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Biology - Module 6 > cellular control > Flashcards

cellular control Flashcards

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1
Q

what is a mutation

A

Change in sequence of base pairs

may results in altered polypeptide

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2
Q

3 types of factors that increase the risk of mutations

A

physical

chemical

biological

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3
Q

what are physical mutagens and how do they work

A

ionising radiation - X rays

break DNA strands

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4
Q

what are chemical mutagens and how do they work

A

deaminating agents

chemically alter bases in DNA

e.g - converting cytosine to uracil

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5
Q

what are biological mutagens and how do they work

A

alkylating agents

(methyl / ethyl groups attaching to bases - incorrect pairing)

base analogs

(inserted into DNA in stead of usual base)

viruses

(viral DNA insert into genome - changing sequence)

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6
Q

how might mutations not effect the phenotype

A

masking

degenerate – many different triplets code for same amino acid = no effect

occur in non-coding sections

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7
Q

what are mutations that dont effect phenotype called

A

silent mutations

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8
Q

how do mutations occur

A

insertion of nucleotides

deletion of nucleotides

substitution of nucleotides

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9
Q

effect of insertion of nucleotides

A

changes amino acid

also has knock on effect further along DNA sequence – frameshift mutation

dramatically changes sequence

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10
Q

effect of deletion of nucleotides

A

changes triplet

knock on effect – frameshift mutation

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11
Q

effect of substitution of nucleotides

A

only change amino acid for the triplet – no knock on effect

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12
Q

types of substitution mutations

A

silent

missence

nonsense

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13
Q

what is a missence mutation

A

alters single amino acids in chain – sickle cell anaemia

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14
Q

what is nonsense mutation

A

creates a premature stop codon – polypeptide chain incomplete – cystic fibrosis

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15
Q

what is a silence mutation

A

does not alter amino acid sequence = degenerate

generally changes in 2nd / 3rd base

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16
Q

give an example of a beneficial mutation to humans

A

early humans Africa – dark skin due to high conc of melanin

provided protection from harmful UV radiation – still allowing vitamin D to be synthesised

as humans moved into cooler – mutations caused decrease in melanin

paler skin – selective advantage – synthesis more vitamin D
= lighter skin absorbs less UVB
= cooler climates – already low levels
= need as much as can get

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17
Q

example of harmful mutation

A

genetic diseases – cystic fibrosis

loss of function of protein

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18
Q

example of neutral mutations

A

ability to taste bitter tasting chemicals in brussel sprouts

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19
Q

what is a chromosome mutation vs gene mutation

A

gene mutations – occur in single genes

chromosome mutations – affect whole chromosome / number of chromosomes

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20
Q

how would chromosome mutations occur

A

deletion – section of chromosome breaks off

duplication – sections copied on chromosome

translocation – section of 1 chromosome breaks off + joins non-homologous chromosome

inversion – section of chromosome breaks off + is reversed + joins back on

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21
Q

what is the purpose of regulatory mechanisms

A

ensure correct genes expressed in correct cells at correct time

allows for specialisation of cells

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22
Q

what are the levels of regulation

A

transcriptional level

post-transcriptional level

translational level

post translational level

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23
Q

examples of regulation at transcriptional level

A

lac operon / transcription factors / chromatin remodelling / histone modification

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24
Q

examples of regulation at post-transcriptional level

A

editing of primary mRNA + removal of introns

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25
examples of regulation at translational level
degradation of mRNA
26
examples of regulation at post - translational level
activation of proteins by cyclic AMP
27
what is a structural gene
codes for proteins that function within a cell
28
what is a regulatory gene
codes for proteins / RNA that control expression of structural genes
29
what is heterochromatin
tightly wound DNA
30
what is euchromatin
loosely wound DNA in interphase
31
what is chromatin remodelling
Simple form of regulation that ensures proteins needed for cell division are made in time
32
how does chromatin remodelling act as a regulatory mechanism
transcription of genes can not occur for heterochromatin RNA polymerase cant access genes Protein synthesis only occurs during interphase
33
benefits of chromatin remodelling
prevents energy-consuming protein synthesis happening in cell division
34
why does DNA coil around histone
Histone – positively charged DNA – negatively charged so coils around
35
how does histone modification act as a regulatory mechanism
Add acetyl groups / phosphate groups – reduces positive charge on histones + DNA coils less tightly (Allows certain genes to be transcribed) Add methyl groups – histones more hydrophobic – bind more tightly to each other + DNA coils more tight (Prevent transcription of genes)
36
what reduces positive charge on histone + its effect
acetyl groups / phosphate groups – DNA coils less tightly
37
what increases positive charge on histone + its effect
methyl groups – bind more tightly to each other + DNA coils more tight
38
what is an operon
group of genes that are under the control of the same regulatory mechanism / promoter are expressed at same time
39
benefits of an operon
allow for smaller / simpler genome structure efficient at saving resources – if certain gene products not needed – all genes switched off
40
what does the lac operon control
controls production of enzyme lactase + 2 structural proteins
41
what is an inducible enzyme
enzyme that is made under certain conditions // dependant on presence of their substrate
42
how is lactase an inducible enzyme
only synthesised when lactose is present = not when glucose is present or no point
43
describe the structure of a lac operon
promoter for structural genes operator structural gene lacZ for lactase structural gene lacY for permease structural gene lacA for transacetylase promotor for regulatory gene regulatory gene lacl that codes for lac repressor protein
44
what is an operator
segment of DNA that a repressor binds to – inhibiting transcription of genes
45
what happens if lactose is absent
transcription of lac genes repressed regulatory gene always switched on lac repressor protein made protein binds to operator region upstream of lacZ now – RNA polymerase unable to bind to promoter region transcription of structural genes cant happen no lactase enzyme is made
46
what happens if lactose is present
uptake of lactose by bacteria lactose binds to second binding site on repressor protein distorts shape – conformational change can not bind to operator RNA polymerase can now bind to promoter Transcription happens Lactase produced
47
what is a transcription factor
Protein that controls transcription of genes by binding to specific region of DNA Bind to promoter region – either allow or prevent transcription
48
what type of hormone is oestrogen
lipid soluble
49
how does oestrogen act as a transcription factor
Oestrogen diffuses through the cell surface membrane into the cytoplasm + nucleus attaches to an ERα oestrogen receptor that is held within a protein complex causes the ERα oestrogen receptor to undergo a conformational change new shape of the ERα oestrogen receptor allows it to detach from the protein complex diffuses towards the gene to be expressed ERα oestrogen receptor binds to a cofactor enables it to bind to the promoter region of the gene stimulates RNA polymerase binding and gene transcription
50
when to use DNA / RNA
all cells = same DNA express diff genes = analyse RNA
51
what are exons
coding sequences eventually be translated into amino acid = polypeptide EXPRESSED
52
what are introns
non coding base sequences
53
what happens in terms of exons / introns in transcription
both exons + introns transcribed on premRNA
54
what happens to modify the premRNA into mRNA
splicing
55
what is splicing
primary / pre-mRNA has exons + introns introns removed from molecule exons fused together – to form continuous mRNA = mature mRNA cap + tail added
56
how are introns removed
5’ splice site at beginning of intron 3’ splice site at end of intron
57
what is a cap + where is it added
modified nucleotide added to 5’ end
58
what is a tail + where is it added
long chain of adenine nucleotides added to 3’ end
59
purpose of cap + tail
tail - help stabilise mRNA + delay degradation in cytoplasm cap – aid binding mRNA to ribosomes
60
describe the control at post-translational level
polypeptides undergo modifications in Golgi / apparatus + cytosol some require activation from cAMP cAMP – activates protein kinase A once activates – can activate other proteins
61
example of control at post-translational level
when muscle cells require energy enzyme = glycogen phosphorylase releases glucose from glycogen This enzyme is activated by cAMP, which changes the shape of the enzyme to expose its active site
62
what do homeotic genes control
polarity – head and tail segmentation – distinct body parts
63
what is morphogenesis + what is it controlled by
Process that causes organisms to form shape homeotic genes
64
what are homeobox genes
Subset of homeotic genes any gene that contains a homeobox
65
what is a homeobox
DNA sequence that codes for a protein transcription factor – 180 base pairs
66
what are the key characteristics of a homeobox
Highly conserved – maintained by natural selection / remain unchanged through evolution Sequences are similar in animals / plants – all code for amino acid sequences that will form transcription factors DNA-binding region of them all must have same shape
67
what is the homeodomain
Sequence of 60 amino acids that the homeobox codes for
68
what shape is a homeodomain
folds into shape with three alpha helices
69
what is a protein with a homeodomain called
transcription factor
70
what is a hox gene
Subset of homeobox genes Involved in correct positioning of body parts
71
where are hox genes found
Only found in bilaterian animals Have half way symmetry Exist in all common ancestors
72
what happens when hox genes are mutated
body parts develop in wrong place
73
whats special about hox genes
show spatial linearity show temporal order
74
what is spatial linearity
Order of genes along chromosome matches expression patterns Those that code for head – at the top end
75
what is temporal order
Starts with expression of anterior hox genes Head ones expressed first – head gets made first
76
how is apoptosis expressed in cells
DNA of cell becoming denser + more tightly packed Nuclear envelope breaking down + chromosomes condensing Vesicles forming with hydrolytic enzymes Phagocytes engulfing + digesting cell = phagocytosis
77
why is apoptosis needed in body plans
some cells made by mitosis earlier may no longer be needed
78
example of apoptosis in body plans
Fingers + toes first develop as combined unit Separated later by apoptosis of cells between digits
79
how is mitosis controlled
by two types genes Proto-oncogenes – stimulate cell division Tumour-suppressor genes – reduce cell division
80
how does cyclins regulate mitosis
Cyclins – regulators CDK’s – catalysts Cyclins bind to CDKs = conformational change // activating the CDK Now CDK capable of phosphorylating target proteins – transfer phosphate from ATP to protein Activate / inactivate proteins – control progression of cell cycle Proteins may release transcription factors
81
what are the internal stimuli that effect mitosis / apoptosis
Irreparable genetic damage Release of hormones RNA decay Internal biochemical changes that lead to cell changes or cellular injury (e.g. oxidative reactions)
82
overall how does apoptosis get activated
stress // hormones activate a protein acts as transcription factor activates genes involved in apoptosis
83
what are the external stimuli that effect mitosis / apoptosis
presence of cell-signalling molecules = cytokines / hormones / growth factors viruses + bacteria change in light intensity lack of nutrients drugs

Biology - Module 6 (6 decks)

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