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Molecular Biology > Lecture 10 Control Of Gene Expression 2 > Flashcards

Lecture 10 Control Of Gene Expression 2 Flashcards

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AP® Biology flashcards Biology 101 flashcards
1
Q

Alternative splicing produces

A

Different forms of proteins form the same gene

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2
Q

RNA splicing can be regulated negatively by______ that prevent splicing machinery access to splice site

A

Repress or molecule

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3
Q

RNA splicing can be regulated positively by ______ that recruits and helps direct splicing machinery

A

Activating molecule

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4
Q

mRNAs leave nucleus through

A

Pores

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5
Q

After mRNAs leave nucleus through pores they travel to

A

Destination using cytoskeletal motors (anchor proteins hold them in place)

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6
Q

If mRNA is not anchored in the cytoskeleton it

A

Gets degraded

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7
Q

miRNA involvement was found in 1 form of Tourette’s syndrome. The variant in what gene is associated to this 1 form

A

SLITRK1 (change on target mRNA leads to increased mRNA binding)

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8
Q

___% of genes in humans undergo alternative RNA processing

A

75%

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9
Q

Intracellular protein, that binds to thousands of Fe3+/molecule, and is found in most cells

A

ferritin

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10
Q

Granules of ferritin

A

Hemosiderin

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11
Q

Excess iron is mainly stored by

A
  • liver
  • lungs
  • pancreas
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12
Q

During 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 (TfR) mRNA
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13
Q

Iron in excess

A
  • need to store excess iron
  • make more ferritin mRNA (makes storage protein)
  • and transport less iron into cell
  • Make less TfR mRNA (makes Fe transport protein)
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14
Q

mRNA regulation of iron transport involves _____ and _____

A

Iron responsive elements (IREs) and Iron responsive regulatory protein (IRP)- aconitase

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15
Q

When Iron responsive protein binds to Iron responsive elements at the 5’ ferritin mRNA there is

A

no ferritin made

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16
Q

When Iron responsive protein binds to Iron responsive elements at 3’ transferrin receptor mRNA there is

A

transferrin receptor made

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17
Q

____ are regulatory RNAs that regulate messenger RNAs

A

microRNAs

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18
Q

microRNAs are ____ RNAs; ____ nucleotides long- that silence expression of specific mRNA targets

A

noncoding, 22

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19
Q

microRNAs bind to complementary sequences in the _____ end of mRNA

A

3’ UT

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20
Q

microRNAs _____ RNA or _____ translation

A

degrade, block

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21
Q

microRNAs are ____ of gene activity

A

repressors

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22
Q

microRNAs originate as ____ nucleotide precursors

A

100

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23
Q

MicroRNAs is made as a primary miRNA: pri-miRNA- RNA with _____ then it is cut down in size to ______ and then further processed to mature miRNA

A

RNA with hairpin loop, pre-miRNA

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24
Q

Precursor miRNA is ____ in the nucleus and forms a ______ structure it is then further cleaved by ____ enzyme and joins with ___ and other proteins to form __________

A

cropped in the nucleus and forms a double stranded loop structure, Dicer, joins with Argonaute and other proteins to form RISC: RNA-inducing silencing complex

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25
Q

RNA-inducing silencing complex base pairs with ____

A

mRNA

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26
Q

After RISC (RNA-induced silencing complex base pairs with mRNA) base pairs with mRNA it cleaves ____ and _____

A

RNA (note that this requires ATP) and shuts down expression

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27
Q

there are more than _____ miRNAs in the human genome

A

5,600

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28
Q

miRNAs occur in ___ in genome

A

clusters

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29
Q

Can a miRNA regulate more than 1 mRNA

A

yes

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30
Q

each miRNA can repress ______ of mRNAs

A

hundreds

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31
Q

miRNAs may target __% of mammalian genes

A

60%

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32
Q

miRNA binding sites are _____

A

widespread

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33
Q

Can 1 miRNA effect a whole biological program

A

yes

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34
Q

miRNAs change their expression profile in _____ states

A

disease (for example certain miRNAs can be elevated in stroke or cardiovascular disease)

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35
Q

can circulating levels of miRNAs can be used to identify cancer

A

Yes

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36
Q

miRNA-____ serum levels are elevated in prostate cancer

A

141

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37
Q

miRNA-____ decreased in expression of heart disease

A

29

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38
Q

Can miRNA serve as a biomarker

A

yes

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39
Q

Are changes in microRNA expression the cause of disease or response

A
  • both
  • miRNAs likely have mutations that cause disease
  • increased miRNA expression down regulates genes in response to disease to limit severity
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40
Q

Neurological disorder manifested by motor and vocal tics

A

Tourette’s syndrome

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41
Q

Tourette’s syndrome affects as many as ___ in ____ individuals

A

1 in 100

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42
Q

miRNA involvement was found with ___ form of Tourette’s syndrome. what is/are the variant(s)

A

1, Variant of SLITRK1 gene shown associated with Tourette’s syndrome, A change in recognition sequence on target SLITRK1 mRNA increases miRNA binding

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43
Q

change in recognition sequence on target SLITRK1 mRNA leads to

A

increased miRNA binding (thus leading to Tourette’s Syndrome)

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44
Q

miR-___ binds more efficiently to target sequence in 3’UT of SLITRK1 gene and decreases SLITRK1 expression thus leading to Tourette’s syndrome

A

189

45
Q

Post translational modifications are require by proteins to be

A

functional

46
Q

proteins must fold into _____ conformations

A

3-D

47
Q

______ help proteins fold appropriately

A

molecular chaperones

48
Q

examples of post transcriptional modifications required proteins to be funcitonal

A
  • proteins must fold into 3-D conformations
  • molecular chaperones help proteins fold appropriately
  • Bind co-factors
  • Modified by protein kinases
  • Glycosylated
  • bind to other protein subunits or protein partners
  • modifying enzymes act on protein
49
Q

What is an example of modifying enzymes acting on protein

A

Thrombin cuts fibrinogen to form fibrin in blood clotting

50
Q

Many molecular chaperones are _______ synthesized in dramatic amounts when temperature is raised (37 degrees C to 42 degrees C)

A

Heat shock proteins (Hsp)

51
Q

why are heat shock proteins needed

A
  • increase in temperature leads to increase in misfiling of proteins
  • There is feedback to synthesize chaperones (Hsp) to help proteins refold
52
Q

What are the two major families of heat shock proteins

A

HSP60 and Hsp70 (70kDa)

53
Q

proteins can be regulated by degradation by the ______

A

proteasome

54
Q

Hollow chamber where proteins are degraded

A

Proteasome

55
Q

The Proteasome has ____ active sites that are ____ dependent

A

6, ATP

56
Q

The cap area ___ to proteins selected for destruction it then acts as a ____ for proteasome

A

binds, gate

57
Q

What is the recognition tag to help proteasome identify proteins for degradation

A

Ubiquitin

58
Q

ubiquitin is about ____ amino acids

A

76

59
Q

____ ubiquitin activating enzyme involved in first step of marking protein for degradation

A

E1

60
Q

The first step of marking a marking of proteins by ubiquitin C-terminus of ubiquitin is initially activated by being linked via a high-energy thioester bond to the _____ side chain on the ____

A

Cysteine, E1 protein

61
Q

The second step of marking a protein with ubiquitin is the ubiquitin is transferred to

A

E2 ubiquitin ligase (with accessory protein E3)

62
Q

after the ubiquitin is transferred to E2 ubiquitin ligase (with accessory protein E3) the complex is now

A

primed to mark proteins for destruction

63
Q

Ubiquitin removes

A

unfolded or abnormal proteins

64
Q

Addition of ______ (with degradation signal) to ubiquitin ligase primed with ubiquitin. And the first ubiquitin chain is added to _____ side chain on protein

A

protein, lysine

65
Q

after the addition of the first ubiquitin each successive ubiquitin added to ____ of ubiquitin chain by ______

A

lysine side chain of ubiquitin chain by E1 enzymes

66
Q

Targeted ubiquitin chain on target protein is recognized by ____

A

proteosome

67
Q

Apparatus that deliberately destroys aberrant protein

A

Proteasome

68
Q

in humans their are ____ E1 ubiquitin activating enzymes

A

two

69
Q

In humans their are ____ type of proteasome

A

1

70
Q

In humans there are ____ types of E2 ubiquitin conjugating enzymes and ____ of E3 accessory proteins

A

30-40 and 600-750

71
Q

Proteasome inhibitors are used to treat

A

multiple myelomas

72
Q

Cancer of plasma cells

A

myelomas

73
Q

Myelomas leads to abnormal cells accumulating in bone marrow and this interferes with ____ production leading to _____

A

RBC production leading to anemia

74
Q

Multiple myelomas are incurable but

A

treatable

75
Q

What is the drug name for an inhibitor of proteasome that is highly effective in treating multiple myeloma

A

Bortezomib

76
Q

what was the first patient treated with Bortezomib

A

pt007 JB

77
Q

The chamber in proteasome has ___ proteolytic sites

A

3

78
Q

Bortezomid interacts with ___ proteolytic sites in proteasome

A

1

79
Q

Ubiquitin ligase is activated by

A
  • phosphorylation by protein kinase
  • allosteric transition caused by ligand binding
  • allosteric transition caused by protein subunit addition
80
Q

ways the target protein degradation signal can be activated

A
  • phosphorylation by protein kinase
  • Unmasking by protein dissociation
  • creation of destabilizing N-terminus
81
Q

Other controls of gene expression

A
  • coordinated expression of genes: genes do not exist in a vacuum
  • Decision for specialization: what kind of cell do I want to become
  • methylation and genomic imprinting: what genes get expressed (or not) from Mom and Dad
  • X-chromosome inactivation: even things out XX vs. XY- 2 X chromosomes vs. 1 X chromosome
82
Q

What is coordinated gene expression

A
  • expression of critical regulatory protein can trigger batter of downstream genes
  • coordinated gene expression in response to need
83
Q

What is an example of coordinated gene expression

A

Glucocorticoid cortisol- response to stress- increase blood sugar- aid in fat, protein, carbohydrate metabolism (hiest at 8am and lowest at midnight)

84
Q

Explain decision for specialization

A
  • combinations of gene control can produce many types of cells
  • Decision at each step
  • result is several different cell types
85
Q

what is an example of decision of specialization

A

Hematopoiesis (HSC becomes HPC that can then become lymphoid lineage or myeloid lineage)

86
Q

what is the effect of DNA methylation on gene expression

A

it represses gene expression

87
Q

Can we inherit DNA methylation

A

yes

88
Q

Cytosine is methylated by _____

A

maintenance methyltransferase

89
Q

DNA methylation of the parent strand

A

serves as a template for daughter strand

90
Q

Genomic imprinting is based on ______

A

DNA methylation

91
Q

what is genomic imprinting

A
  • differential expression of genetic material depending on the parent origin
  • expression of some genes depends on whether genes inherited from mother or father
92
Q

Regulation of expression of gene activity without altering gene structure

A

Epigenetics

93
Q

What is an example of epigenetics

A

methylation

94
Q

Caused by paternal deletion on chromosome 15 in the region of 15q11-q13 (paternal genes expressed) while the maternal is silenced

A

Prader Willi (PWS) syndrome

95
Q

Prader Willi syndrome (PWS) subjects inherit gene deletion from

A

father (note the deletion is on chromosome 15)

96
Q

Stage one of Prader Willi (PWS) syndrome

A

Infantile hypotonia; poor suck; feeding difficulties- failure to thrive

97
Q

Stage two Prader Willi syndrome (PWS)

A

Hyperphagia (uncontrollable eating); onset of early childhood obesity

98
Q

____ is a cardinal feature of Prader-Willi syndrome (PWS) and most significant health problem

A

Obesity

99
Q

What is the major cause of obesity in order will syndrome (PWS)

A

Hyperphagia

100
Q

What is the average age of onset for Prader Willi obesity ___ years ; range _____ years may occur as early as ___ months

A

2 years, range 1-6 years may occur as early as 6 months

101
Q

Prader-willi syndrome may lead to greater than ___% body fat, or ____ times higher than in the general population

A

40%, or 2-3 times higher

102
Q

What are the symptoms of Prader-Wlli syndrome

A
  • obesity
  • Hypogonadism
  • short stature; small hands and feet
  • hypopigmentation
  • mental deficiency; behavioral problems (skin picking, obsessive compulsive disorder)
103
Q

What causes Prader Willi syndrome (PWS)

A

Paternal 15q11-q13 deletion: inherit deletion on chromosome 15 from Dad while maternal genes are not expressed (even though they are normal) this is due to genomic imprinting

104
Q

____ occurs so equal number of genes expressed from X chromosome is equal in males and females

A

dosage compensation

105
Q

The inactivation of one X chromosome in females occurs _____, The inactive chromosome becomes very highly condensed forming a ____. This inactivation is ____

A

early in development, Barr body, random

106
Q

Why are females mosaics of 2 types of cells

A

either the paternal X or maternal X is inactivated

107
Q

Inactivation of X chromosome is maintained post cell divisions. reprogramming of X chromosomes occurs during

A

gamete cell formation

108
Q

The ______ is where inactivation of X chromosome start and spreads

A

X-inactivation center (XIC)

109
Q

The X-inactivation center (XIC) makes _____ RNA that coats entire X chromsome

A

XIST RNA

Molecular Biology (14 decks)

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