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MCB - Exam 3 > Gene Expression 2 > Flashcards

Gene Expression 2 Flashcards

1
Q

This percentage of genes in humans undergo alternative RNA processing/splicing.

A

75%

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2
Q

What are 4 types of alternative splicing mechanisms?

A
  1. optional exon
  2. optional intron
  3. mutually exclusive exons
  4. internal splice site
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3
Q

You can prevent RNA splicing by using a ___ and promote splicing by using a ___.

A

Repressor molecule.

Activating molecule.

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4
Q

mRNAs leave nucleus through ___. mRNAs travel to anchor proteins via what mechanisms?

A

Pores.

mRNAs can travel to anchor proteins via cytoskeleton migration, random diffusion, or random diffusion + degradation.

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5
Q

mRNAs poly-A tail confers stability of mRNA. Once reduced to __ nucleotides, two pathways converge to degrade mRNA.

Most mRNAs half-life is __.
Globin mRNA half-life is __.

A

25.

Most mRNA = 30 minutes.
Globin mRNA = 10 hours.

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6
Q

mRNAs can be degraded from both the 5’ end and the 3’ end. This process, ___, exposes the 5’ end, allowing for degradation. This region, ___, is degraded at the 3’ end.

A

Decapping.

Poly-A tail.

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7
Q

During periods of excess iron, you want to store iron and make more ___ mRNA (not protein) and less ___ mRNA.

During periods of iron starvation, you want to absorb iron by making more of this mRNA ___ and decreasing ___ mRNA.

A

Ferritin/Transferrin.

Transferrin/Ferritin.

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8
Q

What happens when cytosolic aconitase is bound to either ferritin or transferrin mRNA.

A

No ferritin made.

Transferrin receptor made.

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9
Q

What happens when one atom of iron is bound to cytosolic aconitase?

A

Aconitase cannot bind to either ferritin or transferrin mRNA. This results in ferritin being made and transferrin not being made.

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10
Q

Excess iron is mainly stored by what organs?

A

Liver, lungs, and pancreas.

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11
Q

This protein, ___, binds thousands of Iron (Fe3+) molecules and is needed for iron storage, and it also comes together to form granules in the form of ___.

A

Ferritin.

Hemosiderin.

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12
Q

This protein, ___, transports iron into cells.

A

Transferrin.

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13
Q

Erythroid precursors in bone marrow have how many TfR molecules per cell?

A

800,000

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14
Q

What does IRP and IRE stand for? In the case of iron regulation, what does each represent?

A

IRP = iron responsive regulatory protein.

IRE = iron responsive element.

IRP = aconitase.
IRE = recognition site on mRNA for binding.
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15
Q

What is the result of the IRP binding to the IRE at the 5’ end of the mRNA? At 3’ end?

A

At 5’ end, if binding occurs, translation is blocked and no ferritin is made.

If the IRP binds at the 3’ end, then transferrin receptor is made.

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16
Q

What is the result of the IRP NOT binding to the IRE at the 5’ end of the mRNA? At 3’ end?

A

If IRP does not bind to IRE at 5’ end, mRNA is made and ferritin is produced.

IF IRP does not bind to IRE at 3’ end, RNA degrades and no transferrin receptor made.

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17
Q

microRNAs regulate what kind of RNAs? How many nucleotides long are these noncoding, microRNAs? Where do the miRNAs bind to on the mRNA and what is the result?

A

mRNA.

22 nucleotides.

miRNAs bind to a complementary sequence in the 3’ UT end of mRNA, resulting in RNA degradation or blocking of translation.

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18
Q

Describe the origin and maturation of miRNAs.

What does RISC stand for?

A

Originates as 100 nucleotide precursors in a pri-miRNA form (RNA with hairpin loop). Cut down in size to pre-miRNA.

Precursor miRNA is cropped in nucleus. Cleaved by Dicer enzyme in cytosol, then miRNA joins with Argonaute to form RISC.

RISC = RNA-induced silencing complex.

19
Q

What results from the complementary matching of the miRNA and mRNA? In other words, what happens when there is an extensive match and a less extensive match?

A

Extensive match = faster degradation of mRNA.

Less extensive match = reduced translation.

20
Q

T/F: A miRNA can regulate more than 1 mRNA?

T/F: Each miRNA can repress hundreds of mRNAs.

A

True.

True.

21
Q

How many miRNAs, occurring in clusters in the genome, are in the human genome?

A

About 1,000.

22
Q

Name a few disease states where miRNAs could be elevated.

What disease states are miR-141 and miR-29 associated with?

A

Stroke, CVD, cancer.

miR-141 serum levels are elevated in prostate cancer.

miR-29 is decreased in heart disease.

23
Q

Are the changes in miRNA expression causative of disease or responsive to disease?

A

Both!

miRNA mutations likely cause disease, and increased miRNA expression down regulates genes in response to limit disease severity.

24
Q

A variant of this gene, ___, is associated with Tourette’s Syndrome?

How does the mutation of this gene change expression and cause Tourette’s?

A

SLITRK1.

The mutation in SLITRK1 causes miR-189 to bind more efficiently to 3’UT region of SLITRK1, decreasing SLITRK1 expression, leading to Tourette’s.

25
Q

T/F: Post translational modifications are required by proteins to be functional?

Name some ways that proteins can be post-translationally modified?

Name on modifying enzyme that can act on a protein.

A

True.

Binding to co-factors, glycosylated, bind to other protein subunits.

Thrombin cuts fibrinogen to form fibrin.

26
Q

Many molecular chaperones are these kinds of proteins, which are synthesized in high amounts when body temperature rises.

Why are these proteins produced when temp rises?

Name two major families of heat shock proteins.

A

Heat shock proteins.

increase in temperature causes an increase in misfolding of proteins.

Hsp60 and Hsp70.

27
Q

These proteins, __, account for 2% of the cell’s protein, and each one contains this many, __, active sites in the central barrel that are ATP dependent.

A

Proteasomes.

6.

28
Q

Describe the steps of tagging proteins for degradation using ubiquitin tags.

A
  1. Ubiquitin binds to E1
  2. E1 binds to ubiquitin ligase (E2 + E3)
  3. Ubiquitin tag moves from E1 to E2/E3, and E1 dissociates.
  4. Protein signaled for degradation binds to ubiquitin ligase, and ubiquitin tag transferred from E2 to protein (on lysine side chain).
  5. Each successive ubiquitin tag is added to previous ubiquitin by E1 enzyme.
  6. Proteasome recognizes ubiquitin chain as target for degradation.
29
Q

How many E1, E2, and E3 proteins are there?

A 
E1 = 2
E2 = 30-40
E3 = 600-750
30
Q

Proteasome inhibitors have been used to treat this disease, __. What type of cells does this disease affect?

This drug was the first drug used a proteasome inhibitor, and the first patient was “pt007 JB.”

A

Myelomas.

Plasma cells.

Bortezomib.

31
Q

What is the theory behind why inhibiting the proteasome with Bortezomib treats myelomas?

A

proteasome inhibition may prevent degradation of pro-apoptotic factors for cell suicide. Therefore, inhibiting proteasome with bortezomib increases apoptosis.

32
Q

T/F: Increasing proteasome activity could enhance clearance of misfolded proteins in diseases like Alzheimer’s.

A

True.

33
Q

What three ways can ubiquitin ligase become activated?

A
  1. phosphorylation by protein kinase
  2. allosteric binding of ligand.
  3. allosteric binding of protein subunit.
34
Q

What three ways can the protein degradation signal become activated?

A
  1. phosphorylation by protein kinase.
  2. unmasking by protein dissocation.
  3. creation of destabilizing N-terminus.
35
Q

What is one example of coordinated gene expression in response to need?

A

glucocorticoid cortisol (response to stress) increases blood sugar and aids in fat, protein, carb metabolism.

diurnal = high at 8am and low at midnight.

36
Q

Induction of regulatory proteins at each cell division is one way that cells specialize which can produce what?

What type of cells undergo this type of specialization, starting from HSCs, then producing HPCs, and so on? What does HSC and HPC stand for?

A

Several different cell types.

Blood cells.

HSC = hematopoietic stem cell

HPC = hematopoietic pluripotent stem cell.

37
Q

What is the result of DNA methylation?

Cytosine is methylated to form ___.

Can methylation of genes be inherited? If so, how?

A

Methylation shuts down expression of genes.

5-methylcytosine

Yes. Methylation of cytosine by maintenance methyltransferase. DNA methylation of parent strand serves as template for daughter strand.

38
Q

This process of differential expression of genetic material depending on the parent of origin is based on DNA methylation. What is the name of this phenomenon?

A

Genomic Imprinting.

39
Q

T/F: The imprinted allele is the expressed allele.

A

False. The imprinted allele (imprinted with methyl groups) is silent and the non-imprinted allele is expressed.

40
Q

Name a genomic imprinting disorder given during lecture. Describe the inheritance pattern of PWS.

A

Prader Willi Syndrome (PWS).

Subject inherits gene deletion on chromosome 15 from father, and the maternal genes are not expressed due to imprinting. Because of this combination, there is no gene expression, resulting in PWS.

41
Q

Describe some clinical presentations of PWS.

A

Stage One: infantile hypotonia, poor suck, feeding difficulties (failure to thrive).

Stage Two: Hyperphagia (uncontrollable eating); onset of early childhood obesity. (average around 2 years old, can range from 1-6).

Hypogonadism, short stature, small hands/feet, hypopigmentation, mental deficiency, behavioral problems (OCD).

42
Q

X-inactivation occurs in males or females?

This results in females being ___ of 2 types of cells.

A

Females.

Mosaics (Either the paternal X or maternal X is inactivated).

43
Q

Inactivation of the specific X-chromosome is inherited in daughter cells. Inactivation starts and spreads from the ___.

___ is made there, which then coats and inactivates the rest of the X-chromosome.

A

X-inactivation Center (XIC).

XIST RNA.

MCB - Exam 3 (11 decks)

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