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Biology - Module 6 > cellular control > Flashcards

cellular control Flashcards

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
Q

examples of regulation at translational level

A

degradation of mRNA

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26
Q

examples of regulation at post - translational level

A

activation of proteins by cyclic AMP

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27
Q

what is a structural gene

A

codes for proteins that function within a cell

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28
Q

what is a regulatory gene

A

codes for proteins / RNA that control expression of structural genes

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29
Q

what is heterochromatin

A

tightly wound DNA

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30
Q

what is euchromatin

A

loosely wound DNA in interphase

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31
Q

what is chromatin remodelling

A

Simple form of regulation that ensures proteins needed for cell division are made in time

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32
Q

how does chromatin remodelling act as a regulatory mechanism

A

transcription of genes can not occur for heterochromatin

RNA polymerase cant access genes

Protein synthesis only occurs during interphase

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33
Q

benefits of chromatin remodelling

A

prevents energy-consuming protein synthesis happening in cell division

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34
Q

why does DNA coil around histone

A

Histone – positively charged

DNA – negatively charged

so coils around

35
Q

how does histone modification act as a regulatory mechanism

A

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
Q

what reduces positive charge on histone + its effect

A

acetyl groups / phosphate groups – DNA coils less tightly

37
Q

what increases positive charge on histone + its effect

A

methyl groups – bind more tightly to each other + DNA coils more tight

38
Q

what is an operon

A

group of genes that are under the control of the same regulatory mechanism / promoter

are expressed at same time

39
Q

benefits of an operon

A

allow for smaller / simpler genome structure

efficient at saving resources – if certain gene products not needed – all genes switched off

40
Q

what does the lac operon control

A

controls production of enzyme lactase + 2 structural proteins

41
Q

what is an inducible enzyme

A

enzyme that is made under certain conditions // dependant on presence of their substrate

42
Q

how is lactase an inducible enzyme

A

only synthesised when lactose is present = not when glucose is present or no point

43
Q

describe the structure of a lac operon

A

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
Q

what is an operator

A

segment of DNA that a repressor binds to – inhibiting transcription of genes

45
Q

what happens if lactose is absent

A

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
Q

what happens if lactose is present

A

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
Q

what is a transcription factor

A

Protein that controls transcription of genes by binding to specific region of DNA

Bind to promoter region – either allow or prevent transcription

48
Q

what type of hormone is oestrogen

A

lipid soluble

49
Q

how does oestrogen act as a transcription factor

A

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
Q

when to use DNA / RNA

A

all cells = same DNA

express diff genes = analyse RNA

51
Q

what are exons

A

coding sequences

eventually be translated into amino acid = polypeptide

EXPRESSED

52
Q

what are introns

A

non coding base sequences

53
Q

what happens in terms of exons / introns in transcription

A

both exons + introns transcribed on premRNA

54
Q

what happens to modify the premRNA into mRNA

A

splicing

55
Q

what is splicing

A

primary / pre-mRNA has exons + introns

introns removed from molecule

exons fused together – to form continuous mRNA = mature mRNA

cap + tail added

56
Q

how are introns removed

A

5’ splice site at beginning of intron

3’ splice site at end of intron

57
Q

what is a cap + where is it added

A

modified nucleotide added to 5’ end

58
Q

what is a tail + where is it added

A

long chain of adenine nucleotides added to 3’ end

59
Q

purpose of cap + tail

A

tail - help stabilise mRNA + delay degradation in cytoplasm

cap – aid binding mRNA to ribosomes

60
Q

describe the control at post-translational level

A

polypeptides undergo modifications in Golgi / apparatus + cytosol

some require activation from cAMP

cAMP – activates protein kinase A

once activates – can activate other proteins

61
Q

example of control at post-translational level

A

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
Q

what do homeotic genes control

A

polarity – head and tail

segmentation – distinct body parts

63
Q

what is morphogenesis + what is it controlled by

A

Process that causes organisms to form shape

homeotic genes

64
Q

what are homeobox genes

A

Subset of homeotic genes

any gene that contains a homeobox

65
Q

what is a homeobox

A

DNA sequence that codes for a protein transcription factor – 180 base pairs

66
Q

what are the key characteristics of a homeobox

A

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
Q

what is the homeodomain

A

Sequence of 60 amino acids that the homeobox codes for

68
Q

what shape is a homeodomain

A

folds into shape with three alpha helices

69
Q

what is a protein with a homeodomain called

A

transcription factor

70
Q

what is a hox gene

A

Subset of homeobox genes

Involved in correct positioning of body parts

71
Q

where are hox genes found

A

Only found in bilaterian animals

Have half way symmetry

Exist in all common ancestors

72
Q

what happens when hox genes are mutated

A

body parts develop in wrong place

73
Q

whats special about hox genes

A

show spatial linearity

show temporal order

74
Q

what is spatial linearity

A

Order of genes along chromosome matches expression patterns

Those that code for head – at the top end

75
Q

what is temporal order

A

Starts with expression of anterior hox genes

Head ones expressed first – head gets made first

76
Q

how is apoptosis expressed in cells

A

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
Q

why is apoptosis needed in body plans

A

some cells made by mitosis earlier may no longer be needed

78
Q

example of apoptosis in body plans

A

Fingers + toes first develop as combined unit

Separated later by apoptosis of cells between digits

79
Q

how is mitosis controlled

A

by two types genes

Proto-oncogenes – stimulate cell division

Tumour-suppressor genes – reduce cell division

80
Q

how does cyclins regulate mitosis

A

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
Q

what are the internal stimuli that effect mitosis / apoptosis

A

Irreparable genetic damage

Release of hormones

RNA decay

Internal biochemical changes that lead to cell changes or cellular injury (e.g. oxidative reactions)

82
Q

overall how does apoptosis get activated

A

stress // hormones

activate a protein

acts as transcription factor

activates genes involved in apoptosis

83
Q

what are the external stimuli that effect mitosis / apoptosis

A

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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