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Molecular Exam 3 > White- Gene Expression 2 > Flashcards

White- Gene Expression 2 Flashcards

1
Q

True or False: Alternative Splicing produces different forms of proteins from the same gene

A

True

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2
Q

Define a repressor molecule in relation to alternative splicing

A

prevents the splicing machinery from accessing the splice site

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3
Q

Define an activating molecule in relation to RNA splicing

A

it recruits and helps to direct the splicing machinery

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4
Q

What are the 3 ways in which the mRNA is able to travel through the cell? (spatial localization)

A
  1. cytoskeletal motors (anchor proteins and hold mRNA in place
  2. Random movement (diffusion and trapping)
  3. Random movement and degeneration (RNA that is not trapped is degraded)
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5
Q

What is the purpose of the poly A tail?

A

confers stability

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6
Q

Describe the poly A tail in relation to shortening? (how is it shortened? and what does it act as?)

A

shortened by an exonuclease
shortening acts as a timer
once it gets to 25 nucleotides, the two pathways converge and the mRNA is degraded

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7
Q

What are the two ways in which the mRNA can be degraded?

A

decapping (5’ cap protects the RNA from the degrading enzymes- removing= break down)
3’ end via poly A tail degradation

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8
Q

What are the two RNA’s that are involved in iron metabolism? And what do they do?

A

Ferritin mRNA- storage of iron

TfR mRNA- iron absorbance

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9
Q

Describe the iron cycle

A
  1. Iron is absorbed by the intestine
  2. plasma transferrin iron travels to the marrow erythroid precursors (TfR)
  3. goes into the blood stream via circulating erythrocytes
  4. macrophages
  5. recycled back as a plasma transferrin iron

(CAN also go to the liver where it is stored as ferritin)

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10
Q

Describe ferritin.

A

Intracellular protein that is found in most cells

granules=hemosiderin

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11
Q

Where is excess iron stored?

A

Liver, lungs, and pancreas

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12
Q

What happens in the cell during iron starvation?

A
  1. cells do not need to store iron
  2. decrease in ferritin mRNA
  3. cells must transport iron into the cell
  4. make more of the transferrin receptor (TfR) mRNA
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13
Q

What happens in the cell when there is excess iron?

A
  1. need to store the excess iron
  2. make more ferritin mRNA
  3. transport less iron into the cell
  4. make less TfR mRNA
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14
Q

Define IRE and IRP and describe what they do.

A

IRE-iron responsive elements; recognition sites for binding
IRP- aconitase

They bind together and regulate mRNA

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15
Q

What happens if the IRP binds to the IRE at the 5’ end of the ferritin mRNA?

A

translation is blocked

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16
Q

What happens if the IRP binds to the IRE At the 3’ end of the transferrin?

A

The transferrin receptor is made and the mRNA is stable

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17
Q

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

A

mRNA is made and you get ferritin

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18
Q

What happens if the IRP does NOT bind to the IRE at the 3” transferrin receptor?

A

The RNA degrades and no transferrin receptor is made

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19
Q

Describe what happens with IRE/IRP in iron starvation

A

You need more iron obvs sooo

IRP binding to IRE or ferritin, no mRNA is made and you do not need to store iron (bc you want it in the cell)
NO FERRITIN IS MADE

IRP binds to IRE at 3’ transferrin receptor mRNA- transferrin receptor is made and you need to college more iron

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20
Q

What happens with the IRE/IRP when there is excess iron in the body

A

You need to store the iron because you do not need any more;

IRP binds to the iron to inactivate it; ferritin is made with no suppression

IRP does not bind to the TfR IRE and there is not any TfR made

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21
Q

What are microRNA’s and what do they do?

A

They are regulatory RNAs that regulate the messenger RNA’s
REPRESSORS

bind to the complementary sequence in the 3” end of the mRNA

degrade the RNA or block translation; cleaves RNA and shuts down expression

sorry Becky I know that is a lot of words LOL

22
Q

Describe the maturation of the microRNA

A

Starts as a primary miRNA (pri-miRNA)
cuts down in size to a pre-miRNA
processed into mature miRNA

cropped in the nucleus and cleaved by the Dicer enzyme

23
Q

Describe the RISC

A

The RNA induced silencing complex; microRNA joins with the Argonaute and other proteins to form the RISC

24
Q

True or false: An miRNA can only regulate one mRNA

A

False

25
Q

Describe miRNA’s in disease states

A

miRNA can change their expression profile in disease states; can be elevated in CVD or can be used to identify certain cancers

26
Q

Describe how the microRNA’s are causative to the disease

A

The miRNA’s probably have mutations that cause the disease

27
Q

Describe how the miRNA’s are responsive to disease

A

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

28
Q

Describe Tourette’s syndrome

A

It is an example of the microRNA’s being CAUSATIVE

neurological disorder manifested by motor and vocal tics

variant of SLITRK1 gene associated with Tourettes; change in recognition and increased miRNA binding

29
Q

Describe the binding of the miRNA’s involved in tourette’s syndrome

A

miR-189 binds more efficiently to the target sequence of SLITRK1 and decreases its expression (since miRNAs are repressors) and leads to Tourettes

30
Q

Describe the various post-translational modifications and steps required to get to a mature functional protein

A
  1. Nascent polypeptide chain needs to fold into its 3D conformation with the help of chaperones. Can bind to cofactors
  2. the polypeptide can be modified by protein kinases and glycosylated
  3. bind to other proteins
  4. modified enzymes act on the protein
    Mature and functional
31
Q

Describe heat shock proteins. Include what they do, when and why they are made

A

molecular chaperones that help with protein folding

They are made in dramatic amounts with increased temperature

WHY? Because when the temperatures rise, there is more of a chance that the proteins will misfold

32
Q

What are the two families of heat shock proteins?

A

Hsp 60 and Hsp70

33
Q

Describe the proteasome in as much detail as possible

A

Also called the garbage disposal

controls protein activity by deciding which proteins are around

removes misfolded proteins

has a hollow chamber where proteins are degraded; binds to proteins selected for destruction. The hollow chamber acts as a gate for a proteasome- activated upon demand.

34
Q

What is the purpose of ubiquitin?

A

removes unfolded or abnormal proteins via a recognition tag

35
Q

Describe the process of the formation of the ubiquitin ligase that aids in protein destruction.

A
  1. The ubiquitin activating enzyme E1 binds to ubiquitin via a cysteine side chain
  2. ubiquitin is transferred to E2 and E3
  3. complex is primed and marks proteins for destruction
36
Q

Describe the process of adding a protein to the ubiquitin ligase

A

The ubiquitin is added to a lysine side chain on the protein
E1 enzymes continues to add ubiquitin
targeted ubiquitin chain is recognized by the proteasome

37
Q

How can proteosomes be used as therapy?

A

Can treat multiple myelomas- cancer of the plasma cells, abnormal cells accumulate in the bone marrow and interfere with RBC production- specificity of the proteasome inhibits the myeloma cells

proteasome inhibition can prevent the degradation of pro-apoptotic factors for cell suicide; leads to cell apoptosis

38
Q

Describe the activation of the ubiquitin ligase

A
  1. ATP is used to phosphorylate the E2 E3 complex via protein kinase
  2. allosteric transition caused by ligand binding
  3. allosteric transition caused by protein subunit addition
39
Q

Describe the activation of the degradation signal

A
  1. ATP is used to phosphorylate the protein via protein kinase
  2. unmasking via protein dissociation
  3. creation of destabilizing N terminus
40
Q

What are the 4 types of gene expression?

A
  1. coordinated expression of genes; genes do not exist in a vacuum
  2. Decision for specialization; what kind of cell do I want to become?
  3. methylation and genomic imprinting: what genes get expressed from mom and dad
  4. X-chromosome inactivation; evens things out
41
Q

Describe coordinated gene expression

A
  • expression of critical regulatory protein can trigger battery of downstream genes
  • responds to need
    ex: response to stress- increase in blood sugar
42
Q

Describe the decision for specialization

A

The cell is able to make a decision at each step of cell division
(1 or none, 2 or 3, 4 or 5)
different cell types result

43
Q

Describe the various “specializations” that can happen from an HSC (hematopoietic stem cell)

A

HPC: hematopoietic pluripotent stem cell

myeloid lineage and lymphatic lineage

44
Q

What are the cells that come from the myeloid lineage?

A

Erythrocyte, megakaryocyte-> platelets, neutrophil, eosinophil, basophil, and macrophages

45
Q

What are the cells that come from the lymphoid lineage?

A

B cells, T cells, and NK-cells

46
Q

Describe the inheritance of DNA methylation

A

The methylation of cytosine occurs at CG sequences

methylation is inherited

cytosine is methylated by “maintenance methyltransferase”

DNA methylation of the parent strand serves as a template for the daughter strand

47
Q

Define genomic imprinting

A

the expression of some genes based on inheritance from the mother or the father

differential expression of genetic material depending on the parent of origin

48
Q

Define epigenetics

A

The regulation of expression of gene activity without altering gene structure

49
Q

Describe Prader Willi Syndrome

A

caused by a paternal deletion of Chromosome 15; paternal genes are not expressed and maternal genes are not expressed either even though they are present

hypogonadism,
short stature and small hands and feet; behavioral problems,

50
Q

What are the stages of prader will syndrome?

A

1- infantile hypotonia, poor suck, feeding difficulties

2- hyperphagia (uncontrollable eating)

51
Q

Describe X-inactivation

A

Occurs in females; one of the X chromosomes is inactivated via high condensation (heterochromatin)

inactivation is random- can be mom or dads chromosome that is expressed

maintained post cell divisions

52
Q

Where does X inactivation start and spread?

A

At the X inactivation center

XIC makes XIST RNA that coats the entire X chromosome

Molecular Exam 3 (14 decks)

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