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Biology > Topic 20 - Gene Expression > Flashcards

Topic 20 - Gene Expression Flashcards

1
Q

What is a gene mutation?

A

A change in the base sequence of DNA.

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2
Q

What is a substitution gene mutation?

A

DNA nucleotide replaced by a different one. Can have no effect on the base sequence, could change one amino acid.

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3
Q

What is a chromosome mutation?

A

Change in chromosome number. Also arises spontaneously during meiosis (anaphase 1 and 2).

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4
Q

What is a deletion gene mutation?

A

DNA nucleotide removed from DNA sequence. Usually causes a frame shift. No effect if before a STOP codon.

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5
Q

What is an addition gene mutation?

A

DNA nucleotide inserted into DNA sequence. Usually causes a frame shift.

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6
Q

What is a duplication gene mutation?

A

One or more bases are repeated. Causes a frame shift, amino acids change.

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7
Q

What is an inversion gene mutation?

A

Groups of bases spliced and reinserted in the same position, but in reverse order. Causes one amino acid to change (might not change if the reverse codes for the same thing).

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8
Q

What is a translocation gene mutation?

A

Group of bases deleted/removed from DNA sequence of one chromosome and are added into the DNA sequence of another chromosome. Amino acids are the same, one is just removed so will be read slightly differently. May cause frame shift if bases were not coding together.

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9
Q

How does an organism increase in size?

A

New cells form (mitosis) and existing cells grow in size.

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10
Q

What does development involve?

A

Arranging specialised cells into tissues, which are arranged into organs. Cells become specialised via cellular differentiation.

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11
Q

What is a zygote?

A

A precursor for all cells in your body. It contains all the genetic information required to produce all of the cell types found in your tissues and organs.

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12
Q

What is a totipotent stem cell?

A

Can differentiate into any type of specialised body cell.

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13
Q

What is a pluripotent stem cell?

A

Can differentiate into almost any type of specialised body cell.

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14
Q

How do cells lose their totipotency and become specialised?

A

During development, totipotent cells translate only part of their DNA, resulting in cell specialisation.

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15
Q

What is a multipotent stem cell?

A

Can divide to form a limited number of different cell types e.g. bone marrow produces different types of blood cells.

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16
Q

What is a unipotent stem cell?

A

Can divide to form only a single cell type e.g. a phagocyte.

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17
Q

What are the three general properties of all stem cells?

A

1) They can divide and renew themselves over long time periods.
2) They are unspecialised.
3) They can differentiate into other specialised cell types.

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18
Q

What are induced pluripotent stem cells (iPS cells)?

A
  • Can be produced from almost any adult somatic cells e.g. liver, skin, stomach.
  • Acquire characteristics of pluripotent stem cells.
  • Their genes can be induced using ‘appropriate protein transcription factors’.
  • Different to embryonic stem cells because they are capable of self-renewing and dividing in unlimited numbers, so potential limitless supply.
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19
Q

What are some ethical issues surrounding stem cell research?

A
  • Embryos are potential life.
  • Some think it is better to end a person’s suffering, rather than debate an embryo’s right to existence.
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20
Q

What type of stem cell is found in mature plants?

A

Totipotent.

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21
Q

What are the three stages of gene expression?

A

1) Transcription of target gene.
2) Pre-mRNA has to be spliced.
3) Translation has to occur.

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22
Q

What are transcriptional factors?

A

Protein complexes with different subunits that diffuse from cytoplasm to DNA. Diffuse through nuclear pores.

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23
Q

How do transcriptional factors work?

A

1) Each TF has a DNA binding site that is specific to a particular gene.
2) When a specific protein is required, the gene is stimulated by the specific TF.
3) This initiates synthesis of the protein by binding to the DNA at the specific base sequence - the promoter sequence.
4) Stimulates transcription.
5) Pre-mRNA produced, spliced into mRNA before being translated into a protein.

24
Q

What is an inhibitor molecule?

A

Blocks DNA binding site on transcriptional factor so TF can’t bind to DNA.

25
Q

Transcription and translation are regulated via the hormone mechanism, which involves lipid-soluble hormones - such as oestrogen (steroid hormone). How does this work?

A

1) Oestrogen diffuses through phospholipid portion of cell surface membrane.
2) Once inside cytoplasm, binds with site on receptor molecule (they are complementary).
3) Oestrogen changes shape of DNA binding site on TF, which can now bind to DNA.
4) TF can now enter nucleus through nuclear pore and bind to specific base sequences on DNA.
5) Combination of TF with DNA stimulates transcription of the gene that makes up the portion of DNA.

26
Q

What is small interfering RNA (siRNA)?

A
  • Small molecules of double-stranded RNA.
  • Involved in RNA interference.
  • Occurs in eukaryotes and some prokaryotes.
  • Prevents translation of mRNA produced.
27
Q

How is small interfering RNA used to prevent gene expression?

A

1) Double-stranded RNA (dsRNA) produced by RNA dependent RNA polymerase.
2) Enzyme (dicer) breaks up dsRNA making siRNA molecules via hydrolysis reaction.
3) Enzyme 2 combines with one of the two molecules of siRNA - RNA induced slicing complex (RISC).
4) Complimentary base pairing between siRNA and target mRNA.
5) mRNA broken down.
6) mRNA fragments.

28
Q

What is epigenetics?

A

Environmental factors cause heritable changes in gene function, without changing the genome.

29
Q

What is the epigenome made up of?

A

Chemical ‘tags’ which determine the shape of the DNA-histone complex, and therefore influence gene expression.

30
Q

What is the epigenome under the influence of?

A

Environmental factors, and tags respond to environmental changes, which in turn affects transcription.

31
Q

What is the epigenome the accumulation of?

A

Signals received during the lifetime of a cell, so acts like a cellular memory.

32
Q

What was the Barker & Hayles (1986) experiment?

A
  • 16,000 individuals born in Hertfordshire, 191-1930.
  • Anthropometric birth data and mortality rates.
  • Low birth weight = elevated blood pressure, obesity, type 2 diabetes, cholesterol.
  • Coronary heart disease = early mortality.
  • It did not prove that low birth weight led to coronary heart disease as the data was showing a correlation not a causation. There may be other factors leading to CHD.
33
Q

Why is the rate of gene expression higher if a DNA-histone complex is less condensed?

A

If less condensed, the more able for enzymes to get into DNA to start more transcription.

34
Q

What does deacetylation (decreased acetylation) of histones do?

A

Decreased acetylation of histone increases positive charge on histones and thus increases attraction to negative phosphate on DNA. Stronger association between histones and DNA means DNA not accessible to transcriptional factors, so inhibits transcription as more condensed.

35
Q

What does acetylation of histones do?

A

Acetyl joins histone, DNA-histone complex less condensed so transcription increases.

36
Q

What does increased methylation of DNA do?

A

Prevents binding of transcriptional factors to DNA, so inhibits transcription as more condensed.

It also attracts proteins that condense the DNA-histone complex, thus making it inaccessible to transcriptional factors.

37
Q

What does demethylation (decreased methylation) of DNA do?

A

Becomes less condensed so increases transcription.

38
Q

What are characteristics of benign tumours?

A
  • Grow very slowly.
  • Cells are often well differentiated.
  • Much less likely to be life threatening, but can still disrupt functioning of a vital organ.
  • Often have localised effects on the body.
  • Rarely reoccur after treatment.
39
Q

What are characteristics of malignant tumours?

A
  • Cell nucleus often larger and appears darker due to an abundance of DNA.
  • Cells do not produce adhesion molecules and so tend to spread to other regions of body (metastasis), forming secondary tumours.
  • Tumours not surrounded by a capsule so can grow finger link projections into the surrounding tissues.
  • Removal usually involves radiotherapy and/or chemotherapy as well as surgery, and they can come back.
40
Q

How does a tumour grow and spread?

A

1) Tumour enlarges, developing blood and lymphatic vessels.
2) Tumour cells squeeze into blood and lymphatic vessels.
3) Tumour cells circulate in the blood.
4) Tumour cells adhere to blood vessel walls and squeeze through to form distant metastases.
5) Metastasis in lymph node.

41
Q

What is a proto-oncogene?

A

Stimulate cell division.

42
Q

What is an oncogene?

A

Mutations of proto-oncogene means they become permanently switched on.

Some proto-oncogenes code for a cell surface membrane receptor protein, others codes for growth factor protein that is complementary to cell surface membrane receptor.

43
Q

How does an oncogene lead to uncontrolled cell division?

A
  • Receptor protein permanently activated, so cells divide without growth factors.
  • Oncogene codes for growth factor, which is thus produced in excessive amounts.
  • Leads to rapid, uncontrollable cell division = tumour.
44
Q

What is the role of a tumour suppressor gene?

A

Forms normal growth-inhibiting protein so cell division is under control.

45
Q

What may happen in a cell with a mutated tumour suppressor gene?

A

Produces a defective, non functioning protein so cell division is not under control.

46
Q

How does methylation of tumour suppressor lead to uncontrolled cell division?

A

More methylation inhibits the tumour suppressor gene so less made = uncontrolled cell division.

47
Q

How does methylation on oncogenes lead to uncontrolled cell division?

A

Reduced methylation of oncogenes = DNA-histone complex less condensed = transcriptional factors bind more easily = increases transcription = increased expression of oncogenes = increases rate of cell division.

48
Q

Oestrogen and breast cancer.

A
  • Post-menopausal = increased risk of breast cancer.
  • Thought to be due to increased oestrogen concentration.
  • Less oestrogen from ovaries, but more locally produced from fat cells of breasts.
  • Breast tumours produce oestrogen so tumour develops and grows.
49
Q

What is bioinformatics?

A
  • Science of collecting and analysing complex biological data.
  • Uses computers to read, store, and organise biological data.
  • Utilises algorithms to analyse and interpret biological data.
50
Q

What is a whole-genome shotgun (WGS)?

A

Researchers cut DNA into many small, easily sequenced sections, then use computer algorithms to align overlapping segments to assemble the entire genome.

51
Q

What are primers?

A

Short stretches of DNA that target unique sequences and help identify a unique part of a genome.

52
Q

What is a proteome?

A

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

53
Q

What is the significance of the proteome with bacteria?

A

Bacteria reallocate their proteome to relieve metabolic or translational bottlenecks and increase growth rate under a given nutrient limitation.

54
Q

What is genomic medicine?

A

Studying genomes of thousands of people to find patterns in the data. Can then pinpoint individual risks of disease, deliver definitive diagnoses, and select treatments that work best.

55
Q

What is a SNP?

A

Genomic variant at a single base position in the DNA.

56
Q

What is genomic information useful for (NOT medical!)?

A
  • Identifying unknown individuals.
  • DNA fingerprints.
  • Developing genetically modified livestock/plants.
  • Selective breeding processes in agriculture.
  • Environmental monitoring for biological pathogens.

Biology (24 decks)

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