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MCAT Miscellaneous > Review 4 > Flashcards

Review 4 Flashcards

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MCAT flashcards
1
Q

Telomere

A
  1. Protect ends of chromosomes from degradation
  2. If not telomeres:
    a. Genes will be lost
    b. Act as a buffer zone
    c. Prevent chromosomes from sticking to each other
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2
Q

Single Copy DNA

A
  1. Holds most of the organism’s important genetic information
  2. Transcribed and translated
  3. Lower mutation rate
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3
Q

Somewhat Repetitive DNA

A
  1. Found near centromeres
  2. May contain genes that are transcribed and translated
  3. Higher rate of mutation
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4
Q

Highly Repetitive DNA

A
  1. No genes
  2. Not transcribed and translated
  3. E.g. telomeres
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5
Q

Topoisomerase

A
  1. Unwinds DNA

2. Breaks backbone temporarily for DNA

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6
Q

Helicase

A

Breaks H-Bonds

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7
Q

RNA Primer

A

Adds some nucleotides for DNA polymerase to continue catalyzed by DNA primase

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8
Q

Polymerase and addition to the 5’ end

A

It works by not adding to the 5’ end

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9
Q

Strands in Transcription

A

Template strand = Noncoding Strand

Complimentary strand = Coding Strand

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10
Q

Primary modifications to pre-mRNA in Eukaryotes

A
  1. Addition of 5’ Cap - Modified Guanine (Phosphate I think), converts to a 3’end?
  2. 3’ Poly-A tail (adenine addition), act as buffer for exonuclease.
  3. Intron splicing
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11
Q

Functions of 5’ Cap and 3’ poly A tail modifications

A
  1. Helps with translation
  2. Reduces ends from damage
  3. Helps ensure RNA robusticity
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12
Q

Sites on Ribosome and Functions

A
  1. A - Amino-acyl site
  2. P - Peptide bond site
  3. E - Exit Site
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13
Q

Binding Spot of ribosome on mRNA on Eukaryotes vs. Prokaryotes

A

Shine-Dalgarno sequence for Prokaryotes and 5’ cap for eukaryotes

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14
Q

Translation: Prokaryotes vs. Eukaryotes

A

Prokaryotes- 1st amino acid is Formyl-methionine (f-Met) while Methionine in eukaryotes

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15
Q

Function of f-Met detection in Humans

A
  1. Acts as an alarm system in the human body
  2. Means Bacteria is around
  3. Triggers immune response
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16
Q

DNA Repair Systems

A
  1. 3’ Exonuclease activity - Proofreading
  2. Mismatch repair mechanism - After Replication
  3. Nucleotide Excision Repair - DNA Damage
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17
Q

3’ Exonuclease Activity

A
  1. Occurs at 3’ end

2. Nucleotide is excised and replaced with RNA primer

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18
Q

Mismatch Repair Mechanism

A

Done by proteins that recognize a problem because it distorts the sugar molecule:
1. Mark incorrect base with a cut

  1. Exonuclease removes the incorrect nucleotide
  2. DNA pol inserts correct nucleotide
  3. DNA ligase connects nucleotide to the side and correct complement
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19
Q

How Mismatch distinguishes between parental and daughter strand

A

Parental strand is methylated and Daughter strand is not.

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20
Q

3 Damages UV can do to DNA

A
  1. Cause pyrimidine dimer
  2. Distorts DNA, make it stick out
  3. Alters band
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21
Q

Process that fixes DNA UV Damage

A

Nucleotide Excision Repair

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22
Q

Factors that contribute to DNA damage

A

Endogenous - Internal e.g. reactive oxygen species like peroxides, oxides

  1. Exogenous - External - X-rays, UV rays, and gamma rays
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23
Q

Nucleotide Excision Mechanism

A
  1. Endonuclease will remove pyrimidine dimer or particular wrong nucleotide
  2. DNA pol brings the right nucleotide
  3. DNA ligase attaches to next to complimentary to it
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24
Q

What if nucleotide Excision repair does not work?

A
  1. Cells can become dormant (senescence; where it just remains and does nothing)
  2. Apoptosis
  3. Unregulated cell division (cancer)
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25
Q

2 main Moments of Protein modifications

A
  1. Co-translational e.g. acetylation

2. Post-translational (mostly occur in ER and Golgi)

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26
Q

Post-translational Modification that affects structure

A
  1. Glycosylation
  2. Lipidation/Prenylation - addition of lipid groups to certain membrane-bound enzymes
  3. Carboxylation - addition of carboxylic acid groups, usually to serve as calcium-binding sites
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27
Q

Glycosylation

A
  1. Happens to mostly proteins embedded in the cell membrane
  2. Help identify types of cells
  3. Can be useful as receptors
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28
Q

Lipidation

A
  1. Addition of lipids

2. Happens to proteins that tether to the cell.

29
Q

Post-translational Modification that affects function

A
  1. Ubiquitination
  2. Proteolysis
  3. Methylation
  4. Phosphorylation/Dephosphorylation
30
Q

Phosphorylation/Dephosphorylation

A

Addition/removal of Pi (Inorganic phosphate group) e.g. Na/K ATP Pump:

  1. 3 Na+ ions attached to the protein on the intracellular side
  2. Binding causes ATP to hydrolyze to ADP and Pi
  3. Pi attaches to enzyme and this causes enzyme to close to the outside and open to the extracellular space (Phosphorylation)
  4. While open, 3 Na+ is released and 2 K+ ions bind, to the enzyme. When completely bound, Pi is removed (Dephosphorylation).
  5. Dephosphorylation causes the enzyme to open to the intracellular space while close to the extracellular space.
  6. 2 K+ ions are removed.
31
Q

Goal of Na/K+ ATP Pump

A

To have lower Na+ in the cell and higher outside

32
Q

Methylation

A

Specifically histones:

  1. DNA wrapped around histones
  2. Histones are methylated
  3. Turns on or off genes
33
Q

Proteolysis

A

Sometimes proteins need to be cut (maybe twice) to make it active.

34
Q

Ubiquitination

A
  1. Addition of ubiquitin to a protein

2. Marks protein for degradation

35
Q

LEARN LAC OPERON

A

Arrangement

Repressor Promoter -> Repressor Protein (Constitutively expressed) -> Promoter -> Operator -> Lac Z (Beta-galactosidase) -> Lac Y (Lactose permease) -> Lac A

36
Q

Inducer Exclusion

A

Protein in the presence of glucose breakdown binds to Lac Y and prevents lactose entry in the cell but glucose over lactose

37
Q

Chromatin Regulation

A
  1. Histone acetylation

2. Histone Deacetylation

38
Q

Histone Acetylation

A

Lysine residues are bound to acetyl groups. This allows DNA to be open because positive lysine is now removed and electrostatic attraction is reduced. This leads to EUCHROMATIN and promotes transcription

39
Q

Histone Deacetylation

A

Lysine is deacetylated. It is attracted to DNA (-ve) and leads to HETEROCHROMATIN. This works with CpG methylation. It silences genes

40
Q

How does methylation affect genes

A
  1. Physically impedes it (transcriptional proteins to genes0
  2. Methyl-binding Proteins (MBP) - recruit certain proteins like histone proteins (deacetylase and acetylase) and helps in gene silencing.
41
Q

Basic Transcription Apparatus

A
  1. General transcription factors
  2. RNA polymerase
  3. Mediator multiple protein complex
42
Q

Activators

A

DNA-binding protein:

  1. Enhance binding of RNA polymerase:
    a. Interaction with subunits of RNA pol
    b. Changing DNA structure

e.g: CAP - Catabolic Activating Protein in E.coli

43
Q

Enhancers

A
  1. Part of DNA that binds to activators to loop DNA that brings a specific promoter to transcription factors
  2. Does not need to be close to genes but can even be on another chromosome
44
Q

Repressors

A
  1. Bind to operator

2. Prevents promoter RNA pol to transcribe gene

45
Q

Silencers

A
  1. Bind by repressor protein
  2. Similar to enhancers
  3. Can be upstream or downstream
  4. When they bind, it prevent RNA pol from interacting with promoters
46
Q

Prokaryotes Transcriptional Regulation

A

Purpose - Quickly adapt to changing environment

  1. Activators, repressors
  2. Enhancers (rarely)
47
Q

Eukaryotes Transcriptional Regulation

A

Sophisticated (combination of factors)
1. Nuclear envelope - prevents simultaneous transcription and translation.

  1. Spatial and temporal control of gene expression
48
Q

Introns Regulation Process

A
  1. Gets spliced
  2. Non-coding RNA
  3. Performed by spliceosome
    a. Binds to two ends of introns
    b. Loops in a circle and cuts
    c. Ligase DNA
49
Q

RNA editing

A
  1. Process that leads to sequence variation in RNA molecule
  2. Catalyzed by enzymes
  3. Rare
  4. Insertion, deletion, and substitution
50
Q

ADAR and CDAR RNA Editing Enzymes

A

ADAR - Adenosine Deaminating Acting RNA (A to Inosine)

CDAR - Cytosine Deaminating Acting RNA (C to Uridine)

51
Q

Non-coding RNA

A

TRANSCRIPTION:
1. micro RNA (miRNA) - gene silencing, prevent translation, degradation

Translation:

  1. ribosomal RNA
  2. Transfer RNA tRNA
  3. Small NUCLEOLAR RNA (snoRNA)
    - Guide covalent modifications of rRNA,tRNA< etc.

a. Methylation
b. Pseudoridylation - addition of isomer (nucleotide uridine)

Pre-mRNA:

  1. snRNA (small NUCLEAR RNA)
    a. Process pre-mRNA in the nucleus
    b. Regulation of TF
    c. Maintain telomeres
52
Q

Spliceosome

A

snRNA + proteins (example of snRNP):

a. Two sequential transesterification reactions
i. Splice out introns
ii. Ligate the two exons

53
Q

Mitogen

A

Something that encourages a cell to start cell division

- Triggers mitosis

54
Q

Three things to trigger an oncogene

A
  1. Point mutation/Deletion
  2. Gene Amplification/Instability
  3. Chromosomal Rearrangement
55
Q

Deletion/Point Mutation

A

Removal/Change in nucleotides

  • Hyperactive protein
  • Overexpressed protein
56
Q

Gene Amplification

A

a. increased mRNA instability
b. Increased expression in cell and activity
c. Overexpressed protein

57
Q

Chromosomal Rearrangement

A

a. Translocation to a regulatory sequence
b. Fusion to actively transcribed region
c. Overexpressed or hyperactive protein

58
Q

Oncogene Examples

A
  1. Src - Sarcoma
  2. Ras - GTPase
  3. Myc - TF
  4. RTK - Receptor Tyrosine Kinase
  5. CTK - Cytoplasmic Tyrosine Kinase
59
Q

Src

A
  1. Sarcoma
  2. Tumor of mesenchyma or connective tissue
  3. Codes for non-receptor kinase
60
Q

Ras

A
  1. GTPase
  2. GTP -> GDP + Pi
  3. MAPK and other downstream cascade activation
61
Q

Myc

A
  1. Transcription factor
  2. Chromsome 8 and 14
  3. Burkitt’s Lymphoma
62
Q

RTK

A
  1. Receptor Tyrosine Kinase
  2. E.g:
    a. VEGF
    b. EGFR
    c. PDGF
63
Q

CTK

A
  1. Cytoplasmic Tyrosine Kinase
    a. Survival
    b. Migration
    c. Differentiation
    d. Proliferation

E.g:
Bcr -> Abl gene -> CML aka Philadelphia Chromsome

64
Q

Characterize Oncogene and Tumor Suppressor Genes

A

Mutated Oncogene - Dominant

Mutated Tumor Suppressor Genes - Recessive

65
Q

Tumor Suppressor Genes

A
  1. p53

2. pRb - Retinoblastoma Protein

66
Q

pRb

A
  1. Prevents retinal cells from replicating when DNA damage
  2. Halts G1 -> S when DNA damage detected
  3. Histone Deacetylation (lowers transcription)
  4. Mutation = Retinoblastoma
67
Q

p53

A
  1. Halts G1 -> S when DNA damage detected
  2. Bind DNA and activates p21 which binds to cyclin CDK and holds cell hostage at G1->S phase
  3. Apotosis
68
Q

Mutation of p53

A

Can also lead to deviation from 2 hit hypothesis
1. Prevents product of normal p53 from working

  1. Dominant negative region and deviation from 2 hit hypothesis

MCAT Miscellaneous (17 decks)

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