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Biology Block 1 > Genes > Flashcards

Genes Flashcards

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1
Q

spearman/pearson test

A

correlation coefficient AND looking for correlation between two variables

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2
Q

mutation in transcription factor

A

dna of cell changed
tertiary structure change
TF not complementary to gene
cannot bind - little mRNA for gene produced and translated
less available for drug/something else to bind to

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3
Q

mutation in cells that prevent cell division

A

mRNA transcription change
change in protein structure - non-functioning/faulty
uncontrollable division

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4
Q

samples

A

ethical = death/suffering

large number = improve reliability

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5
Q

tumours measured in volume

A

have varying depth

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6
Q

standard deviation

A

spread of distribution around the mean/degree of variation from the mean

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7
Q

SD overlap

A

difference is statistically insignificant
not conclusive
could be down to chance/equal results

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8
Q

change in sequence of DNA bases

A

change in primary structure
change in hydrogen bonds
alters tertiary structure
substrate cannot bind - no ES complexes

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9
Q

DNA structure

A
  1. Sugar-phosphate back bone = provides strength
  2. Long molecule = store lots of information
  3. Helix = compact
  4. Base sequence = transcription
  5. Double stranded = replication occur semi-conservatively
  6. Hydrogen bonds = stable
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10
Q

human vs bacterium

A

different enzymes

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11
Q

tumour suppressor genes mutation

A 
abnormal methylation as a mutation
inactive
methyl groups added
tertiary structure altered
genes don't produce mRNA so not transcribed
proteins that slow division not produced
uncontrollable cell division
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12
Q

control groups

A

same conditions without trialled/independent variable

unethical to deny treatment

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13
Q

percentages

A

to compare

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14
Q

promoter regions

A

where RNA-polymerase binds to DNA
mutation = “ “ unable to bind to promoter
no mRNA made so no transcription of gene

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15
Q

siRNA

A

specific tertiary structure and shape
complementary so binds to mRNA only
mRNA cut - prevents translation
gene inhibited so protein not made

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16
Q

sample size

A

small = not representative
big = reliable
repeats in lab experiment

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17
Q

cancer

A

much higher rate of cell division? cancer IS uncontrollable cell division

18
Q

hormone oestrogen therapy not always cancerous

A

genetic differences with TSG
bodies may have little OE and hrt restores it
body already has processes to remove cancer

19
Q

getting rid of main source

A

controlled

20
Q

conclusion

A

lowest/most COMPARED TO ….
SD overlap = results by chance and not conclusive need stat test
lab study = repeats needed
drugs - side effects, human vs mice differences
small sample size = not rep or reliable
does it cure/stop?
results with little effect

21
Q

tumour develops

A

advanced cancer investigated

22
Q

in transcription, not all genes are expression - this is controlled by….

A

transcription factors

bind to specific DNA sites (promoters)

23
Q

TF’s control expression by controlling….?

A

rate of transcription
ACTIVATORS - incr rate by helping enzyme bind to DNA
REPRESSORS - decr rate by binding w/ start of target gene so preventing RNA Polymerase

24
Q

OESTROGEN

A

binds to TF called OE receptor
lipid-soluble
receptor-hormone complex binds to specific DNA site and stimulates transcription

25
Q

miRNA

A

translation of target mRNA blocked

26
Q

epigenetics

A

heritable change in gene function without change to the base sequence of DNA

27
Q

acetylation

A

COCH3 binds to histone proteins
chromatin = less condensed
protein separated from DNA= more exposure
gene switched on - transcribed!

28
Q

hypermethylation

A

CH3 attaches to DNA bases at CpG site
change in tertiary structure
no transcription - gene switched off

29
Q

hypomethylation

A

too little CH3
proto-oncogenes act as oncogenes
incr. prod of proteins that encourage cell /
= uncontrollable cell /

30
Q

cell division controlled by 2 genes

A

proto-oncogenes = stimulate cell division

tumour suppressor genes = slow cell division

31
Q

PROTO-ONCOGENES

A

proteins produced BUT mutation…? p-o = oncogene
gene is overactive
cell divides uncontrollably

32
Q

TUMOUR SUPPRESSOR GENES

A

mutation…?
gene is inactivated
protein not produced - uncontrollable dividision

33
Q

benign vs malignant

A

slow vs fast

covered in fibrous tissue vs invades other tissues

34
Q

TRANSCRIPTION + TRANSLATION

A

1) DNA strands separate by DNA helicase
nucleotides join to DNA template strand
Uracil binds to Adenine
RNA polymerase joins to nucs = mRNA

2) mRNA to ribosome
mRNA codon binds with tRNA’s comp anti-codon
amino acid attached to each tRNA
formation of peptide bonds between aa’s

35
Q

mutagenic agents

A

increase rate of mutations
e.g. UV or ionising radiation, chemicals/viruses

-alter bases or act as base or change DNA structure

36
Q

same protein produced if mutation in dna?

A

genetic code is degenerate and mutations could occur in introns

37
Q

mutation definition

A

alteration to DNA base sequence - often arises spontaneously during replication

38
Q

frameshift

A

amino acid sequence produced is different

39
Q

scatter graph

A

relationship between two independent variables

40
Q

genome

A

organisms complete set of DNA

Biology Block 1 (3 decks)

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