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gene expression Flashcards

1
Q

What are stem cells?

A

*Undifferentiated / unspecialised cells capable of:
1. Dividing (by mitosis) to replace themselves indefinitely
2. Differentiating into other types of (specialised) cells

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2
Q

Describe how stem cells become specialised during development

A

*Stimuli lead to activation of some genes (due to transcription factors - see 8.2.2)
● So mRNA is transcribed only from these genes and then translated to form proteins
● These proteins modify cells permanently and determine cell structure / function

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3
Q

Describe totipotent cells

A

● Occur for a limited time in early mammalian embryos
● Can divide AND differentiate into any type of body cell (including extra-embryonic cells eg. placenta)

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4
Q

Describe pluripotent cells

A

● Found in mammalian embryos (after first few cell divisions)
● Can divide AND differentiate into most cell types (every cell type in the body but not placental cells)

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5
Q

Describe multipotent cells

A

● Found in mature mammals
● Can divide AND differentiate into a
limited number of cell types

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6
Q

Describe unipotent cells, using an example

A

● Found in mature mammals
● Can divide AND differentiate into just one cell type

Example: unipotent cells in the heart can divide and differentiate
into cardiomyocytes (cardiac muscle cells)

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7
Q

Explain how stem cells can be used in the treatment of human disorders

A

● Transplanted into patients to divide in unlimited numbers
● Then differentiate into required healthy cells (to replace faulty / damaged cells)

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8
Q

Explain how induced pluripotent stem (iPS) cells are produced

A
  1. Obtain adult somatic (body) cells (non-pluripotent cells or fibroblasts) from patient
  2. Add specific protein transcription factors associated with pluripotency to cells so express genes associated with pluripotency (reprogramming)
    ○ Transcription factors attach to promoter regions of DNA, stimulating or inhibiting transcription
  3. Culture cells to allow them to divide by mitosis
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9
Q

Evaluate the use of stem cells in treating human disorders

A

For:
* can divide and differentiate into required healthy cells, so could relieve human suffering by saving lives and improving quality of life

  • embryos are often left over from IVF and so would otherwise be destroyed.
  • iPS cells unlikely to be rejected by patient’s immune system as made with patient’s own cells.

*iPS cells can be made without destruction of embryo and adult can give permission

Against:
*ethical issues with embryonic stem cells as obtaining them requires destruction of an embryo and potential life (embryo cannot consent)

*Immune system could reject cells and immunosuppressant drugs are required

*cells could divide out of control, leading to formation of tumours / cancer

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10
Q

Examples of treatments using stem cells

A

● Potential treatment of Type 1 diabetes by creating healthy islet cells that produce insulin
● Bone marrow stem cell transplant for sickle cell disease / blood cancers
1. Destroy patient’s bone marrow before treatment → so no faulty cells are produced
2. Transplant stem cells from healthy person → divide and differentiate into healthy cells

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11
Q

What are transcription factors?

A

● Proteins which regulate (stimulate or inhibit) transcription of specific target genes in eukaryotes
● By binding to a specific DNA base sequence on a promoter region

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12
Q

Describe how transcription can be regulated using transcription factors

A
  1. Transcription factors move from cytoplasm to nucleus
  2. Bind to DNA at a specific DNA base sequence on a promoter region (before / upstream of target gene)
  3. This stimulates or inhibits transcription (production of mRNA) of target gene(s) by helping or preventing RNA polymerase binding
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13
Q

Explain how oestrogen affects transcription

A
  1. Oestrogen is a lipid-soluble steroid hormone so diffuses into cell across the phospholipid bilayer.
  2. In cytoplasm, oestrogen binds to its receptor, an inactive transcription factor, forming an oestrogen-receptor complex
  3. This changes the shape of the inactive transcription factor, forming an active transcription factor
  4. The complex diffuses from cytoplasm into the nucleus
  5. Then binds to a specific DNA base sequence on the promoter region of a target gene
  6. Stimulating transcription of target genes forming mRNA by helping RNA polymerase to bind
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14
Q

Explain why oestrogen only affects target cells

A

Other cells do not have oestrogen receptors

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15
Q

What is RNA interference (RNAi)?

A

● Inhibition of translation of mRNA produced from target genes, by RNA molecules eg. siRNA, miRNA
● This inhibits expression of (silencing) a target gene

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16
Q

Describe the regulation of translation by RNA interference

A

*siRNA/miRNA binds to a protein,
*forms an RNA-induced silencing complex (RISC)
*single stranded miRNA / siRNA within RISC binds to target mRNA with a comp base sequence.
*leads to hydrolysis of mRNA into fragments which then degraded OR prevents ribosomes binding.
*reducing / preventing translation of target mRNA into protein

17
Q

Describe what is meant by epigenetics

A

● Heritable changes in gene function / expression without changes to the base sequence of DNA
● Caused by changes in the environment (eg. diet, stress, toxins)

18
Q

Describe what is meant by epigenome

A

All chemical modification of DNA and histone proteins - methyl groups on DNA and acetyl groups on histones

19
Q

To inhibit transcription

A

methylation increased and acetylation decreased

20
Q

Allow transcription

A

methylation decreased and acetylation increased

21
Q

Explain how methylation can inhibit transcription

A
  1. Increased methylation of DNA - methyl
    groups added to cytosine bases in DNA
  2. So nucleosomes (DNA wrapped around
    histone) pack more tightly together
  3. Preventing transcription factors and
    RNA polymerase binding to promoter
22
Q

Explain how low acetylation can inhibit transcription

A
  1. Decreased acetylation of histones
    increases positive charge of histones
  2. So histones bind DNA (negatively
    charged) more tightly
  3. Preventing transcription factors and
    RNA polymerase binding to promoter
23
Q

Describe how tumours and cancers form

A

● Mutations in DNA / genes controlling mitosis can lead to
uncontrolled cell division
● Tumour formed if this results in mass of abnormal cells
○ Malignant tumour = cancerous, can spread by metastasis
○ Benign tumour = non-cancerous

24
Q

Describe the function of tumour suppressor genes

A

Code for proteins that:
● Inhibit / slow cell cycle (eg. if DNA damage detected)
● OR cause self-destruction (apoptosis) of potential tumour cells (eg. if damaged DNA can’t be repaired)

25
Q

Explain the role of tumour suppressor genes in the development of tumours

A

● Mutation in DNA base sequence → production of non-functional protein
○ By leading to change in amino acid sequence which changes protein tertiary structure
● Decreased histone acetylation OR increased DNA methylation → prevents production of protein
○ By preventing binding of RNA polymerase to promoter region, inhibiting transcription
● Both lead to uncontrolled cell division (cell division cannot be slowed)

26
Q

Describe the function of (proto-)oncogenes

A

Code for proteins that stimulate cell division
(eg. through involvement in signalling pathways that control cell responses to growth factors)

27
Q

Explain the role of oncogenes in the development of tumours

A

● Mutation in DNA base sequence → overproduction of protein OR permanently activated protein
○ By leading to change in amino acid sequence which changes protein tertiary structure
● Decreased DNA methylation OR increased histone acetylation → increases production of protein
○ By stimulating binding of RNA polymerase to promoter region, stimulating transcription
● Both lead to uncontrolled cell division (cell division is permanently stimulated)

28
Q

What is an oncogene

A

(An oncogene is a mutated / abnormally expressed form of the corresponding proto-oncogene)

29
Q

Suggest why tumours require mutations in both alleles of a tumour suppressor gene but only one allele of an oncogene

A

● One functional allele of a tumour suppressor gene can produce enough protein to slow the cell cycle
OR cause self-destruction of potential tumour cells → cell division is controlled

● One mutated oncogene allele can produce enough protein to lead to rapid / uncontrolled cell division

30
Q

Explain the role of increased oestrogen concentrations in the development
of some (oestrogen receptor-positive) breast cancers

A

*some breast cancers cells have oestrogen receptors,
*If oestrogen concentration is increased, more oestrogen binds to oestrogen receptors, form more oestrogen-receptor complexes which are active transcription factors.
3. These bind to promoter regions of genes that code for proteins stimulating cell division.
4. This increases transcription / expression of these genes, increasing the rate of cell division

31
Q

Suggest how drugs that have a similar structure to oestrogen help treat
oestrogen receptor-positive breast cancers

A

● Drugs bind to oestrogen receptors (inactive transcription factors), preventing binding of oestrogen
● So no / fewer transcription factors bind to promoter regions of genes that stimulate the cell cycle.

32
Q

Differences between malignant and benign tumours

A

*malignant- spread by metastasis - cells break off and spread to other parts of the body benign doesnt metastasise

*mal- grow faster, ben slower
*mal- cells have irregular nuclei, ben- normal, regular nuclei
*mal- poorly differentiated/specialised, ben- well diffrentiated/specialised

33
Q

Where is oestrogen produced in women with menopause

A

the fat cells in the breast tissue

34
Q

Explain the relevance of epigenetics in cancer treatment

A

● Increasing DNA methylation OR decreasing histone acetylation of oncogene
○ To inhibit transcription / expression
● Decreasing DNA methylation OR increasing histone acetylation of tumour suppressor gene
○ To stimulate transcription / expression

Bio (23 decks)

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