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control of gene expression Flashcards

1
Q

substitution

A

one or more bases swapped for another

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2
Q

deletion

A

one or more bases removed

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3
Q

addition

A

one or more bases added

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4
Q

duplication

A

one or more bases repeated

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5
Q

inversion

A

a sequence of bases is reversed

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6
Q

translocation

A

sequence of bases moved from one location in genome to another
(could be within same or different chromosomes)

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7
Q

when do gene mutations occur?

A

spontaneously during DNA replication

mutagenic agents increase the rate of mutation

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8
Q

effects of mutations

A

different amino acid sequence made in polypeptide

change in sequence may change tertiary structure of protein
could stop it functioning

eg if its an enzyme, active site won’t be complementary shape to substrate

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9
Q

what does degenerate mean? and its impact on mutations

A

some amino acids coded for by more than one DNA triplet

means not all mutations change amino acid sequence

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10
Q

what is a frame shift?

A

happens due to mutations
- often addition, duplication and deletions
happens as they change the number of bases in a DNA code

changes nature of all base triplets that follow, code read in a different way
- affects amino acid sequence

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11
Q

examples of mutagenic agents

A

UV radiation
ionising radiation
chemicals

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12
Q

how can mutagenic agents increase rate or mutations? (3)

A

act as a base
- substitute for a base
- causes substitution mutations
- changes base sequence

alter a base
- can delete or alter bases
- changes sequence

changing DNA structure
- causes issues in replication
- increases likelihood of mutations

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13
Q

causes of cancer

A

when mutations happen in genes that control cell division
- tumour supressor genes
- proto-oncogenes

causes uncontrolled cell growth
results in tumour
- mass of abnormal cells which invade and destroy surrounding tissue

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14
Q

malignant tumours

A

cancers
- grow rapidly
- invade and destroy surrounding tissue
- cells can break off and spread in bloodstream

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15
Q

benign tumours

A

not cancerous
- grow slower
- covered in fibrous tissues, stops invading
- often harmless, can become malignant

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16
Q

what do tumour cells look like?

A
  • irregular shape
  • larger and darker nucleus
  • different antigens
  • divide more frequently (don’t respond to regulating processes)
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17
Q

role of tumour suppressor genes

A

working normally:
- slow cell division
- produce proteins to stop cell division or to make cells self destruct

can be inactivated by a mutation:
- doesn’t produce protein to slow division
- stimulates cells divide uncontrollably = tumour

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18
Q

role of proto-oncogenes

A

working normally:
- stimulate cell division
- produces proteins to make cell divide

effect can be increased due to mutation:
- gene becomes overactive
- stimulates cells to divide uncontrollably = tumour

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19
Q

what are oncogenes?

A

Mutated proto oncogene
caused by hypomethylation

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20
Q

what is methylation?

A

adding a methyl group

methylation of DNA controls weather or not the DNA is transcribed and translated

abnormal methylation is when it happens to much or too little
- hypomethylation
- hypermethylation

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21
Q

how can abnormal methylation cause tumours?

A
  • hypermethylation of tumour - suppressor genes
  • gene isn’t transcribed
  • protein to slow division not made
  • divide uncontrollably = tumour
  • hypomethlyation of proto-oncogenes
  • act as oncogenes
  • increases amount of proteins that stimulate cell division
  • divide uncontrollably = tumour
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22
Q

how does oestrogen cause cancer?

A

increased exposure over long periods of time - increased risk of breast cancer

  1. can stimulate certain breast cells to divide
    more cell division taking place increases chance of mutations and cells becoming cancerous
  2. the ability to stimulate division mean any cancerous cells would be able to divide even faster
    tumour form more quickly
  3. may be able to introduce mutations directly in DNA causing mutations
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23
Q

2 types of risk factors

A

something that increases someones chance of developing cancer

genetic - linked to specific inherited alleles - if inherited, more at risk

environmental - exposure to radiation, smoking, increased alcohol and fat diet increase risk

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24
Q

how can understanding roles of the genes be used in prevention?

A

if a specific mutation causing cancer is known, it can be screened for

knowing this risk can allow for prevention
- screened more often
- lifestyle choices
increased recovery when found early

knowing genes can also mean better tests for cancers
- easier and more accurate diagnosis

25
how can understanding roles of the genes be used in treatment and cures?
treatments are different for different mutations - allows for more specific treatments to be made - more effective in targeting it - more treatment (eg higher doses) can be used for more aggressive cancers caused by different mutations gene therapy - replace faulty genes with working ones knowing which gene cause the cancers can also them be to changed
26
what are stem cells?
unspecialised cells that can differentiate into other types of cell
27
what are totipotent cells?
stem cells that can divide and produce any type of body cell only translate part of their DNA, allowing them to become specialised only present in mammals in first few divisions of embryo - then become pluripotent
28
what are pluripotent cells?
found in embryos can specialise into any cell but ones that make up placenta
29
multipotent stem cells
found in adult mammals able to differentiate into few types of cell eg red and white blood cells from bone marrow
30
unipotent stem cells
only differentiate into one type of cell found in adult mammals
31
how to stem cells become specialised?
only transcribe and translate part of their DNA all contain same genes due to conditions, some genes are expressed and other switched off mRNA only transcribed from specific genes so only specific proteins made in translation proteins modify cell eg structure = specialised
32
unipotent cells in the heart
cardiomyocytes - heart muscle cells thought that heart cells couldn't be regenerated (issue if damaged) now thought there is small supply of unipotent stem cells in heart - specials to replace damaged cells
33
use of pluripotent stem cells in treating disorders
as they can specialise into any type of cell, can be used to replace damaged cells - bone marrow contains stem cells that can specialise into any blood cell - bone marrow transplants are used to replace faulty bone marrow in patents with abnormal blood cells - cells in transplant divide and specialise into healthy blood cells eg leukaemia
34
sources of stem cells
adult stem cells - body tissues of adult eg bone marrow obtained in simple operation but not as flexible - multipotent (a few types) embryonic stem cells - embryos in early stages of development created in lab using in vitro fertilisation (outside of womb) stem cells remove and embryo destroyed pluripotent - any number of any cell iPS cells
35
what are iPS cells?
induced pluripotent stem cells created in a lab reprogramming specialised adult body cells to become pluripotent - made to express transcription factors associated with pluripotent cells - cause there body cells to express genes associated with the stem cells will be useful in medicine and ethical (see benefits of stem cells)
36
how are iPS cells made?
made to express transcription factors to make them express genes associated with pluripotent stem cells - infect with specific modified virus - virus has genes coding for transcription factors in its DNA - when it infects, genes passed on to adult cells DNA, cell produces transcription factors
37
benefits of stem cell treatments
save many lives eg those waiting for transplants, new organs made from stem cells to reduce waiting improve quality of life replace damaged cells eg blindness iPS cells are from adult stem cells - more ethical but can still specialise into any cell iPS made from patients cells - genetically identical less chance of rejection
38
issues of using stem cells treatments
ethical issues of using embryonic stem cells - results in destruction of embryo, could become fetus - less objection to those from egg cells that haven't been fertilised, wouldn't become fetus should use adult stem cells - doesn't destroy embryo but can't specialise into any cell
39
why do cells have different functions?
cells in an organism all have the same genes but structure and function varies as not all genes are expressed (transcribed and translated) different genes expressed = different proteins made, determine structure and processes
40
what are transcription factors?
proteins that control whether or not genes are transcribed bind to promotor reigons upstream of gene
41
promotor region
section of DNA upstream of a gene binding site for transcription factors
42
how do transcription factors work?
control expression by controlling rate of transcription not transcribed = not expressed - move from cytoplasm to the nucleus, through pores - bind to promotor region (upstream of the gene they control the expression of) activators - stimulate or increase rate of transcription help RNA polymerase bind to start of target gene = activate transcription repressors - inhibit or decrease rate of transcription prevent RNA polymerase from binding = inhibited
43
how does oestrogen initiate transcription?
oestrogen is a steroid hormone affects transcription - diffuses into cells through phospholipid bilayer (lipid soluble) - binds to complementary site on transcription factor (oestrogen receptor) - forms an oestrogen - oestrogen receptor complex complex changes shape - moves from cytoplasm to nucleus, thorugh nuclear pores binds to specific base sequence near start of target gene (promoter) complex acts as an activator helps RNA polymerase bind initiates transcription
44
what is a steroid hormone? (oestrogen)
small and lipid soluble can diffuse directly through membrane
45
what is RNA interference? (RNAi)
where small, double stranded RNA molecules (non-coding) stop mRNA from target genes being translated into proteins also affects gene expression (inhibits) done by siRNA (small interfering) or miRNA (micro)
46
how is siRNA made?
DNA transcribed and replication = Double stranded RNA Broken up by enzymes into double stranded siRNA DICER, hydrolyses Hydrogen bonds broken Joined to enzyme (eg RISC) Creates siRNA
47
how does siRNA work in mammals? (miRNA in plants)
DNA transcribed and replicated = double stranded RNA broken up by enzymes into pieces (eg DICER) hydrogen bonds broken = single stranded siRNA associates with enzyme (eg RISC) in cytoplasm: siRNA then binds to target mRNA - base sequence of siRNA complementary to base sequence of target mRNA Enzyme with siRNA, cut the mRNA into fragments - can't be translated fragments move to processing body where they are degraded
48
how does miRNA work?
miRNA not always complementary to target mRNA - is less specific than siRNA, can target more than one mRNA molecule miRNA associates with enzymes and binds to target mRNA in cytoplasm miRNA - protein complex blocks the translation of target mRNA mRNA then moved into processing body and stored or degraded (stored to be translated later)
49
what is epigenetic control? (+ how it works)
determines whether or not a gene is expressed (transcribed and translated) changes gene function without changing base sequence works by attachment or removal of chemical groups - epigenetic marks to or from DNA or histones - changes how easy it is for machinery to interact heritable - changes due to changes in environment eg stress reversible
50
types of epigenetic changes (2)
increased methylation of DNA decreased acetylation of histones = genes not expressed
51
inheritance of epigenetic marks
organisms inherit DNA base sequence from parents some epigenetic marks are passed on to offspring (most removed) means expression of some gene in offspring affected by environmental changes that impacted their parents
52
how does increased methylation inhibit transcription?
methyl group (epigenetic mark) is attached to the DNA coding for a gene attaches at a CpG site (where cytosine and guanine are joined by a phosphodiester bond) increased methylation changes the DNA structure transcriptional machinery can't interact (eg enzymes) gene isn't transcribed (not expressed)
53
how does decreased acetylation inhibit transcription?
DNA wraps around histones to make chromatin can be highly or less condensed due to presence of acetyl groups (epigenetic marks) histones can be acetylated - add acetyl group - makes chromatin less condensed - DNA more accessible to machinery - can be transcribed acetyl groups can be removed from histones - chromatin highly condensed - genes in DNA less accessible, machinery can reach it - not transcribed histone deacetylase (HDAC) responsible for removing acetyl group
54
how does epigenetics lead to development of disease?
methylation controls which genes are expressed abnormal methylation of certain genes can result in cancers: hypermethylation of tumour suppressor genes hypomethylation of proto-oncogenes controls which genes are expressed, lead to uncontrolled cell growth (decreased acetylation of tumour suppressor increased acetylation of proto oncogenes)
55
how can drugs treat epigenetic changes?
epigenetic changes are reversible drugs designed to counteract epigenetic changes increased methylation = gene switched off drugs can stop DNA methylation so gene still expressed decrease acetylation = gene switched off drugs can inhibit histone deacetylase (which remove the acetyl group) so genes remain acetylated, can be expressed but drugs must be specific as epigenetic changes can happen naturally, must target right cells
56
epigenetic cancer treatment
removal of methyl groups from tumour suppressor genes - allows them to be expressed = division slowed removal of acetyl groups from histones of oncogenes - more condensed = can't be transcribed, division slowed
57
Pre transcriptional control
Transcription factors Increased or decrease transcription
58
Post transcriptional control
RNA interference Stop translation
59
development of a tumour
tumour supressor genes mutated or silenced - mutations = inactive - silenced - epigenetics/RNAi proto oncogenes = oncogenes - mutations = over active - not switched off (hypomethylation, increased acetylation)

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