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20. Gene expression Flashcards

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1
Q

What is meant by ‘cell differentiation’?

A

The process by which each cell develops into a specialised structure suited to the role that it will carry out.

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2
Q

How is every cell capable of making everything that the body can produce?

A

All the cells in an organism are derived by mitotic divisions of the zygote. It follows that they all contain exactly the same genes.

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3
Q

Why do the cells of the small intestine produce maltase rather than insulin, and B cells of the pancreas produce insulin rather than maltase?

A

Although all cells contain all genes, only certain genes are expressed in any one cell at any one time.

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4
Q

Why do differentiated cells differ from each other?

A

Because they each produce different proteins. The proteins that a cell produces are coded for by the genes that are expressed.

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5
Q

What are totipotent cells?

A

Cells such as fertilised eggs, which can mature into any type of body cell.

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6
Q

Which ways are genes prevented from expressing themselves?

A
  • Preventing transcription and the production of mRNA

- Preventing translation

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7
Q

What are stem cells?

A

Undifferentiated dividing cells that occur in embryos and in adult animal tissues that require constant replacement, e.g. bone marrow.

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8
Q

Name different places stem cells originate in mammals:

A
  • Embryonic stem cells
  • Umbilical cord blood stem cells
  • Placental stem cells
  • Adult stem cells
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9
Q

What are totipotent stem cells?

A

Found in the early embryo and can differentiate into any type of cell. Since all body cells are formed from a zygote, the zygote is totipotent. As the cell divides and matures, its cells develop into slightly more specialised cells called pluripotent stem cells.

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10
Q

Pluripotent stem cells

A

Found in embryos and can differentiate into almost any type of cell. E.g. embryonic stem cells and fetal stem cells

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11
Q

What are multipotent stem cells

A

Found in adults and can differentiate into a limited number of specialised cells. They usually develop into cells of a particular type: e.g. stem cells in the bone marrow can produce any type of blood cell.

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12
Q

What are unipotent stem cells?

A

They can only differentiate into a single type of cell. They’re derived from multiple types of stem cells and are made in adult tissue.

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13
Q

What are induced pluripotent cells?

A

Induced pluripotent stem cells are a type of cell produced by unipotent stem cells. Involves inducing genes and transcriptional factors within the cell to express themselves. The genes that were turned off are turned on.
They’re capable of self renewal, and can divide indefinitely to produce a limitless supply. Therefore they could replace embryonic stem cells, removing the ethical issues surrounding use of embryos in research.

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14
Q

Give 3 examples of pluripotent cells in treating human disorders

A
  • Heart muscle cells- can treat heart damage/heart attacks.
  • Skeletal muscle cells- Muscle dystrophy.
  • B cells of the pancreas- type 1 diabetes
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15
Q

Suggest a reason why skin cells retain an ability to divide by being unipotent when the cells of other organs do not

A

Skin cells, being on the outside on the body are subject to external environments so need replacing frequently. Other organs are less prone to damage and need little cell replacement.

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16
Q

All cells possess the same genes and yet a skin cell can produce the protein keratin but not the protein myosin, while a muscle cell can produce myosin but not keratin. Explain why.

A

In skin cells, the gene that codes for keratin is expressed, but not the gene for myosin. The genetic code for keratin is translated into the protein keratin which the cell produces, but the genetic code for myosin isn’t translated.
In muscle cells, the gene for myosin is expressed but not the gene for keratin. In the same way, the genetic code for myosin rather than keratin is translated so only myosin is produced.

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17
Q

What is a gene mutation?

A

A change to one or more nucleotide bases in DNA resulting in a change in genotype which may be inherited.

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18
Q

What is base substitution?

A

The type of gene mutation in which a nucleotide in a section of a DNA molecule is replaced by another nucleotide that has a different base.

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19
Q

Why might substitution of bases not change the sequence of amino acids?

A

The genetic code is degenerate so most amino acids have more than one codon. The mutation therefore has no effect on the polypeptide produced.

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20
Q

What is base deletion?

A

The loss of a nucleotide base from a DNA sequence.

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21
Q

Why does deletion of a base result in a non-functional protein?

A

A frame shift is created because the reading frame that contains the codon has been shifted to the left by one base. The gene is now read in the wrong triplet code and the information is altered. Most triplets will be different, as well as the amino acids they code for. The polypeptide will be different and lead to the production of a non-functional protein that could considerably alter the phenotype.

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22
Q

What is base addition?

A

An extra base becomes inserted in the sequence. This causes a frame shift to the right, and the whole sequence of triplets is altered. If 3 extra bases are added there will not be a frame shift. The resulting polypeptide will be different but not to the extent of a frame shift.

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23
Q

What is base duplication?

A

One or more bases are repeated, producing a frame shift to the right.

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24
Q

What is base inversion?

A

A group of bases become separated from the DNA sequence and rejoin at the same position but in the inverse order. The base sequence of this portion is therefore reversed and effects the amino acid sequence that results.

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25
Q

What is base translocation?

A

A group of bases become separated from the DNA sequence on one chromosome and become inserted into the DNA sequence of a different chromosome. Translocations often have significant effects on gene expression leading to an abnormal phenotype. These effects include the development of certain forms of cancer and reduced fertility.

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26
Q

What are mutagenic agents?

A

Outside factors which increase the basic mutation rate

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27
Q

Give 2 examples of mutagenic agents.

A
  • High energy ionising radiation

- Chemicals, e.g. nitrogen dioxide

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28
Q

Give advantages of mutations

A

They produce genetic diversity necessary for natural selection and speciation.

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29
Q

A translocation mutation is a combination of 2 other types of gene mutation. Deduce which 2 types of mutation they are.

A

Deletion and addition because the bases are deleted from one chromosome and added to a different one.

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30
Q

Explain why the effects of a single additional base in a sequence of DNA bases may have little effect on the polypeptide produced

A

If the additional base is inserted at the end of the sequence few, if any, codons will be changed. Few, if any, amino acids they code for will differ and the resulting polypeptide will be normal.

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31
Q

A mutation causes 3 bases in the DNA of a gene to become duplicated. Explain how the effects of this mutation might differ if the duplicated bases are consecutive rather than in 3 separate locations on the DNA molecule.

A

Where the duplicated bases are consecutive, the frame shift is 3 bases long and so the subsequent codons are not affected. The polypeptide will have an additional amino acid but otherwise will be unchanged. If the bases are separate the frame shift will initially be one base long, becoming two bases long after the second duplicate base is added. Codons after both the duplications will be changed and the polypeptide will have many different amino acids. After the third duplicate base the codons will be unchanged.

32
Q

Suggest 2 reasons why the addition of a single base into a DNA sequence may not alter the amino acid sequence in the resultant polypeptide.

A
  • Some codons will be changed to ones that code for the same amino acids (degenerate code).
  • The frame shift might not alter some codons because the replacement bases are the same as the originals.
33
Q

What causes cancer?

A

A disease caused by damage to the genes that regulate mitosis and the cell cycle. This leads to unrestrained growth of cells. A group of abnormal cells, called a tumour, develops and expands in size.

34
Q

Conpare benign and malignant tumours

A

Both can grow to a large size.
Benign- grow slowly, malignant- grow rapidly.
Benign- nucleus appears normal, malignant- nucleus is larger and appears darker due to lots of DNA.
Benign- cells well-differentiated, malignant- cells unspecified.
Benign- adhesion molecules/primary tunours, malignant- metastasis/secondary tumours.
Benign- surrounded by a capsule of dense tissue/compact structure, malignant- not surrounded by a capsule, project into surrounding tissue.
Benign- less likely to be life-threatening, malignant- more likely to be life-threatening.
Benign- localised effect on body, malignant-systemic effects: weight loss/fatigue.
Benign- removed by surgery, removed by radiotherapy/chemotherapy
Benign- rarely reoccur, malignant- frequently reoccour

35
Q

What are the 2 main genes involved in cell division?

A
  • Oncogenes

- Tumour supressor gene

36
Q

What are oncogenes?

A

Mutations of proto-oncogenes stimulate a cell to divide when growth factors attach to a protein receptor on its cell surface membrane. This activates genes that cause DNA to replicate and the cell to divide. Oncogenes are permanently activated causing uncontrolled cell division.

37
Q

What factors cause oncogenes to become permemnatly activated?

A
  • The receptor protein on the cell surface membrane can be permenantly activated, so that cell division is swithed on even in absence of growth factors.
  • The oncogene may code for a growth factor that is then produced in excessive amounts, again stimulating excessive cell division.
38
Q

What is the role of normal functioning tumour supressor genes?

A

Slow down cell divison, repair mistakes in DNA and control apoptosis.
(Have opposite role of proto-oncogenes).

39
Q

What happens when tumour suppressant gene gets switched off?

A

Stops inhibiting cell division and cells can grow out of control. Mutated cells form structurally different from normal cells, most of these die.

40
Q

Describe how hypermethylation of tumour suppressor genes can cause cancer

A
  • Hypermethylation occurs in promotor region of tumour suppressor genes.
  • This leads to the tumour suppressor gene being inactivated.
  • As a result, transcription of the promotor regions of the tumour suppressor genes is inhibited.
  • The tumour suppressor gene is therefore silenced.
  • As the tumour suppressor gene normally slows down the rate of cell division, its inactivation leads to increased cell division and the formation of a tumour.
41
Q

Does oestrogen concentration increase risk of breast cancer?

A

The fat cells of the breats tend to produce more oestrogen after menopause, triggering breast cancer in postmenopause.
Once the tumour has developed, it further increases oestrogen concentration which therefore leads to increase development of the tumour. White blood cells are drawn to the tumour increase oestrogen production, leading to greater development of the tumour.

42
Q

How does oestrogen affect gene transcription, causing formation of a tumour?

A

Fat cells of the breasts tend to produce more oestrogen after menopause. These locally produced oestrogens release an inhibitor molecule causing proto-oncogenes of breast tissue to develop into oncogenes. These oncogenes increase the rate of cell division leading to the development of a tumour.

43
Q

Explain why the activation of a proto-oncogene might casue breast cancer in post-menapausal women

A

Proto-oncogenes increase the rate of cell division and so their activation produces a mass of cells, but tumour suppressor genes decrease the rate of cell devision and so their deactivation produces a tumour.

44
Q

Suggest 2 reasons why the surgical removal of a benign tunour is usually sufficient treatment to prevent the tumour growing again.

A

Cells of a benign tumour produce adhesion molecules that make them stick together and are surrounded by a capsule of dense tissue. The tumour therefore remains a compact structure so surgical removal is likely to remove all tumour cells.

45
Q

Suggest why the surgical removal of a malignant tumour requires follow up treatments such as chemotherapy and radiotherapy.

A

Malignant tumours spread to other regions of the body and so even though surgery removes the larger tumours, tiny ones will require other therapies to prevent them regrowing new tumours.

46
Q

The enzyme histone deacetylase removes acetyl groups from the histones. Phenylbutyric acid is an inhibitor of the enzyme. Suggest how phenylbutyric acid might be used to treat cancer. Explain your answer.

A

HADC removes acetyl groups from histones, inhibiting transcription and switching off the gene. Some cancers are the result of genes that normally help repair DNA being switched off. By inhibiting HADC, phenybutyric acid could prveent the removal of acetyl groups from histones and switch the protective gene back on.

47
Q

How do transcriptional factors affect the expression of a gene?

A
  • For transcription to begin, the gene is switched on by transcriptional factors, which have a binding site specific to the DNA sequence in the nucleus.
  • mRNA is produced and the information carried is translated into a polypeptide.

-When a gene is switched off, the site on the transcriptional factor that binds to DNA isn’t active, preventing transcription and protein synthesis.

48
Q

How does oestrogen stimulate transcription, causing gene expression?

A
  • Oestrogen is lipid-soluble and diffuses easily through the phospholipid membrane.
  • Oestrogen binds with a site on a receptor of the transcriptional factor. The shape of this site is complementary to oestrogen.
  • By binding to the site, the oestrogen changes the shape of the DNA binding site on the TF which is now activated to bind to DNA.
  • The TF can now enter the nucleus and bind to specific sequences on DNA.
  • The combination of the transcriptional factor with DNA stimulates transcription of the gene that makes up the portion of DNA.
49
Q

What is epigenetics?

A

Epigenetics is a new scientific field that provides explanations to how environmental factors, such as diet, stress and toxins, can cause heritable changes in gene function without changing the base sequence of DNA.

50
Q

What is the ‘epigenome’

A

Chemical tags that form a second layer around the DNA-histone complex. Determines the shape of the complex.

51
Q

How does the epigenome activate/switch on genes?

A

The chemical tags respond to environmental changes and unwraps active genes so that DNA is exposed and easily transcribed.

52
Q

How does the epigenome de-activate/switch off genes?

A

The chemical tags respond to environmental changes and keeps inactive genes in a tightly packed arrangement so DNA can’t be read and transcribed. Known as epigenetic silencing.

53
Q

How is the epigenome created?

A

The accumulation of signals received during its lifetime, originally signals from foetal cells. Throughout life environmental factors affect the epigenome along with signals within the body, such as hormones.
The environmental signal stimulates proteins to carry a message, by a series of proteins, into the nucleus. Signal passes to specific protein attached to specific DNA bases. It can change:
-Acetylation of histones
-Methylation of DNA

54
Q

How does the DNA-histone complex affect transcription.

A

When association of histones with DNA is weak, the DNA-histone complex is less condensed. DNA is accessible to transcriptional factors, which can initiate mRNA production.
When association is stronger, the complex is more condensed. DNA is more accessible by transcription factors, therefore can’ t initiate mRNA production.

55
Q

Describe how decreased acetylation of associated histones causes gene inactivation

A

Deacetylation involves the removal of the acetyl group from a molecule. It increases the positive charges on histones and therefore increases their attraction to the phosphate groups of DNA. The association between DNA and histones is stronger and the DNA is not accessible to transcriptional factors. These transcriptional factors can’t initiate mRNA production from DNA, switching the gene off.

56
Q

What evidence is there to suggest epigenetic inheritance takes place?

A
  • Experiments on rats show that female offspring who received good care when young, respond better to stress later in life and nurture offspring better than female offspring receiving low-quality care. Good maternal behaviour in rats transmits epigenetic information onto their offspring’s DNA without passing through egg or sperm.
  • In humans, when a mother has gestational diabetes, the foetus is exposed to high concentrations of glucose. This causes epigenetic changes in the daughter’s DNA, increasing the likelihood that she will develop the disease.
57
Q

How do epigenetic changes cause disease?

A

Altering any epigenetic processes can cause abnormal activation or silencing of genes. In some cases the activation of a normally inactive gene causes disease, in other cases the inactivation of a normally active gene that can cause disease, e.g. cancer.

58
Q

Give evidence that epigenetic changes cause cancer

A

In 1983, researchers found diseased tissue taken from cancer patients had less DNA methylation than normal tissue. DNA methylation normally inhibits transcription. This means that patients with less DNA methylation would have higher gene activity/more genes switched on, e.g. oncogenes.
Specific sections of DNA near promotor regions are highly methylated, causing genes to be switched off, e.g. tumour suppressor genes.

59
Q

How does increased methylation of DNA inhibit transcription?

A

Methylation is the addition of a methyl group to the cytosine bases of DNA. Inhibits transcription by:

  • Preventing the binding of transcriptional factors of DNA
  • Attracting proteins that condense the DNA-histone complex, by inducing deacetylation, making the DNA inaccessible to transcription factors.
60
Q

How can diseases be treated with epigenetic therapy?

A

-Drugs inhibit certain enzymes involved in histone acetylation or DNA methylation, can reactive silenced genes.
Must be specifically targeted on cancer cells, on normal cells they could active gene transcription and make them cancerous.
-Development of diagnostic tests to detect early stages of diseases. Can identify the level of DNA methylation and histone acetylation at an early stage, early treatment, increased chance of cure.

61
Q

How can siRNA interfere with gene expression

A
  • An enzyme cuts large double-stranded molecules of RNA into smaller sections called small interfering RNA.
  • 1 of the 2 siRNA strands combines with the enzyme.
  • The siRNA molecule guides the enzyme to a mRNA molecule by pairing up its bases with complementary ones on a section of mRNA.
  • Once in position, the enzyme cuts the mRNA into smaller sections.
  • The mRNA is no longer capable of being translated into a polypeptide.
  • The gene can’t be expressed.
62
Q

One of the 2 strands of siRNA combines with an enzyme and guides it to an mRNA molecule which it then cuts. Explain why the mRNA is unlikely to be cut if the other siRNA strand combines with the enzyme.

A

siRNA strand not complementary to mRNA. Therefore the siRNA, with enzyme attached would not be able to bind to the mRNA and so would be unaffected.

63
Q

How could siRNA be used to identify the roles of genes in a biological pathway?

A

Some siRNA that blocks a particular gene could be added to cells. By observing the effects we could determine what the role of the blocked gene is.

64
Q

How could siRNA be used to prevent a disease?

A

By blocking the gene that causes it.

65
Q

Enzyme histone deacetylase removes acetyl groups from histones. Suggest what the effect of this enzyme would be on the arrangement of chromatin and trasncription.

A

Chromatin/DNA-histone complex would be more condensed due to positive charge of histone attracting negatively charged phosphate.
Transcription would cease as transcriptional factors have no way of binding to the gene’s promotor region.

66
Q

Which lifestyle factors contribute towards cancer?

A
  • Smoking
  • Diet
  • Obesity
  • Physical activity
  • Sunlight
67
Q

Define ‘genome’

A

A complete map of all the genetic material in an organism.

68
Q

How many genes are in the human genome?

A

20000

69
Q

How many base pairs in the human genome?

A

3 billion

70
Q

How is the genome of an organism determined?

A

Whole genome shotgun/WGS sequencing- involves researchers cutting DNA into small, easily sequenced sections and using computer algorithms to align overlapping segments to assemble the entire genome.

71
Q

Give examples of medical advances made as a result of sequencing the genome

A
  • Over 1.4M single nucleotide polymorphisms found. SNPs are single-base variations in the genome associated with disease/disorders.
  • Medical screening of individuals allows quick identification of medical problems and early intervention to treat it.
  • Sequencing DNA has helped establish evolutionary links between species.
72
Q

Define ‘proteome’

A

All the proteins in a given type of cell or organism, at a given time, under specified conditions.

73
Q

Why are genomes of prokaryotic and single-celled eukaryotic organisms being sequenced as part of the Human Microbiome Project?

A

Its hoped that the information gained will help cure disease and provide knowledge of genes that can be usefully exploited.

74
Q

Why is determining the proteome of prokaryotic organisms relatively easy?

A
  • The vast majority of prokaryotes have just one circular piece of DNA that is not associated with histones
  • There are no non-coding portions of DNA which are typical of eukaryotic cells.
75
Q

Give an advantage of having knowledge of bacteria’s proteome

A

Identification of proteins that act as antigens on the surface of human pathogens- can be used in vaccines.

76
Q

Why is it difficult to translate knowledge of the genome into the proteome for complex organisms?

A

The genome of complex organisms contains many non-coding genes as well as coding genes.
In humans as few as 1.5% of genes code for proteins.

Biology (21 decks)

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