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A2 biology > 8.1 gene expression > Flashcards

8.1 gene expression Flashcards

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1
Q

give the type of gene mutation in which a nucleotide in a section of a DNA molecule is replaced by another nucleotide with a different base.

A

substitution.

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2
Q

give the type of gene mutation which results in the loss of a nucleotide base from a DNA sequence.

A

deletion.

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3
Q

apart from substitution and deletion, give the four other types of gene mutation.

A
  • addition.
  • duplication.
  • inversion.
  • translocation.
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4
Q

what is a frameshift?

A
  • a mutation that shifts the “reading” frame of the genetic code by inserting or deleting a nucleotide.
  • the gene is now read in the wrong three-base groups and the coded information is altered.
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5
Q

the addition and duplication of bases causes a frameshift in which direction? explain how this is different from the deletion of bases.

A
  • addition and duplication mutations cause a frameshift to the right hand side.
  • this is different to deletion, which causes a frameshift to the left hand side.
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6
Q

explain cell differentiation.

A

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

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7
Q

what are totipotent cells?

A

cells, such as fertilised eggs, that can mature into and give rise to any type of body cell.

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8
Q

explain how different cells may become specialised.

A
  • during the process of cell specialisation, only some genes are expressed, meaning that only part of the DNA of a cell can be translated into proteins.
  • the cell therefore only produces the proteins that it requires to carry out its specialised function.
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9
Q

although specialised cells are capable of producing all types of proteins, these are not needed so it would be wasteful to produce them. in order to conserve energy and resources, a variety of stimuli (controlling factors) ensure the genes for the production of other proteins are not expressed. give the two ways in which genes are prevented from expressing themselves.

A
  • preventing transcription, and so preventing the production of mRNA.
  • preventing translation.
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10
Q

explain what is meant by the term ‘stem cell’, and describe where stem cells are found.

A

stem cells are undifferentiated dividing cells that occur in adult animal tissues and need to be constantly replaced.

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11
Q

stem cells originate from various sources in mammals. list four of these sources.

A
  • embryonic stem cells.
  • umbilical cord blood stem cells.
  • placental stem cells.
  • adult stem cells.
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12
Q

there a number of different stem cells which are classified according to their ability to differentiate. give the four main types of stem cell, where they are found and an example for each.

A

totipotent stem cells - found in the early embryo, and can differentiate into any type of cell.

pluripotent stem cells - found in embryos, and can differentiate into almost any type of cell. an example of a pluripotent stem cell is a fetal stem cell.

multipotent stem cells - found in adults and can differentiate into a limited number of specialised cells. multipotent stem cells usually differentiate into cells of a particular type. an example of a multipotent stem cell is an umbilical cord blood cell.

unipotent stem cells - can only differentiate into a single type of cell. they are derived from multipotent stem cells and are made in adult tissue.

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13
Q

induced pluripotent stem cells (iPS cells) are a type of pluripotent cell. give the type of stem cell iPS cells are produced from.

A

unipotent stem cells, which may be almost any body cell.

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14
Q

in order to produce iPS cells, unipotent cells are genetically altered in a lab so that they acquire the characteristics of embryonic stem cells (pluripotent stem cells). describe how these unipotent cells are genetically altered to give iPS cells.

A

making the unipotent cell acquire the new characteristics of a pluripotent cell involves inducing genes, and other transcriptional factors within the cell to express themselves.

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15
Q

the fact that these induced genes are capable of being reactivated within the unipotent cell shows what?

A

the fact that these genes are capable of being reactivated shows that adult cells retain the same genetic information that was present in the embryo.

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16
Q

give one feature of iPS cells and a consequence of this feature.

A
  • iPS cells are capable of self-renewal, meaning that they can potentially divide indefinitely to provide a limitless supply.
  • they could replace embryonic cells in medical research and treatment, overcoming many of the ethical issues surrounding the use of embryos in stem cell research.
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17
Q

give three potential uses of human cells produced from stem cells.

A

heart muscle cells - heart damage, for example, as a result of a heart attack.

nerve cells - strokes.

blood cells - leukaemia.

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18
Q

what are transcriptional factors?

A

specific molecules that move from the cytoplasm to the nucleus to express (switch on) a gene so that transcription may begin.

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19
Q

explain how transcriptional factors cause a region of DNA to begin the process of transcription.

A
  • each transcriptional factor has a site that binds to a specific base sequence of the DNA in the nucleus.
  • when it binds, it causes this region of DNA to begin transcription.
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20
Q

explain what happens to a transcriptional factor if a gene is not being expressed.

A
  • when a gene is not being expressed, the transcriptional factor that binds to the DNA is not active.
  • therefore, it cannot stimulate transcription and polypeptide synthesis.
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21
Q

give an example of a molecule which can express a gene and start transcription by combining with a receptor site on the transcriptional factor.

A

steroid hormones, such as oestrogen.

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22
Q

explain why oestrogen is able to easily diffuse through the cell-surface membrane of a cell.

A

oestrogen is a lipid-soluble molecule, therefore diffuses easily through the phospholipid portion of cell-surface membranes.

23
Q

once inside the cytoplasm of a cell, oestrogen binds with a site on a receptor molecule of the transcriptional factor. explain why this is able to take place.

A

the shape of the site on the receptor molecule and the shape of the oestrogen molecule are complimentary to one another.

24
Q

explain what occurs when oestrogen binds with the binding site on a receptor molecule.

A

by binding with the site, the oestrogen changes the shape of the DNA binding site on the transcriptional factor, which can now bind to DNA (it is activated)

25
Q

the transcriptional factor can now enter the nucleus. give the part of the nucleus which the transcriptional factor enters through.

A

the nuclear pore.

26
Q

the combination of the transcriptional factor with DNA stimulates the transcription of what?

A

transcription of the gene that makes up the portion of DNA.

27
Q

what is epigenetics?

A

changes to the phenotype caused by environmental factors that can cause heritable changes in gene function without changing the base sequence of DNA.

28
Q

give three environmental influences that could subtly alter the genetic inheritance of an organism’s offspring.

A
  • diet.
  • stress.
  • toxins.
29
Q

what is the epigenome?

A

a chemical layer surrounding chromatin (the combination of DNA and histones) the epigenome determines the shape of the DNA-histone complex.

30
Q

what is epigenetic silencing?

A
  • the epigenome can keep inactive genes in a tightly packed arrangement, therefore ensuring that they cannot be read.
  • this is known as epigenetic silencing.
31
Q

explain why the epigenome is described as ‘flexible’.

A
  • the epigenome is described as ‘flexible’ because its chemical tags respond to environmental changes.
  • factors like diet and stress can cause the chemical tags to adjust the wrapping and unwrapping of DNA, switching genes on and off.
32
Q

environmental signals stimulate proteins to carry messages inside of cells, where the signal is passed by a series of other proteins onto the nucleus. here, the message passes onto a specific protein which can be attached to a specific sequence of bases on the DNA. give the two possible effects that could occur following attachment of the protein.

A
  • acetylation of histones leading to the activation or inhibition of a gene.
  • methylation of DNA by attracting enzymes that can add or remove methyl groups.
33
Q

explain what happens to the DNA-histone complex where the association of histones is weak.

A
  • where the association of DNA with histones is weak, the DNA-histone complex is less condensed.
  • in this condition, the DNA is accessible by transcription factors, which can initiate the production of mRNA.
34
Q

explain what happens to the DNA-histone complex where the associate of histones is stronger.

A
  • where the association of DNA with histones is stronger, the DNA-histone complex is more condensed.
  • in this condition, the DNA is not accessible by transcription factors, which therefore cannot initiate the production of mRNA.
35
Q

condensation of the DNA-histone complex inhibits transcription. explain how this can be brought about.

A
  • by decreased acetylation of the histones.
  • by methylation of DNA.
36
Q

explain how decreased acetylation can inhibit transcription factors.

A
  • decreased acetylation increases the positive charge 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 transcription factors.
37
Q

explain how increased methylation can inhibit transcription factors.

A
  • by preventing the binding of transcriptional factors to the DNA.
  • by attracting proteins that condense the DNA-histone complex, making the DNA inacessible to transcription factors.
38
Q

give the two types of tumours, whether or not they can spread to other tissues, and if they are cancerous.

A

benign tumours - non-cancerous, cannot spread to other tissues.

malignant tissues - cancerous, can spread to other tissues.

39
Q

give four features of a benign tumor.

A
  • grow very slowly.
  • cells are often specialised.
  • less likely to be life-threatening, but can disrupt functioning of a vital organ.
  • tend to have localised effects on the body.
40
Q

give four features of a malignant tumour.

A
  • grow rapidly.
  • cells become unspecialised.
  • more likely to be life-threatening as abnormal tumour tissue replaces normal tissue.
  • often have systematic (whole body) effects such as weight loss and fatigue.
41
Q

give the two main types of gene that play a role in cancer.

A
  • tumour suppressor genes.
  • oncogenes.
42
Q

most oncogenes are mutations of proto-oncogenes. explain how proto-oncogenes stimulate cell division.

A
  • proto-oncogenes stimulate a cell to divide when growth factors attach to a protein receptor on its cell-surface membrane.
  • this then activates genes that cause DNA to replicate and the cell to divide.
43
Q

give two reasons why an oncogene can become permanently activated if a proto-oncogene mutates into a oncogene.

A
  • the receptor protein on the cell-surface membrane can be permanently activated, so that cell division is switched on even in the absence of growth factors.
  • the oncogene may code for a growth factor that is then produced in excessive amounts, again stimulating excessive cell division.
44
Q

what is the role of a tumour suppressor gene?

A

tumour suppressor genes slow down cell division, repair mistakes in DNA, and stimulate apoptosis (programmed cell death)

45
Q

if a tumour suppressor gene becomes mutated it is inactivated. explain what happens as a result of this.

A
  • the tumour suppressor gene stops inhibiting cell division and the cells can divide uncontrollably.
  • the mutated cells that are formed are usually structurally and functionally different from normal cells.
  • whilst most of these die, those that survive can make clones of themselves and form tumours.
46
Q

give the two forms of abnormal methylation of tumour suppressor genes.

A
  • hypermethylation (increased methylation)
  • hypomethylation (reduced methylation)
47
Q

where in tumour suppressor genes does hypermethylation occur? explain how this limits transcription.

A
  • hypermethylation occurs in the promoter region of tumour suppressor genes, leading to the inactivation of the gene.
  • as a result, transcription of the promoter regions of the tumour suppressor gene is inhibited.
48
Q

explain how oestrogen can cause a tumour to develop.

A

oestrogen can cause proto-oncogenes of cells in breast tissue to develop into oncogenes, leading to the development of a tumour.

49
Q

what is the genome?

A

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

50
Q

what is whole-genome shotgun (WGS) sequencing?

A

WGS sequencing involves cutting DNA into many small, easily sequenced sections and then using computer algorithms to align overlapping segments to assemble the entire genome.

51
Q

what are single nucleotide polymorphisms (SNPs)?

A

SNPs are single-base variations in the genome that are associated with disease and other disorders.

52
Q

what is the proteome?

A

the proteome is the all the proteins produced in a given type of cell or organism at a given time under specified conditions.

53
Q

give two reasons why determining the proteome of prokaryotic organisms, such as bacteria, is easier than determining the proteome of eukaryotic organisms.

A
  • the majority of prokaryotes have just one, circular piece of DNA that is not associated with histones.
  • there are none of the non-coding portions of DNA (introns) which are typical of eukaryotic cells.
54
Q

explain why is it difficult to determine the genome and proteome of complex organisms.

A
  • the genome of complex organisms contains many non-coding genes as well at others that have a role in regulating other genes.
  • this makes it difficult to determine the genome and proteome of complex organisms.

A2 biology (9 decks)

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