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Molecular Exam 3 > Control of Gene Transcription II > Flashcards

Control of Gene Transcription II Flashcards

1
Q

Alternative Splicing produces _____ forms of proteins from the _____ gene.

A

Different

Same

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2
Q

What is negative regulation of alternative splicing?

A

Repressor molecule prevents splicing machinery access to splice site

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3
Q

What is positive regulation of alternative splicing?

A

Activating molecule recruits and helps direct splicing machinery

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4
Q

What are the 3 ways the mRNA can leave the nucleus through pores?

A
  1. mRNA use cytoskeletal motors to travel to destination. Anchor proteins hold mRNA in place
  2. mRNA randomly move and some are trapped by anchor proteins
  3. mRNA randomly move and those that are not trapped by anchor proteins are degraded
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5
Q

What are the 2 modifications that make RNA stable?

A

3’ poly- A tail

5’ cap

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6
Q

Poly- A tail

A

Confers stability

Gradually shortened by exonuclease
- shortening acts like a timer

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7
Q

What happens to the RNA once its poly- A tail has been reduced to 25 nucleotides?

A

mRNA is degraded

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8
Q

What is the function of the 5’ cap?

A

Serves to protect RNA from RNA degrading enzymes

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9
Q

Name and describe the 2 RNA degrading pathways.

A

Decapping
- mRNA degraded from 5’ end

Poly- A tail timer
- mRNA degraded from 3’ end through poly- A tail into coding region

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10
Q

Describe Ferritin mRNA

A

Very large intracellular protein that stores iron

Binds thousands of iron per molecule

Found in most cells

Granules of Ferritin = Hemosiderin

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11
Q

Where is excess iron stored?

A

Liver
Lungs
Pancreas

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12
Q

Describe Transferrin- Receptor mRNA (TfR)

A

Absorbs iron

TfR binds diferric Tf

  • enters membrane via clathrin- coated invagination
  • increase in [H+] causes iron to break off Tf
  • TfR are recycled back outside membrane
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13
Q

Describe what is happening to iron and Ferritin/ TfR in Iron Starvation

A

Cells do not need to store iron
- decrease Ferritin mRNA (encodes storage protein)

Cells must transport iron into cells
- make more transferrin receptor mRNA (TfR)

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14
Q

Describe what is happening to iron and Ferritin/ TfR in Iron Excess

A

Cells need to store excess iron
- make more Ferritin mRNA

Cells transport less iron into cells
- make less TfR mRNA

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15
Q

What are IREs?

A

Iron Responsive Elements

Acts as recognition sites for binding

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16
Q

What re IRPs?

A

Iron Responsive Regulatory Protein

Bind to IREs

Aconitase

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17
Q

Describe the action/ result of IRP binding at 5’ Ferritin mRNA

A

IRP binds to IRE at 5’ Ferritin mRNA

No Ferritin is made

Translation is blocked

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18
Q

Describe the action/ result of IRP binding at 3’ Transferrin Receptor mRNA

A

IRP binds to IRE at 3’ Transferrin Receptor mRNA

Transferrin Receptor is made

mRNA is stable

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19
Q

What happens if IRP does NOT bind to IRE at 5’ Ferritin mRNA?

A

mRNA is made

Makes Ferritin

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20
Q

What happens if IRP does NOT bind to IRE at 3’ Transferrin Receptor mRNA?

A

RNA degrades

No Transferrin Receptor made

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21
Q

Describe iron starvation with respect to IRP and IRE

A

Cell needs to transport more iron

IRP binding to IRE of Ferritin:

 - No mRNA made
 - Do not need to store iron

IRP binds to IRE at 3’ Transferrin Receptor mRNA

 - Transferrin Receptor made
 - Need to collect more iron
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22
Q

Describe iron excess with respect to IRP and IRE

A

Cell needs to store more iron

Need Ferritin not TfR

IRP binds to iron to inactivate it
- Ferritin made with no suppression

No binding of IRP to TfR IRE
- No TfR made

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23
Q

What are microRNAs?

A

Regulatory RNAs that regulate mRNAs

Noncoding RNAs

Function to silence expression of specific mRNA targets

  • act as repressors
  • degrade RNA or block translation
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24
Q

Where do microRNAs bind on mRNA?

A

Bind to complementary sequences in 3’ UT end of mRNA

25
Q

What is the formation pathway of miRNAs?

A
  1. Precursor miRNA
  2. Cropped in nucleus
  3. Forms double stranded loop structure
  4. Cleaved by Dicer enzyme
  5. Joined by Argonaute and other proteins to form RISC
  6. Base pairs with mRNA
  7. Cleaves RNA
  8. Shuts down expression
26
Q

What is the result of miRNA overlapping with a LARGE portion of mRNA?

A

mRNA is degraded

27
Q

What is the result of miRNA overlapping with a SMALL portion of mRNA?

A

Translation is reduced

28
Q

T/F: miRNA can regulate more than 1 mRNA

A

True

29
Q

What are examples of miRNAs changing their expression profile in disease states?

A

Circulating levels of miRNAs can be used to identify cancers
- miR- 141 serum levels are elevated in prostate cancer (serves as biomarker)

miR- 29 is decreased in expression in heart disease

30
Q

What does it mean if changes in miRNA expression are causative?

A

miRNA likely have mutations which cause disease

31
Q

What does it mean if changes in miRNA expression are responsive?

A

Increased miRNA expression down regulates genes in response to disease to limit severity

32
Q

How is Tourette’s Syndrome an example of miRNA changes being causative?

A

Neurological disorder (motor and vocal tics)

miRNA involved in 1 form - variant of SLITRK1

  • change in recognition sequence on target SLITRK1 mRNA
  • leads to increased miRNA binding
  • miR-189 binds more efficiently to target sequence in 3’ UT of SLITRK1 gene
  • leads to decrease in SLITRK1 expression
  • leads to Tourette’s Syndrome
33
Q

What is required in order for proteins to functional?

A

Post- translational modifications

Must fold into their proper 3D conformations
- aided by molecular chaperones

34
Q

What are some examples of protein regulation by post- translational processing and modification?

A

Binding cofactors

Modification by protein kinases

Glycosylation

Bind to other protein subunits / protein partners

Modifying enzymes act on protein
- ex: thrombin cuts fibrinogen to form fibrin in blood clotting

35
Q

Heat shock proteins

A

Synthesized in dramatic amounts when temperature is raised

Increase in temperature leads to increase in misfolding of proteins

Feedback mechanisms help synthesize chaperones to help proteins refold

36
Q

How does the proteasome control protein activity?

A

Chooses what proteins are around

Removes misfolded protein

Destroys aberrant proteins

37
Q

What are the components of the proteasome?

A

Hollow chamber and caps

Caps bind to proteins selected for destruction

  • acts as a gate for proteasome
  • activated upon demand

Has 6 active sites - ATP dependent

38
Q

What is ubiquitin’s role in regulation by protein degradation?

A

Removed unfolded or abnormal proteins

Identifies protein to destroy
- acts as a recognition tag

39
Q

Describe pathway from E1 to E3

A

E1 ubiquitin activating enzyme = start
- ubiquitin is linked to cytosine side chain of E1

Ubiquitin is transferred to E2 ubiquitin conjugating enzyme with accessory protein E3 ubiquitin ligase

At this point, primed to mark proteins for destruction

40
Q

Ubiquitin chain is added to the _____ side chain on protein.

Where is each successive ubiquitin added?

A

Lysine

Each successive ubiquitin added to lysine of ubiquitin chain by starts with E1 enzymes

41
Q

T/F: E1, E2, and E3 provide a lot of specificity for binding to specific proteins

A

True

Can make a lot of combinations of E1, E2, and E3 enzyme

42
Q

How are proteasome inhibitors used to treat myelomas?

A

Myelomas interferes with RBC production

Bortezomib = proteasome inhibitor, very effective

Proteasome chamber has 3 proteolytic sites

  • Bortezomib interacts with 1 proteolytic sites
  • reversibly inhibits proteasome
  • may prevent degradation of pro-apoptotic factor for cell suicide
    • triggers programmed cell death in neoplastic cancer cells
43
Q

Proteasome inhibition in cancer cells leads to _____ which makes it a great target for therapy

A

Apoptosis

44
Q

What are the two ways to enhance clearance of misfolded proteins?

A

Activation of ubiquitin ligase

Activation of target protein degradation signal

45
Q

Describe activation of ubiquitin ligase

A

Phosphorylation by protein kinase

Allosteric transition caused by ligase binding

Allosteric transition caused by protein subunit addition

46
Q

Describe activation of target protein degradation signal

A

Phosphorylation by protein kinase

Unmasking by protein dissociation

Creation of destabilizing N- terminus

47
Q

What are examples of controls of gene expression?

A
  1. Coordination of gene expression
  2. Decision for specialization
  3. DNA Methylation
  4. X Chromosome Inactivation
48
Q

Describe coordination of gene expression

A

Expression of critical regulatory protein can trigger battery of downstream genes

Occurs in response to need

Ex: glucocorticoid cortisol

  - released in response to stress
  - leads to increased blood sugar
  - high in morning, low at night
49
Q

Describe decision for specialization

A

Combinations of gene control can produce many types of cells

Make a decision at each step
- 1 or none –> 2 or 3 –> 4 or 5, etc.

Result in several different cell types

Ex: hematopoiesis

50
Q

Describe DNA methylation

A

Methylated cytosines

Functions to repress gene expression

51
Q

Can DNA methylation be inherited? If so, describe this process

A

Yes, methylation is inherited

Occurs at CG sequence

DNA methylation of parent strand serves as template for daughter strand

52
Q

What is genetic imprinting?

A

Differential expression of genetic material depending on the parent of origin

Expression of some genes dependent on whether genes are inherited from mother or father

Form of epigenetic

53
Q

What is Prader- Willi Syndrome an example of?

A

A genomic imprinting disease

54
Q

Describe Prader- WIlli Syndrome’s cause

A

Caused by paternal deletion on Chromosome 15

Inherit deletion on chromosome 15 from father

Genes in this chromosomal region not expressed when inherited from mom

Paternal genes are not expressed and maternal genes are not expressed even though they are present
- Result = lack of gene expression

55
Q

Describe Prader- WIlli Syndrome’s presentation

A

Stage 1: infantile hypotonia

        - poor suck - feeding difficulties 
        - failure to thrive

Stage 2: Hyperphagia - uncontrollable eating
- onset of early childhood obesity

56
Q

Describe the role of obesity in Prader- Willi Syndrome

A

Obesity is the cardinal feature of PWS

Most significant health problem in these cases

Caused by hyperplasia

Average age of onset = 2 years

Children have greater than 40% body fat

57
Q

Describe the characteristics of children with Prader- Willi Syndrome

A

Short stature

Small hands and feet

Hypopigmentation

Mental deficiency

Behavioral problems

58
Q

Describe X chromosome inactivation

A

Females have double the number of genes on X chromosome (have 2 X’s, males have 1)

Humans cannot deal well with extra segments on chromosomes or extra chromosomes
- Dosage compensation occurs so equal number of genes expressed from X chromosomes is equal in males and females

1 X chromosome is inactivated in females

  • occurs early in development
  • becomes highly condensed
    • Heterochromatin - Barr Body
  • random
59
Q

What does it mean that females are ‘mosaics’?

A

Either the paternal X or maternal X is inactivated

- we don have all of one type inactivated

Molecular Exam 3 (2 decks)

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