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2B > Gene Expression > Flashcards

Gene Expression Flashcards

1
Q

Define mutation

A

Any change to the base (nucleotide) sequence of DNA

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2
Q

When do mutations occur?

A

During errors in DNA replication

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3
Q

How can the rate of mutation be affected?

A

Mutagenic agents

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4
Q

What are the 6 types of mutations?

A

Substitution, deletion, addition, inversion, duplication and translocation

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5
Q

Define substitution

A

One or more bases is swapped for another

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6
Q

Define deletion

A

One or more bases are removed

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7
Q

Define addition

A

One or more bases are added

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8
Q

Define duplication

A

One or more bases are repeated

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9
Q

Define inversion

A

A sequence of bases is reversed (ATGCCT now ACCGTT)

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10
Q

Define translocation

A

A sequence of bases is moved from one location in the genome to another.

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11
Q

What is a hereditary mutation?

A

When a gamete containing a mutation for a genetic disorder is fertilised, the mutations will be present in the new foetus.

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12
Q

Why do mutations not always have an effect?

A

Due to the degenerate nature of the genetic code - meaning some AA are coded for by more than one triplet.

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13
Q

Give examples of mutagenic agents.

A
  • high ionising radiation; e.g. short wave radiation such as X-rays
  • chemicals; e.g. nitrogen dioxide may directly alter the structure of DNA
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14
Q

What are acquired mutations?

A

Mutations that occur in individual cells after fertilisation

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15
Q

What happens if an acquired mutations occurs in a gene that controls cell division?

A

Can cause uncontrolled cell growth

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16
Q

Which two genes cause cell division?

A

Tumour suppressor genes and proto-oncogenes

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17
Q

Outline how mutations in tumour suppressor genes cause cancer.

A

When functioning normally, tumour suppressor genes slow cell division by producing proteins that stop cells dividing or cause them to self destruct (apoptosis).

If a mutation occurs, the protein for this isn’t produced. So the cells divide uncontrollably, resulting in a tumour.

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18
Q

Outline how mutations in photo-oncogenes cause cancer.

A

When functioning normally, PO genes stimulate cell division (by producing proteins that make the cell divide).

If a mutation occurs, the gene can become overactive. This stimulates the cells to divide uncontrollably and cause a tumour.

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19
Q

Difference between malignant or benign tumours?

A

Malignant spread throughout the body and grow rapidly. They are cancers.

Benign tumours are localised and grow slowly. They are not cancerous.

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20
Q

In what way are tumour cells different to normal cells?

A
  • irregular shape
  • different antigens on their surface
  • divide (by mitosis) more frequently
  • nucleus is darker and larger
21
Q

Outline hypermethylation.

A

When tumour suppressor genes are hypermethylated, there genes aren’t transcribed - so the proteins they produce (to slow cell division) aren’t made.
This means that cells are available to divide uncontrollably by mitosis.

22
Q

Outline hypomethlation

A

Hypomethylation of protons-oncogenes cause ten to act as oncogenes - increasing the production of proteins that encourage cell division.
This stimulates the cell to divide uncontrollably, which causes the formation of tumours.

23
Q

Outline how increased oestrogen may contribute to breast cancer.

A
  • oestrogen can stimulate certain breast cells to divide and replicate, so with more cell divisions taking place, this naturally increases the chance of mutations occurring, and so increases the chance of cells becoming cancerous.
  • the ability to stimulate division could also mean that if cells do become cancerous, their rapid replication could be further assisted by oestrogen helping tumours to form quickly.
24
Q

Outline genetic factors involved in the risk of cancer.

A

Some cancers are linked with specific inherited alleles. Therefore if you inherit said allele, you’re more likely to get that type of cancer.

25
Q

Outline environmental factors involved in the risk of cancer.

A

Exposure to radiation, lifestyle choices e.g. smoking, increased alcohol consumption and a high fat diet have all been linked to an increased chance of developing some cancers.

26
Q

How can understanding a specific mutation in a cancer related gene help to treat cancer?

A

If a specific causing mutations is known, then it’s possible to screen for the mutation in a person’s DNA (e.g. BRCA1 tumour suppressor gene). Preventative steps can then be taken e.g. mastectomy.

27
Q

At what stage of development can totipotent cells be found in mammals?

A

In the first few cell divisions of an embryo.

28
Q

Describe the difference between pluripotent and multipoint stem cells.

A

Pluripotent cells are made after totipotent cells. They can specialise into any cell, but lose the ability to become cells that make up the placenta.

Multipotent cells are only able to differentiate into a few types of cells - e.g. RBC and WBC made from multipoint cells found in bone marrow.

29
Q

How do stem cells become specialised?

A
  1. mRNA is only transcribed from specific genes.
  2. The mRNA from these genes is then translated into proteins.
  3. These proteins modify the cell (they determine the cell structure and control cell processes (inc the expression of more genes which produces more proteins)).
  4. These changes to the cell produced cause the cell to become specialised. These changes are difficult to reverse, so stays specialised.
30
Q

Name 2 conditions stem cell treatment could be used to treat?

A

Heart disease; stem cells used to replace damaged heart tissue.
Organ transplant; organs grown from stem cells to provide new organs for people on organ donor waiting lists.

31
Q

One difference between adult and embryonic stem cells

A

Adult cell - obtained from body tissue of adult cell. Also can only specialise into a limited range of cells (they’re multipotent)
Embryonic cell - obtained from embryos at an early stage of development. Also can divide into all types of body cells (they’re pluripotent)

32
Q

What do transcription factors do?

A

Control the transcription of target genes

33
Q

What is the basic principle of transcription?

A

DNA into mRNA , using RNA polymerase

34
Q

If all cells in and organism carry the same DNA, why is the structure and function different?

A

Because not all the genes in the cell are expressed (transcribed and used to make a protein).

Because different genes are expressed, different proteins are made and these proteins modify the cell; they determine the cell structure and cell processes.

35
Q

What kind of molecule is a TF?

A

Protein

36
Q

Outline the basic way that Bfs work.

A
  1. In eukaryotes, TFs move from the cytoplasm to the nucleus.
  2. In the nucleus, they bind to specific DNA sites near the start of their target genes.
37
Q

What are activators?

A

A TF that stimulates / increases the rate of transcription.

38
Q

What are repressors?

A

Bfs that inhibit / decrease the rate of transcription.

39
Q

Outline how oestrogen can initiate the transcription of target genes.

A
  1. Oestrogen binds to a TF, forming an oestrogen-oestrogen receptor complex.
  2. The complex moves from cytoplasm into nucleus where it binds to specific DNA sites near the start of the target gene.
  3. The complex can act as an activator of transcription (e.g. helping RNA polymerase bind to the start of the target gene).
40
Q

Outline how siRNA can inhibit the translation of mRNA

A
  1. Once mRNA has been transcribed, it leaves the nucleus to the cytoplasm.
  2. In the cytoplasm, double stranded siRNA associates with several proteins and unwinds. A single strand then binds to target mRNA (complementary base sequences).
  3. The proteins associated with the siRNA cut the mRNA into fragments; so it can no longer be translated. The fragments then move into a processing body where they’re degraded.
41
Q

Outline how miRNA can inhibit translation.

A
  1. Associates with proteins and binds to target mRNA in the cytoplasm.
  2. The miRNA-protein complex physically blocks the translation of the target mRNA.
  3. The mRNA is then moved into a processing body, where it’s degraded or stored.
42
Q

Why is miRNA stored?

A

So it can be returned and translated at another time.

43
Q

Difference between siRNA and miRNA?

A

The base sequence of siRNA is complementary to the base sequence in the sections of the target mRNA, but isn’t fully complementary in miRNA, so is less specific.

Also, siRNA cuts the mRNA into fragments, whereas the miRNA-protein complex physically blocks the translation of the target mRNA.

44
Q

Outline increased methylation.

A

The addition of a methyl group (CH3) to a molecule, at a CpG site (where C and G are next to each other).

Inhibits transcription in two ways:

  • prevents the binding of TFs to the DNA.
  • attracts proteins that condense the DNA-histone complex(by inducing deacetlyation of histone), making the DNA inaccessible to TFs.
45
Q

Outline how decreased acetylation of histones can switch off genes.

A
  1. When histones are acetylated, the chromatin is less condensed, meaning the TF can access the DNA, so is transcribed.
  2. When acetyl groups are removed from the histones, the chromatin becomes highly condensed and the genes in the DNA can’t be transcribed because the transcriptional machinery can’t physically access them.
46
Q

Which type of molecule are responsible for removing acetyl groups?

A

Histone deacetylase (HDAC) - enzymes.

47
Q

Give a characteristic that varies due to both environmental and genetic factors.

A

Overeating:

environmental: increased availability of food in developed countries.
genetic: food consumption increases dopamine in the brain, so once enough had been released, people would stop eating.

48
Q

Define epigenetic.

A

Heritable changes in gene function, without changes to the base sequence.

2B (26 decks)

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