Epigenetics

epigenetics

the heritable changes in gene function, WITHOUT changing the base sequence of DNA

histones (4)

• proteins that organise the DNA

• present in all eukaryotic cells (not in most prokaryotic)

• organise DNA into chromosomes

• regulate transcription

charge of histones

positive to associate with the negative DNA

• -ve phosphate ion in DNA (PO4^3-)

• +ve alkaline R groups in histones

how DNA is packaged

• nucleosome has 8 histones with DNA wrapped around them

• nucleosome is supercoiled and turns into a chromosome

heterochromatin vs euchromatin

dictated by epigenetics

euchromatin

DNA is loosely packed → TF can bind to DNA → transcription can occur

heterochromatin

DNA is tightly coiled → TF cannot bind → no transcription

methylation of DNA

• increased methylation of DNA leads to decreased transcription of DNA (nucleosomes more tightly packed together)

• happens to cytosine bases

acetylation of DNA

• increase acetylation of histones (tails) leads to increased transcription of DNA (nucleosomes more loosely packaged)

• acetyl group donated by acetyl coA

apoptosis

when cells with mutated DNA that cannot be fixed undergo programmed cell death

cancerous cells

undergo uncontrolled cell division

proto-oncogene

stimulate cell division when activated by growth factors

oncogene

when a proto-oncogene has mutated to be permanently activated, meaning cell division is always stimulated

tumour suppressor gene

a gene that regulates the replication and division of cells e.g. slows down cell division

benign tumour (4)

• grow slowly

• not invasive

• more compact

• less likely to be life-threatening

malignant tumour

• grow more quickly

• invasive - metastasis → forms secondary tumour

• less compact

• more likely to be life-threatening

genetic nature of tumours

• tumours are derived from one cell with mutated DNA

• mutation causes the cell to undergo uncontrolled mitosis.

• further mutations are acquired in descendant cells that will change the appearance and growth of further daughter cells

consequences of permanent proto-oncogene activation

• growth factor receptor on the cell membrane becomes permanently activated → no longer requires the binding of the growth factor to be active

• oncogene could code for a growth factor that ends up being produced in excessive amounts, stimulating excess cell division

inactivation of tumour suppressor genes…

…cause cancer

oestrogen

can stimulate the transcription of proteins that stimulate cell division and growt

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risk of breast cancer after menapause

• increases

• fat cells in breast produce more oestrogens which can trigger tumour formation

• tumour then produces more oestrogen

• white blood cells are drawn to the tumour and further increase oestrogen production