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Genetics > Lecture 5: Protein Translation and Gene Regulation > Flashcards

Lecture 5: Protein Translation and Gene Regulation Flashcards

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Biology 101 flashcards
1
Q

What is important to know about the genetic code? 5

A
  1. It is NON-OVERLAPPING with 3 different reading frames
  2. Degenerate/Redundant: more than one code for some AAs
  3. Non-ambiguous: each code is only for 1 AA
  4. Continuous
  5. Vectorial: 5’ –> 3’
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2
Q

First AA in eukaryotes?

A

Methionine

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3
Q

First AA in prokaryotes?

A

N-formyl-methionine (fMET)

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4
Q

Stop codons?

A

UUA
UGA
UAG

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5
Q

What defines the ORF?

A

The AUG

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6
Q

What defines the beginning of the UTR?

A

Stop codon

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7
Q

Start codon?

A

AUG

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8
Q

What are 4 types of mutation? Describe each.

A
  1. Misssense: results in the change of amino acid
  2. Nonsense: results in stop codon
  3. Frame-shift: change “reading-frame” of genetic message due to addition or deletion
  4. Chromosome rearrangements
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9
Q

What bonds between tRNA and AA?

A

Covalent bonds

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10
Q

3 stages of translation?

A
  1. Initiation: tRNA-Met binds to the P site on small subunit, large subunit binds
  2. Elongation: New tRNA-AA enters at A site, peptide bond is formed between the two AAs attached to the tRNA in the A site
  3. Termination: tRNA-Met moves to E site and is released and tRNA-peptide moves to P site
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11
Q

How can a protein be targeted for degradation? How are they degraded? What to note?

A

Covalent attachment of multiple ubiquitins

Degraded by the 26S proteasome into mainly dipeptides

This leaves the ubiquitins intact for reuse

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12
Q

What 2 diseases are associated with defects in the ubiquitin-proteasome system?

A
  1. Sporadic Parkinson’s disease (meaning no known genetic cause)
  2. Familial Parkinson’s disease
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13
Q

If there are 2 Mets coded for in one protein, how does the ribosome know which one is the start codon?

A

The Kozak sequence which is found on the 5’ side of the start codon

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14
Q

2 types of promoters? Describe each.

A
  1. Basal: sequence located within about 40 base pairs (bp) of the start site
  2. “Upstream”: may extend hundreds to thousand of base pairs upstream of the start of transcription
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15
Q

What is the TATA box?

A

DNA sequence that positions RNA Pol at the start of transcription

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16
Q

7 elements needed in gene regulation?

A
  1. Exons
  2. Introns
  3. Transcription start site
  4. Promoter
  5. TATA box
  6. Enhancers
  7. TATA-binding protein
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17
Q

Other name for basal promoter?

A

Core promoter

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18
Q

Where are enhancers located with regards to the gene?

A

Either 5’ or 3’

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19
Q

Where is the TATA box located with regards to the gene?

A

Between basal promoter and exons/introns

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20
Q

List and explain the 11 ways that gene expression can be regulated in eukaryotes.

A
  1. Chromatin Structure: Post-translation modifications of the histones and CpG methylation of DNA affect accessibility of the chromatin to RNA polymerases and transcription factors
  2. Epigenetic Control
  3. Transcriptional Initiation: Specific factors including transcriptional activator and repressor proteins exert control through proximal promoter and enhancer sequences to affect the activity of RNA polymerase
  4. Transcript Processing and Modification: Eukaryotic mRNAs are capped and polyadenylated, and the introns removed
  5. RNA Transport: A fully processed mRNA must leave the nucleus in order to be translated into protein.
  6. Transcript Stability: Eukaryotic mRNAs’ stability can vary greatly from minutes to hours
  7. Control of Transcript mRNA Levels by non-coding RNAs: This small RNA-mediated control can be exerted either at the level of the translatability of the mRNA, the stability of
    the mRNA or via changes in chromatin structure
  8. Post-Translational Modification: Common modifications include glycosylation, acetylation, fatty acylation, disulfide bond formations, etc.
  9. Protein Transport: In order for proteins to be biologically active following translation
    and processing, they must be transported to their site of action
  10. Control of Protein Stability: Many proteins are rapidly degraded, whereas others are highly stable
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21
Q

What is the most important mode for control of eukaryotic

gene expression?

A

Transcriptional initiation

22
Q

Where does post-transcriptional modifications occur?

A

Nucleus

23
Q

What is heterochromatin?

A

Condensed chromatin

24
Q

How can we find regions of eurochromatin? What does this mean?

A

By using DNAse1 (made in pancreas) which cleaves DNA and will bind to eurochromatin

Means it’s a potential regulatory region

25
Q

How is HAT recruited?

A

Through physical interactions with a DNA-bound transcriptional activator

26
Q

What have histone deacetylase inhibitors been used to treat?

A

Mood stabilization and epilepsy

More recently: cancers and inflammatory disease

27
Q

Are enhancers position dependent?

A

NOPE

28
Q

What do enhancers function with?

A

Heterologous promoters

29
Q

How can transcriptional activators be regulated to regulate gene expression? 3 ways, explain each.

A
  1. Regulation of Nuclear Localization: regulatory proteins often reside in the cytoplasm, away from their target genes, until a stimulus signals it to enter the nucleus and activate transcription. The stimulus is often
    phosphorylation which can interconvert a transcription factor back and forth between inactive and active forms
  2. Regulation of DNA Binding: the activity of a transcription factor is also controlled through alteration of its DNA-binding ability. Ligand binding can increase or decrease the affinity for DNA. A transcription factor can also multimerize with itself or another factor modifying its
    control of gene expression
  3. Regulation of Transactivation: some transcriptional activators are already bound to their target sites in gene promoters but remain transcriptionally inactive until they are stimulated (protein modification, phosphorylation)
30
Q

How do DNA-binding proteins interact with DNA?

A

DNA-binding proteins fit into the major groove of the double helix and through amino acid side group interactions with the DNA bases can identify specific sequences

31
Q

How does p53 bind to DNA?

A

As a tetramer

32
Q

How can we utilize CRISPR to regulate genes?

A

Attach DNA-binding proteins to inactive Cas-9 and the guide RNA to target a gene

33
Q

3 modes of hormone action? Describe each.

A
  1. Endocrine action: the hormone is distributed in blood and binds to distant target cells.
  2. Paracrine action: the hormone acts locally by diffusing from its source to target cells in the neighborhood.
  3. Autocrine action: the hormone acts on the same cell that produced it.
34
Q

How do glucocorticoids raise blood glucose?

A

Breakdown of fats and proteins

35
Q

Impact of glucocorticoids on immune system?

A

Suppress the immune system and inhibit the inflammatory response

36
Q

Describe the 2 step model of steroid hormone action.

A
  1. The hormone is transported bound to something in blood b/c hydrophobic ==> it then diffuses through the plasma membrane and binds to the steroid receptor quickly because of hydrophilic cytoplasm, which kicks off the inhibitor bound to the receptor
  2. Activated hormone receptor complexes goes to nucleus and binds DNA as a homodimers
37
Q

3 domains of steroid hormone receptors?

A
  1. AD: activation domain
  2. DBD: DNA binding domain
  3. LBD: ligand binding domain
38
Q

Where are steroid hormone nuclear receptors sequestered?

A

Cytosol

39
Q

What is an oncogene?

A

Gene that has the potential to cause cancer. In tumor cells, they are often mutated or expressed at high levels.

40
Q

What is a tumor suppressor gene?

A

Gene that regulates the growth of cells and can
prevent and inhibit the growth of tumors. When tumor suppressor genes are altered or inactivated (due to a mutation), cell growth is uncontrolled leading to cancer.

41
Q

% of human tumors that contain a mutation or deletion of p53?

A

50%

42
Q

When does the p53 protein accumulate in the cell?

A

When the cell is under stress conditions

43
Q

Are BRCA1 and 2 oncogenes or tumor suppressor genes? Explain.

A

TSG

The proteins are recruited when there is damaged DNA

44
Q

What is c-Myc?

A

A transcription factor that regulates 15% of our genome and is an oncogene`

45
Q

What disease is associated with c-Myc? How so?

A

Burkitt lymphoma

Reciprocal translocation of the c-Myc locus on chromosome 8 with immunoglobulin enhancer on chromosome 14 ==> c-Myc is overexpressed in immune cells

46
Q

3 clinical variants of Burkitt lymphoma? Describe each.

A
  1. The endemic variant is the most common malignancy of children in equatorial Africa and often co-occurs with Epstein-Barr virus (EBV) and malaria infection.
  2. The sporadic variant is a form of non-Hodgkin’s lymphoma and is found outside of Africa.
  3. The immunodeficiency variant usually is associated with HIV infection or occurs in posttransplant patients that are taking immunosuppressive drugs.
47
Q

What causes sickle cell disease? Symptoms?

A

Point mutation in hemoglobin beta subunit (HbS) which causes the formation of sickle-shaped cells that are not flexible and can stick to vessel walls. This causes a blockage that slows or stops blood flow, restricting oxygen delivery to nearby tissues that is accompanied by intense pain

48
Q

What is a potential treatment for sickle cell disease?

A

Increasing the body’s production of fetal hemoglobin by using FOXO3 variants to upregulate expression of HbF

49
Q

When does fetal hemoglobin exist?

A

The last seven months of development and persists in the newborn until ~6 months

50
Q

Genes for adult Hb vs fetal?

A

Adult: alpha2beta2

Fetal: alpha2gamma2

Genetics (5 decks)

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