Genes Flashcards
spearman/pearson test
correlation coefficient AND looking for correlation between two variables
mutation in transcription factor
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
mutation in cells that prevent cell division
mRNA transcription change
change in protein structure - non-functioning/faulty
uncontrollable division
samples
ethical = death/suffering
large number = improve reliability
tumours measured in volume
have varying depth
standard deviation
spread of distribution around the mean/degree of variation from the mean
SD overlap
difference is statistically insignificant
not conclusive
could be down to chance/equal results
change in sequence of DNA bases
change in primary structure
change in hydrogen bonds
alters tertiary structure
substrate cannot bind - no ES complexes
DNA structure
- Sugar-phosphate back bone = provides strength
- Long molecule = store lots of information
- Helix = compact
- Base sequence = transcription
- Double stranded = replication occur semi-conservatively
- Hydrogen bonds = stable
human vs bacterium
different enzymes
tumour suppressor genes mutation
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
control groups
same conditions without trialled/independent variable
unethical to deny treatment
percentages
to compare
promoter regions
where RNA-polymerase binds to DNA
mutation = “ “ unable to bind to promoter
no mRNA made so no transcription of gene
siRNA
specific tertiary structure and shape
complementary so binds to mRNA only
mRNA cut - prevents translation
gene inhibited so protein not made
sample size
small = not representative
big = reliable
repeats in lab experiment
cancer
much higher rate of cell division? cancer IS uncontrollable cell division
hormone oestrogen therapy not always cancerous
genetic differences with TSG
bodies may have little OE and hrt restores it
body already has processes to remove cancer
getting rid of main source
controlled
conclusion
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
tumour develops
advanced cancer investigated
in transcription, not all genes are expression - this is controlled by….
transcription factors
bind to specific DNA sites (promoters)
TF’s control expression by controlling….?
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
OESTROGEN
binds to TF called OE receptor
lipid-soluble
receptor-hormone complex binds to specific DNA site and stimulates transcription
miRNA
translation of target mRNA blocked
epigenetics
heritable change in gene function without change to the base sequence of DNA
acetylation
COCH3 binds to histone proteins
chromatin = less condensed
protein separated from DNA= more exposure
gene switched on - transcribed!
hypermethylation
CH3 attaches to DNA bases at CpG site
change in tertiary structure
no transcription - gene switched off
hypomethylation
too little CH3
proto-oncogenes act as oncogenes
incr. prod of proteins that encourage cell /
= uncontrollable cell /
cell division controlled by 2 genes
proto-oncogenes = stimulate cell division
tumour suppressor genes = slow cell division
PROTO-ONCOGENES
proteins produced BUT mutation…? p-o = oncogene
gene is overactive
cell divides uncontrollably
TUMOUR SUPPRESSOR GENES
mutation…?
gene is inactivated
protein not produced - uncontrollable dividision
benign vs malignant
slow vs fast
covered in fibrous tissue vs invades other tissues
TRANSCRIPTION + TRANSLATION
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
mutagenic agents
increase rate of mutations
e.g. UV or ionising radiation, chemicals/viruses
-alter bases or act as base or change DNA structure
same protein produced if mutation in dna?
genetic code is degenerate and mutations could occur in introns
mutation definition
alteration to DNA base sequence - often arises spontaneously during replication
frameshift
amino acid sequence produced is different
scatter graph
relationship between two independent variables
genome
organisms complete set of DNA
