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AP BIO > Gene Regulation > Flashcards

Gene Regulation Flashcards

1
Q

genomic equivalence

A

each somatic cell type in the body contains the same genome

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2
Q

differential gene expression

A

each somatic cell has same genome but express a different subset of genes that is regulated at many stages

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3
Q

common control point for gene expression for both bacteria and eukaryotes?

A

transcription

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4
Q

activators

A

specific transcription factors that increase gene expression

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5
Q

repressors

A

specific transcription factors that decrease gene expression/silence genes

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6
Q

How is controlling gene expression in eukaryotes?

A

since it is complex, there are many additional control points to regulate gene expression

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7
Q

What plays a direct role in regulating transcription?

A

Histone Modification

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8
Q

What charge are histones?

A

Positive

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9
Q

What are histones?

A

Positive charges protein that DNA is wrapped around

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10
Q

Nucleosome

A

DNA and histone together

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11
Q

Amino end of DNA

A

N terminus

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12
Q

What does the N terminus of each histone have?

A

Provides outward forming “histone tails”

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13
Q

How are histone tails modified?

A

By the addition or removal of specific chemical groups like acetyl groups

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14
Q

What charge is DNA?

A

negative because of phosphate groups

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15
Q

Histone acetylation

A

Acetyl groups are attached to a positive charged amino acid in the tails
Positive charges are neutralized so that the tails no longer bind to negative charge phosphates of DNA in neighboring nucleosomes

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16
Q

What does histone acetylation allow?

A

Promotes a more relaxed structure that allows transcription to occur

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17
Q

Deacetylation

A

Removal of acetyl groups which promotes compact structure that stops transcription

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18
Q

DNA methylation

A

Enzymes add methyl groups to certain genes in a DNA molecule and usually turn off the molecule

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19
Q

Example of DNA methylation

A

Barr Body forms when methyl groups attach to one of a females X chromosome

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20
Q

DNA methylation in genomic imprinting

A

Deletion in chromosome 15
Father - Pradeep-Will
Mother - Angelman
Methyl groups permanently inactivate the expression of either maternal or paternal genes at the start of development

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21
Q

Epigenetic inheritance

A

Above the genome- when traits are transmitted by offspring by mechanisms not involved with the nucleotide/DNA sequence
Histone modifications and DNA methylation

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22
Q

What do epigenetic variation explain regarding twins?

A

One identical twin acquires a genetically based disease while the other does not despite identical genomes

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23
Q

Enhancer

A

Distant/distal control elements that serve as binding sites for specific transcription factors proteins called activators or repressors

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24
Q

What does the enhancer control?

A

Controls the initiation of transcription

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25
Q

Where is an enhancer located?

A

Thousands of nucleotides upstream or downstream from the gene they regulate

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26
Q

What happens when an activator binds to a distal controlled enhancer on a DNA molecule?

A

Causes a DNA bending protein to bring the bound activators closer to the promoter region on DNA

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27
Q

What happens when activators are near a promoter region?

A

Mediator proteins help hold the activators close so that general transcription factor proteins and RNA polymerase can come in to make a mRNA and thus activate transcription

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28
Q

Knowing which proteins to make come from?

A

What protein activators are available in the cell which starts on embryonic development

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29
Q

Scientists used to think that all chromatin during interphase was?

A

Amorphous - “bowl of spaghetti” forming a tangled mass

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30
Q

What are scientists now discovering about chromatin?

A

It cloudiest a specific area within the nucleus and has a defined architecture and does not become entangled and some chromatin is highly condensed during interphase

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31
Q

Heterochromatin

A

Highly condensed chromatin

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32
Q

Traditional loose form of chromatin

A

Euchromatin

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33
Q

Where is heterochromatin mostly located?

A

At the centromeres and telomeres and sometimes arms

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34
Q

Which type of chromatin is available for gene expression?

A

Euchromatin - is accessible for being transcribed
Heterochromatin- is not accessible for being transcribed

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35
Q

Alternative RNA splicing

A

When different mRNA molecules are produced from the same DNA template depending upon which RNA segments are treated as exons and which are treated as introns

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36
Q

Intron and exons choices are controlled by?

A

Proteins specific to a cell type affecting where spliceosome makes its cuts in a mRNA molecule

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37
Q

Alternative splicing explains what?

A

According to Beadle and Tatums hypothesis, “one gene one protein”
We should have 100,000 genes as we have 100,000 proteins
But we have 21,000 genes instead

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38
Q

Are euchromatin and heterochromatin on the same chromosome?

A

Yes

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39
Q

Diff between liver cell, and lens cell expression?

A

If albumin gene is expressed, albumin is made (a blood and egg white protein)
If crystalline gene is expressed, only crystalline is made (a protein of the kens of the eye)
Even tho both cells have both genes

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40
Q

bacterial mRNA is typically degraded by enzymes within how long of its synthesis?

A

few minutes

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41
Q

what does the quick degradation of bacterial mRNA allow for?

A

the bacteria to change protein production quickly if the environment changes

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42
Q

how long does eukaryotic mRNA last?

A

typically survives for hours, days, or even months
*mRNA for making hemoglobin are stable and last for months

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43
Q

how many mRNAs do we have?

A

100,000 mRNA

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44
Q

what have a lifespan before degradation occurs?

A

completed protein like cyclin proteins at the 3 chemical checkpoints in the cell cycle are relatively short lived to allow the cell cycle to function properly

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45
Q

what happens to mark a protein for destruction?

A

the cell attaches a small protein called ubiquitin

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46
Q

what happens once ubiquitin is attached?

A

giant protein/enzyme complexes called proteasomes recognize the ubiquitin tagged proteins that both unfold and begins to degrade them

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47
Q

what happens after proteasomes?

A

proteases, enzymes that break down proteins, break the proteins down to amino acids

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48
Q

what are linked to mutations of proteasomes?

A

cancers rendering cell specific proteins impervious to degradation

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49
Q

steps of protein degradation

A

ubiquitin attaches to protein
complex enters proteasome and turns into peptides
proteases turn peptides into aa

50
Q

are proteasomes and ubiquitin recycled?

A

yes

51
Q

how much of our DNA codes for mRNA that creates proteins?

A

1.5% (~90 M)

52
Q

what are RNA that dont code referred to as?

A

ncRNA (non coding RNA)

53
Q

examples of ncRNA

A

every RNA except mRNA

54
Q

how many ncRNA code for other RNAs>

A

a small fraction - rRNA, tRNA

55
Q

what do ncRNAs hint at?

A

a large and diverse population of RNA molecules in the cell that play critical roles in gene expression

56
Q

Endogenous way to control translation example

A

miRNA

57
Q

what are miRNA?

A

microRNA are single stranded RNA molecules that either degrade target mRNAs or block target mRNAs, stopping translation

58
Q

what are miRNAs made from?

A

a big folded RNA molecule comprised of double stranded hairpin structures

59
Q

Endogenous

A

start inside our cells

60
Q

pre miRNA

A

double stranded RNA with hairpin turns present in our cells

61
Q

what enzyme cuts off the hairpin turn?

A

dicer

62
Q

what does dicer do?

A

cuts off hairpin and trims the end and cuts the hairpin turn into small pieces

63
Q

what happens to one strand of the dsRNA when it is turned into miRNA?

A

one strand of the double strand is degraded

64
Q

what happens once miRNA is created?

A

it links together with an enzyme-protein complex called RISC (RNA induced silencing complex)

65
Q

what does the miRNA and RISC complex do?

A

binds to a complementary target on mRNA to either degrade the mRNA or block translation

66
Q

how much of our genes are regulated by miRNA?

A

about 1/2

67
Q

how does the miRNA and RISC complex cut up mRNA?

A

slicer in RISC cuts it up

68
Q

Exogenous way to control translation

A

using siRNAs by the process of RNAi

69
Q

how did researched discover RNAi?

A

they were trying to make a purple petunia darker, and added another copy of the gene that makes purple and produced an white petunia instead

70
Q

what is RNAi?

A

RNA interference - a process
when an introduced gene is added to existing DNA, the cell thinks the added gene is from a virus, and as the introduced gene is oftentimes slightly different, the cell co-suppresses the expression of all genes (existing and introduced) that express the protein as a precaution

71
Q

where else has co-suppression been observed?

A

by injecting cells with dsRNA with the same or similar sequence to the cell’s existing RNA

72
Q

what RNA do most viruses have?

A

dsRNA

73
Q

what does dicer do in RNAi?

A

interferes by cleaving the dsRNA into small interfering RNA (siRNA) which are 19-25 base pairs long

74
Q

what do the siRNA doe next after forming?

A

bind to RISC which binds complementary to mRNA, and slicer stops translation by cutting and turns off gene expression

75
Q

how is the therapeutic potential to use RNAi process to silence undesirable genes advantageous?

A

method of choice to defend against viral diseases
alternative to vaccination
may be the cure to turning off genes in many protein diseases

76
Q

exogenous

A

starts outside of cell
-virus or researcher injects dsRNA

77
Q

what can random spontaneous mutations lead to?

A

cancer

78
Q

what are the random spontaneous mutations be triggered by?

A

environmental influences

79
Q

what is another way of getting cancer?

A

genetics

80
Q

oncogenes

A

cancer causing genes

81
Q

onco

A

tumor

82
Q

proto oncogenes

A

normal versions of the genes that code for proteins that stimulate normal growth and division

83
Q

genetic changes that create oncogenes often involve?

A

increasing the amount of protein product created

84
Q

cancer cells frequently contain what type of chromosomes?

A

chromosomes that have broken and rejoined incorrectly from one chromosome to another - translocated fragments

85
Q

proto

A

before

86
Q

healthy cells contain what genes that create proteins necessary in cells for cell division?

A

tumor suppressor genes

87
Q

what do tumor suppressor genes do? (3)

A

inhibit excessive cell division
repair damaged DNA
control cell anchorage

88
Q

a mutation in a tumor suppressor gene can lead to what?

A

onset of cancer or uncontrolled cell growth

89
Q

two key tumor suppressor genes

A

Ras proto-oncogene
p53 tumor

90
Q

mutations in ras account for how much of cancer?

A

30%

91
Q

mutations in p53 account for how much of cancer?

A

more than 50%

92
Q

what does the ras gene code for?

A

encodes a Ras G protein involved in ultimately stimulating the cell cycle

93
Q

when does the pathway begin in a cell cycle?

A

when growth factors bind to receptor tyrosine kinase proteins (monomers) which then form a phosphorylated dimer

94
Q

what happens once the dimer is made?

A

activates G protein called Ras, GDP turns to GTP, and this signal passes to a series of protein kinases which activates transcription in the end to stimulate the cell cycle

95
Q

what is the mutation in ras gene?

A

turns on Ras G protein even though no growth factor is present, leading to excessive cell division

96
Q

3 steps involved in cellular response?

A

reception
transduction
cellular response

97
Q

what does the transcription factor (activator) do in the ras gene pathway?

A

turns on a specific gene that increases cell division

98
Q

what does the p53 code for?

A

a transcription factor protein that is involved with cell cycle inhibiting proteins (repressor)

99
Q

what happens if p53’s DNA gets damaged?

A

the p53 gene does not make the proteins that inhibit the cell cycle and can lead to the development of cancer

100
Q

how is p53 involved in DNA repair?

A

it activated a “suicide” gene when DNA is irreparable

101
Q

nickname of p53

A

Guardian Angel of the Genome

102
Q

3 things p53 does to mutated DNA

A

stop cell division
fix DNA
cause apoptosis for the irreparable ones

103
Q

how many somatic mutations are needed to produce a full fledged cancer cell?

A

more than one

104
Q

relation between life and cancer

A

longer we live, the more susceptible we are to cancer

105
Q

how does one get colorectal cancer?

A

multistep path that starts out with a tumor gradually becoming malignant and invading other tissues (metastasis)

106
Q

what is the development of colorectal cancer parallel to?

A

gradual accumulation of mutations that convert proto-oncogenes to oncogenes and knock out tumor suppressor genes

107
Q

an individual inheriting an oncogene or a mutant allele of a tumor suppressor gene is more likely to?

A

develop certain cancers

108
Q

inherited predisposition with breast cancer precentage

A

5-10% of patients

109
Q

how common is breast cancer in the US?

A

2nd most common

110
Q

mutations in what genes are associated with susceptibility to breast cancer

A

BRCA 1
BRCA 2

111
Q

BRCA

A

BReast CAncer

112
Q

BRCA 1

A

60% probability of developing breast cancer before the age 50

113
Q

BRCA 2

A

mutations are found in at least 1/2 of inherited breast cancers

114
Q

wild types of BRCA1 and BRCA2

A

tumor suppressor genes that regulate how breast cell divide and repair DNA mutations - almost like p53

115
Q

mutant alleles of BRCA 1 and BRCA2 are recessive or dominant?

A

recessive

116
Q

what percentage of human cancers do viruses play a role in?

A

~15% of the cases

117
Q

what is the Epstein Barr virus associated with?

A

mononucleosis
Burkitt’s lymphonma

118
Q

what type of virus is HPV?

A

papillomavirus

119
Q

what is HPV?

A

most common sexually transmitted infection in the US

120
Q

what is HPV asoociated with?

A

cervical cancer

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