the nucleotide has the triphosphate?

A

5’ end

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

name the purines and their basic structure

A

Adenine and Guanine
2 rings
“PURe As 2 Gold rings”

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Name the pyrimidines and their basic structure

A

Cytosine, Uracil, and Thymine
1 ring
“CUT the PY(pie)”

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Thymine has a ____

A

“thymine has a meTHYl”

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Which nucleotide bonds are stronger and why?

A

G-C bonds have 3 H bonds and are stronger that A-T bonds that only have 2H bonds
Increased G-C content= increased melting temperature of DNA.
“C-G bonds are like Crazy Glue”

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

Which amino acids are necessary for purine synthesis

A

Glycine, Aspartate, and Glutamine

“cats Purr until they GAG”

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

Deamination of cytosine forms ___

A

Deamination of cytosine forms Uracil

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

Deamination of adenine forms ___

A

Deamination of adenine forms hypoxanthine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

Deamination of guanine forms ___

A

Deamination of guanine forms xanthine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

Deamination of 5-methylcytosine forms ___

A

Deamination of 5-methylcytosine forms thymine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

what is the difference between Uracil and thymine?

A

Uracil is found in RNA, Thymine is found in DNA

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

Methylation of uracil forms ___

A

Methylation of uracil forms thymine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

Draw out De novo pyrimidine and purine synthesis

A

I don’t have Brainscape Pro, so I can’t add a picture

Check Page 36 in FA 2018

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

Drugs that interfere with Pyrimidine synthesis and their MOA

A
  1. Leflunomide- inhibits dihydroorotate dehydrogenase
  2. methotrexate (MTX)-HUMAN
    trimethoprim (TMP)- BACTERIA
    pyrimethamine-PROTOZOA
    these inhibit dihydrofolate reductase (which leads to a decrease in deoxythmidine monophosphate [dTMP] in specified organisms
  3. 5-fluorouracil (5-FU) and its prodrug capecitabine- form 5-F-dUMP which inhibits thymidylate synthase (leading to decrease in dTMP)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

drugs that interfere with purine synthesis and their MOA

A
  1. 6-mercaptopurine (6-MP) and its prodrug azathioprine- inhibit denovo purine synthesis
  2. Mycophenolate and ribavirin- inhibit inosine monophosphate dehydrogenase
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

drug that interferes with both purine and pyrimidine synthesis and its MOA

A

hydroxyurea- inhibits ribonucleotide reductase

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

which amino acid is required for pyrimidine base production?

A

aspartate

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

where are the carbamoyl phosphate synthetase enzymes located?

A 
CPS1= in the m1tochondria (urea cycle)
CPS2= in the cyTWOsol
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

Draw purine salvage pathway

A

I don’t have Brainscape Pro, so I can’t add a picture

Check Page 36 in FA 2018

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

Explain Biochem of Adenosine Deaminase (ADA) Deficiency

A 
Adenosine Deaminase (ADA) is required for degradation of adenosine and deoxyadenosine.
in ADA Deficiency increased dATP leads to lymphotoxicity
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

___ is the major cause of AR SCID

A

Adenosine Deaminase (ADA) Deficiency

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

how is ADA deficiency inherited

A

AR

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

Explain Biochem of Lesch-Nyhan Syndrome

A

defective purine salvage bc absent HGPRT which converts hypoxanthine&raquo_space;> IMP and guanine&raquo_space;>GMP.
without HGPRT&raquo_space;>excessive uric acid production and de novo purine synthesis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

how is Lesch-nyhan syndrome ingerited?

A

X-linked recessive

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

Clinical Findings: Lesch-Nyhan Syndrome

Remember: HGPRT pneumonic

A
  • Hyperuricemia (orange “sand” [sodium urate crystals] in diaper)
  • Gout
  • Pissed off (aggression, self-mutilation)
  • Retardation (intellectual disability)
  • dysTonia
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

tx for Lesch Nyhan Syndrome

A

1st: allopurinol
2nd: febuxostat

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

Genetic code features: unambiguous

A

each codon specifies only 1 amino acid

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

Genetic code features: Degenerate/redundant

A

most amino acids are coded by multiple codons bc of the wobble position; exceptions: Methionine (AUG) and tryptophan (UGG) encoded by only 1 codon.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
47
Q

describe the wobble position and how it relates to the degenerate/redundant feature of genetic code

A

codons that differ in the 3rd “wobble” position may code for the same tRNA/amino acid.
specific base pairing is usually required only in the first 2 nucleotide positions of mRNA codon.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
48
Q

Genetic code features: commaless, nonoverlapping

A

read from a fixed starting point as a continuous sequence of bases.
exceptions: some viruses

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
49
Q

Genetic code features: Universal

A

genetic code is conserved throughout evolution.

exception in humans: Mitochondria

50
Q

DNA replication is ___, involves both ___ and ___ synthesis, and occurs in the ___ direction

A

DNA replication is semiconservative, involves both continuous and discontinuous synthesis, and occurs in the 5’-3’ direction

51
Q

Origin of DNA replication

A

may be single (prokaryotes) or multiple (eukaryotes).

AT-rich sequences (TATA box regions) found in promoters and origins of replication

52
Q

what is the replication fork?

A

y-shaped region along DNA template where leading and lagging strands are synthesized

53
Q

Role of Helicase in DNA replication

A

unwinds DNA template at replication fork

“Helicase Halves DNA”

54
Q

Role of Single-stranded binding proteins in DNA replication

A

prevent DNA stands from reannealing

55
Q

Role of DNA topoisomerases in DNA replication

A

create single- or double-stranded break in helix to add or remove supercoils

56
Q

Topoisomerases inhibited by drugs in eukaryotes vs prokaryotes

A

In Eukaryotes:
-Topoisomerase (TOP) I: inhibited by irinotecan/topotecan
-TOP II: inhibited by etoposide/teniposide
In Prokaryotes:
-TOP II (DNA gyrase) and TOP IV: inhibited by fluoroquinolones

57
Q

Role of primase in DNA replication

A

make RNA primer for DNA polymerase III to bind and initiate replication

58
Q

Role of DNA polymerase III in DNA replication

A

IN PROKARYOTES ONLY
elongate leading stand by adding deoxynucleotides to 3’ end.
elongate lagging strand until reach primer of preceding fragment.
3’-5’ exonuclease activity “proofreads”

59
Q

Role of DNA polymerase I in DNA replication

A

Prokaryotic ONLY

degrade RNA primer, replace with DNA, + all functions of DNA polymerase III

60
Q

Role of DNA Ligase in DNA replication

A

joins Okazaki fragments with phosphodiester bond

“Ligase Links DNA”

61
Q

Role of Telomerase in DNA replication

A

EUKARYOTES ONLY
a reverse transcriptase (RNA dependent DNA polymerase) that adds DNA (a TTAGGG sequence) to the 3’ ends of chromosomes to avoid loss of genetic material with every duplication

often fucked up in cancer cells&raquo_space;> unlimited replication

“Telomerase TAGS for Greatness and Glory”

62
Q

Mutations in DNA ranked from least sever to most severe

A

silent &laquo_space;missense < nonsense < frameshift

63
Q

which types of mutations are point mutations?

A

silent
missense
nonsense

64
Q

what is a transition mutation

A

purine to purine
or
pyrimidine to pyrimidine

65
Q

what is a transversion mutation

A

purine to pyrimidine
or
pyrimidine to purine

66
Q

What is a silent mutation?

A

nucleotide substitution, but codes for same/ synonymous amino acid

67
Q

What is a missense mutation?

A

nucleotide substitution that leads to a different amino acid.
Called “conservative” if the new amino acid is similar in chemical structure

68
Q

example of missense mutation leading to disease

A

Sickle Cell Disease

substitution of glutamic acid with valine

69
Q

What is a nonsense mutation

A

nucleotide substitution results in early stop codon.
Usually results in nonfunctional protein

“Stop the Nonsense”

70
Q

what are the stop codons?

A

UAA “u are annoying”
UGA “u go away”
UAG “u are gone”

71
Q

What is a frameshift mutation?

A

deletion or insertion of a number of nucleotides not divisible by 3. results in misreading of all nucleotides downstream.
protein might be shorter or longer, and its function may be disrupted or altered.

72
Q

Examples of diseases caused by frameshift mustations

A

Duchenne muscular dystrophy

tay-sachs disease

73
Q

What is a splice site mutation?

These mutations are rare causes of what?

A

mutation at splice site causes retained introns in the mRNA that lead to the productino of a protein with impaired or altered function

Rare causes of cancer, dementia, epilepsy, and some types of beta-thalassemia

74
Q

What are the two situations in which the Lac operon will be activated to switch to lactose metabolism?
What happens in each?

A
  1. Low glucose&raquo_space;> increased adenylate cyclase activity»> increased generation of cAMP from ATP&raquo_space;> acitvation of catabolite activator protein (CAP)&raquo_space;> increased transcription of Lac-Z,-Y, and -A
  2. High lactose»> unbinds repressor protein from repressor/operator site&raquo_space;> increased transcription
75
Q

What are the 3 single stranded DNA repair mechanisms

A
  1. nucleotide excision repair
  2. base excision repair
  3. mismatch repair
76
Q

What kind of lesions are repaired by Nucleotide Excision Repair?

A

bulky, helix distorting lesions

77
Q

Explain Nucleotide Excision Repair

A

Specific Endonucleases cut out the oligonucleotides containing the damaged bases.
DNA Polymerase fills gap and ligase reseals the cut.

78
Q

When does Nucleotide excision repair occur in the cell cycle?

A

G1 phase

79
Q

Nucleotide excision repair is defective in what condition?

A

Xeroderma Pigmentosum

80
Q

Explain Base Excision Repair

A

Base-specific glycosylase removes altered base and creates an AP site (apurinic/apyrimidinic)
one or more nucleotides removed by AP-Endonuclease which cleaves 5’ end.
Lyase cleaves 3’ end.
DNA polymerase-beta fills the gap
DNA ligase seals it

81
Q

When does base excision repair occur?

A

occurs throughout cell cycle

82
Q

In what specific instance in base excision repair important?

A

repair of spontaneous/toxic deamination

83
Q

Explain Mismatch Repair

A

newly synthesized strand recognized as fucked up.
mismatched nucleotides are removed.
gap is filled and resealed

84
Q

when does mismatch repair occur?

A

predominantly in S phase

85
Q

Defective mismatch repair mechanisms are found in what syndrome?

A

Lynch Syndrome (hereditary nonpolyposis colorectal cancer [HNPCC])

86
Q

What are the 2 Double stranded DNA repair mechanisms

A
  1. non-homologous end joining

2. homologous recombination

87
Q

explain non homologous end joining

A

bring together 2 ends of DNA fragments

does not require homology.

88
Q

in what disorders will you find defective nonhomologous end joining?

A

ataxia telangiectasia

fanconi anemia

89
Q

what sucks about non homologous end joining?

A

you might lose some DNA

90
Q

explain homologous recombination

A

need two homologous DNA duplexes.
a strand from the damaged dsDNA is repaired using a complementary strand from the intact homologous dsDNA as a template.
restores duplexes accurately w/o loss of nucleotides

91
Q

where will you find defective homologous recombination?

A

breast and ovarian cancers with BRCA1 mutations

92
Q

mRNA start codon

A

AUG (rarely GUG) “aye u, GO”
codes for…
-eukaryotes: methionine
-prokaryotes: N-formylmethionine (fMet)

93
Q

fMet stimulates ___.

A

neutrophil chemotaxis

94
Q

What is a promoter?

A

site where RNA polymerase II and other transcription factors bind to DNA upstream from gene locus.
AT-rich upstream sequence w/ TATA and CAAT boxes

95
Q

what happens if a promoter is mutated?

A

dramatic decrease in level of transcription of that gene

96
Q

What is an enhancer?

A

DNA locus where activators bind to increase the expression of a gene on the same chromosome

97
Q

What is a silencer?

A

DNA locus where repressors bind to decrease expression of a gene on the same chromosome

98
Q

Where are enhancers and silencers located with respect to the gene they regulate?

A

can be close to, far away from, or within (like in a intron) the gene it regulates.

99
Q

RNA polymerase I makes ___

A

rRNA

100
Q

Where is RNA polymerase I located?

A

only in the nucleolus

101
Q

RNA polymerase II makes ___

A

mRNA

102
Q

RNA polymerase III makes ___

A

tRNA

103
Q

Which type of RNA is most common?

A

rRNA

104
Q

___ is the smallest RNA, and ___ is the largest.

A 
tRNA = tiny
mRNA = massive
105
Q

Besides making RNA, what does RNA polymerase II do?

A

opens DNA at the promoter site.

106
Q

True or false: RNA polymerases have proof-reading function.

A

False

107
Q

the initial ___ is modified and becomes mRNA

A

heterogeneous nuclear RNA (hnRNA)

108
Q

How and where does hnRNA become mRNA?

A

the following processes occur in the nucleus:
1. capping of 5’ end (by adding 7-methylguanosine cap)
2. polyadenylation of 3’ end (~200 A’s)
3. splicing out of introns.
Once all three actions are complete, it is now mRNA

109
Q

where is mRNA translated

A

cytosol

110
Q

what the fuck is a P-body?

A

A “processing body” in the cytoplasm that contains exonucleases, decapping enzymes, and microRNAs.
mRNA may be degraded or stored in the P-body for future translation

111
Q

what is the polyadenylation signal

A

AAUAAA

112
Q

What are microRNAs

A

small, conserved, noncoding RNA molecules that posttransciptionally regulate gene expression by targeting the 3’ untranslated region of specific mRNA for degradation or translational repression.

113
Q

Where do animo acids bind on a tRNA?

A

at the Acceptor stem with the CCA 3’ end

“Can Carry Amino acids”

114
Q

What is the function of the T-arm of tRNA

A

necessary for ribosome binding

“T-arm Tethers tRNA to ribosome”

115
Q

What is the function of the D-arm of tRNA?

A

has dihydrouridine residues that are necessary for tRNA recognition by the correct aminoacyl-tRNA synthetase

116
Q

Steps of Protein Synthesis

A
  1. initiation
  2. Elongation
  3. termination
117
Q

Protein Synthesis: Initiation

A
  1. Eukaryotic initiation factors (eIFs) identify the 5’ cap or an internal ribosome entry site (IRES)
  2. eIFs help assemble 40S ribosomal subunit with the initiator tRNA. released when mRNA and 60S subunit assemble with the complex.
    Needs GTP
118
Q

What is the energy source for protein synthesis initiation?

A

GTP

119
Q

Protein Synthesis: Elongation

A
  1. Aminoacyl-tRNA bind to A site, require elongation factor + GTP
  2. rRNA catalyzes peptide bond formation, transfers growing polypeptide to aminoacid in A site.
  3. ribosome advances 3 nucleotides toward 3’ end of mRNA, moving peptidyl tRNA to P site (translocation)
120
Q

___ is required to “charge” the tRNA

A

ATP

121
Q

Protein Synthesis: Termination

A
  1. Release factor recognizes stop codon and halts translation
  2. completed polypeptide is released from ribosome
    Requires GTP

Board Review (11 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions