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Biology > 20. GENE EXPRESSION > Flashcards

20. GENE EXPRESSION Flashcards

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1
Q

What is the single cell produced from fertilisation called?

A

Zygote

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2
Q

How does a zygote produce more cells to become an embryo and then a foetus?

A

Mitosis

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3
Q

What causes cells to become differentiated?

A

Certain genes stay switched on, and certain genes are switched off

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4
Q

Which proteins do the genes that are switched on in a cell code for?

A

The proteins that are required to carry out the cell’s specialised function

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5
Q

Which proteins do the genes that are switched off in a cell code for?

A

The proteins that are not required to carry out the cell’s specialised function

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6
Q

Which genes are usually always switched on in most cells?

A

The genes that code for respiratory enzymes

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7
Q

Define what stem cells are

A

Stem cells are undifferentiated cells that have the ability to keep dividing

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8
Q

Define what cell potency is

A

Cell potency is the varying ability of stem cells to differentiate into different specialised cells

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9
Q

What happens to the potency of most cells as they become more specialised?

A

Cells gradually lose potency as they become more specialised

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10
Q

Name the types of potency a cell can have, from the highest to the lowest potency

A

Totipotent, Pluripotent, Multipotent and Unipotent

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11
Q

How many types of cells can multipotent cells differentiate into?

A

Multipotent cells can differentiate into any cell type

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12
Q

Give an example of totipotent stem cells

A

Embryonic stem cells

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13
Q

How many types of cells can pluripotent cells differentiate into?

A

Pluripotent cells can differentiate into almost any cell type

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14
Q

Give an example of pluripotent stem cells

A

Embryonic and foetal stem cells

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15
Q

How many types of cells can multipotent cells differentiate into?

A

Multipotent cells can differentiate into a limited number of cell types

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16
Q

Give an example of multipotent stem cells

A

Adult and umbilical stem cell

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17
Q

How many types of cells can unipotent cells differentiate into?

A

Unipotent cells can only differentiate into one cell type

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18
Q

Give an example of unipotent cell

A

Differentiated adult somatic cells

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19
Q

Which potency of cell are the only ones that can rise to a whole new organism?

A

Totipotent (stem) cells

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20
Q

Why are pluripotent stem cells useful for treating certain conditions of organs?

A

Because they can differentiate into and therefore replace the many different cell types within an organ

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21
Q

Describe the two disadvantages of using pluripotent stem cells to treat conditions of organs

A

The might differentiate into the wrong cell type, or divide uncontrollably to form a tumour

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22
Q

Which potency of cell are useful for treating conditions caused by non-functioning blood cells?

A

Multipotent (adult) stem cell

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23
Q

Define what iPS cells are

A

iPS (induced pluripotent stem) cells are a type of pluripotent stem cell produced from unipotent stem cells

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24
Q

Describe how iPS cells are produced from unipotent cells

A

Unipotent cells are genetically altered by using transcription factors to switch genes on

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25
Q

How are iPS cells used?

A

Once iPS cells are formed from a patient’s cell, they are induced to become another type of unipotent cell. This can then be used to treat conditions in the patient.

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26
Q

Why are iPS cells useful in treating conditions?

A

The new unipotent cell wouldn’t be rejected as it contains the patient’s DNA.

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27
Q

Define what gene expression / gene regulation is

A

The control of the protein production

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28
Q

Name the two ways gene expression occurs in cells

A

Transcriptional control, and translational control

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29
Q

How is gene transcription controlled?

A

Transcriptional factors

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30
Q

Describe the structure of a transcriptional factor

A

A receptor, which contains the binding site for another molecule. A DNA binding site, which binds to the gene’s promoter.

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31
Q

If a transcriptional factor is switching a gene on, will it be active or inactive before the molecule bind to the receptor site?

A

Inactive

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32
Q

Describe the effect of the molecule binding to the receptor site

A

It changes the tertiary shape of the transcriptional factor, making the DNA binding site complementary to the gene promoter

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33
Q

Describe the effect of the DNA binding site of the transcriptional factor binding to the gene promoter

A

This allows RNA Polymerase to bind to the promoter, initiating transcription and forming mRNA

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34
Q

Name an example of a steroid hormone that binds to a transcriptional factor

A

Oestrogen

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35
Q

How would a mutation in the gene that coded for the transcription factor reduce the production of a protein?

A

The mutation would cause a change in the tertiary shape of the transcription factor, making it non-complementary to the gene.

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36
Q

What is siRNA short for?

A

Short Interfering RNA

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37
Q

What are siRNAs?

A

Short double-stranded sections of RNA.

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38
Q

How do siRNAs control gene expression?

A

By initiating the breakdown of mRNA to control translation

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39
Q

siRNAs start as large double-stranded molecules of RNA. How are they processed into siRNAs?

A

They are cut into smaller siRNAs, which become single stranded

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40
Q

What do siRNAs combine with before they act?

A

An enzyme

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41
Q

How do siRNAs bind to their target mRNA?

A

The bases on the siRNA bind to the mRNA by complementary base pairing

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42
Q

How does the siRNA break down the target mRNA?

A

The enzyme cuts the target mRNA into smaller pieces

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43
Q

How could siRNAs be used to treat cancer?

A

They could be artificially produced to silence genes that contribute to the growth of tumours

44
Q

Why do DNA and histones attract each other?

A

Because DNA is negatively charged, and histones are positively charged

45
Q

What is chromatin?

A

The complex that is formed when DNA winds around histones

46
Q

Name the two types of chromatin

A

Euchromatin and heterochromatin

47
Q

How is euchromatin formed?

A

When the DNA is loosely wound around the histones

48
Q

If DNA is in the form of euchromatin, what effect will this have on gene expression?

A

It will increase gene expression, as the genes are easily accessible for transcription because transcription factors can bind

49
Q

How is heterochromatin formed?

A

When the DNA is tightly wound around the histones

50
Q

If DNA is in the form of heterochromatin, what effect will this have on gene expression?

A

It will decrease gene expression, as the genes are not easily accessible for transcription, because transcription factors cannot bind

51
Q

What is the epigenome?

A

A layer of chemical tags attached to the genome

52
Q

Name the two types of chemical tags in the epigenome

A

Methyl groups and acetyl groups

53
Q

Name five factors that can affect the amount of methylation and acetylation of an individual’s epigenome

A

Diet, stress, toxins, mutagenic agents, carcinogens

54
Q

Define epigenetics

A

The heritable changes in gene function, without changes to the base sequence of DNA

55
Q

Describe how epigenetics occurs by methylation

A

Methyl groups are added and removed directly to or from the DNA by binding to cytosine

56
Q

What charge do methyl groups have?

A

Positive

57
Q

Describe the effect of increased methylation on chromatin

A

Increased DNA methlyation causes DNA to wind up tighter (heterochromatin)

58
Q

Why does increased DNA methylation cause heterochromatin?

A

Because the positively charged methyl groups are attracted to the negatively charged DNA

59
Q

Describe the effect of increased methylation on gene expression

A

Increased methylation decreases gene expression by decreasing transcription

60
Q

Describe the effect of decreased methylation on chromatin

A

Decreased DNA methlyation causes DNA winding to loosen (euchromatin)

61
Q

Why does decreased DNA methylation cause euchromatin?

A

Because fewer methyl groups means there is less attraction to the negatively charged DNA

62
Q

Describe the effect of decreased methylation on gene expression

A

Decreased methylation increases gene expression by increasing transcription

63
Q

Describe how epigenetics occurs by acetylation

A

Acetyl groups are added and removed from the histones

64
Q

What charge do acetyl groups have?

A

Negative

65
Q

Describe the effect of decreased acetylation on chromatin

A

Decreased histone acetylation causes DNA to wind up tighter (heterochromatin)

66
Q

Why does increased DNA acetylation cause heterochromatin? RECHECK

A

Fewer acetyl groups causes the histones to become more positive, increasing the attraction between the histones and the DNA

67
Q

Describe the effect of increased methylation on gene expression RECHECK

A

Increased acetylation decreases gene expression by decreasing transcription

68
Q

Describe the effect of increased acetylation on chromatin

A

Increased histone acetylation causes the winding of DNA around histones to loosen (euchromatin)

69
Q

Why does increased DNA methylation cause heterochromatin? RECHECK

A

More acetyl groups causes the histones to become less positive, decreasing the attraction between the histones and the DNA

70
Q

Describe the effect of increased methylation on gene expression RECHECK

A

Decreased acetylation increases gene expression by increasing transcription

71
Q

Define what a tumour is

A

A mass of undifferentiated cells formed from uncontrolled cell division

72
Q

What can uncontrolled cell division be caused by?

A

Mutations

73
Q

Name the three genes that can lead to tumour formation when mutated

A

Proto-oncogenes, tumour suppressor genes, and p53 (an example of a tumour suppressor gene)

74
Q

What are proto-oncogenes?

A

Genes that code for protein involved in the initiation of DNA replication and mitosis

75
Q

How can proto-oncogenes become mutated to form oncogenes?

A

Hypomethylation

76
Q

What are oncogenes?

A

Mutated proto-oncogenes that are now permanently switched on

77
Q

Describe and explain the effect of oncogenes on tumour formation

A

Transcription occurs continuously, which causes DNA replication, mitosis and therefore cell division to occur continuously.

78
Q

What are tumour suppressor genes?

A

They code for proteins involved in slowing down cell division, and causing cell death (apoptosis) if DNA replication errors are detected

79
Q

How can tumour suppressor genes become mutated?

A

A gene mutation, or hypermethylation

80
Q

How do tumour suppressor genes cause tumours if caused by a gene mutation?

A

The primary amino acid sequence is altered, translating into a non-functioning protein. This causes uncontrolled cell division.

81
Q

How do tumour suppressor genes cause tumours if caused by hypermethylation?

A

Transcription is inhibited. This causes unconctrolled cell division.

82
Q

What is p53?

A

A protein that stops the cell cycle when the DNA becomes damaged, which prevents mitosis producing more cells with damaged DNA

83
Q

How do p53 genes become mutated?

A

Gene mutation

84
Q

How does the mutated version of p53 cause tumour formation?

A

Mitosis will continue to occur, producing more cells with faulty DNA. These cells are more likely to become cancerous and undergo uncontrolled cell division.

85
Q

Name the two types of tumours

A

Benign and Malignant

86
Q

What is metastasis?

A

Spreading to other parts of the body

87
Q

Describe the growth rate of benign tumours

A

Slow (but can grow large)

88
Q

Why are benign tumours not cancerous?

A

Because they cannot metastasise or invade neighbouring tissues

89
Q

Explain why benign tumours don’t metastasise

A

They produce adhesion molecules that stick the tumour cells together, and they are surrounded by a capsule

90
Q

Why do benign tumours rarely return after surgery?

A

They are surrounded by a capsule, so total removal is easier.

91
Q

Describe the growth rate of malignant tumours

A

Fast (and grow large)

92
Q

Explain why malignant tumours grow faster

A

The cells can become unspecialised again (and therefore larger) and the tumour can develop its own blood supply

93
Q

Why are malignant tumours cancerous?

A

Because they can metastasise and invade neighbouring tissues

94
Q

Explain why malignant tumours can metastasise

A

They do not produce adhesion molecules, and are not surrounded by a capsule

95
Q

Why are malignant tumours harder to remove by surgery?

A

Because they do not have a capsule around them, and they can invade neighbouring tissues

96
Q

Why are malignant tumours more likely to recur after surgery

A

Because they are more difficult to remove with surgery, and they can metastasise

97
Q

Why are patients with malignant tumours more likely to require radiotherapy and chemotherapy?

A

Because malignant tumours are more difficult to remove with surgery, and they can metastasise

98
Q

Name the two tumour suppressor genes linked to breast cancer

A

BRCA1 and BRCA2

99
Q

What are the two main ways breast cancer is caused?

A

A mutated tumour suppressor gene (BRCA1 or BRCA2) or oestrogen switching on an oncogene

100
Q

Where is oestrogen produced before and after menopause?

A

Before menopause, in the ovaries. After menopause, in the fat tissue in the breasts

101
Q

How does oestrogen switch on oncogenes in the breasts?

A

It binds to the proto-oncogene, permanently switching it on and forming an oncogene

102
Q

Define what gene sequencing is

A

Gene sequencing is determining the nucleotide sequence of genetic material

103
Q

Name the project that sequenced the human genome over 13 years

A

The Human Genome Project

104
Q

Why is the translation of the genome to the proteome complex in eukaryotes?

A

Because of the presence of non-coding DNA, the epigenome and regulatory genes means not all genes in the genome are translated into proteins in the proteome

105
Q

Name one application of sequencing genes in pathogens

A

Sequencing the genes for potential antigens for use in vaccinations

Biology (26 decks)

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