GAP/GROWTH 1 - cell grows,neworganelles,proteins and mRNA made
SYNTHESIS - DNA replication,2N —> 4N for mitosis
GAP/GROWTH 2 - cell grows, new organelles, proteins and mRNA made
CHECKPOINTS
G1 - checks if cell is big enough and proteins are made, if fail goes into G0
S - checks if DNA has been replicated
G2 - checks if it’s big enough to enter mitosis and if replication was correct
1, PROPHASE (MITOSIS)
chromosomes condense, becoming short and fat
become visible under microscopes
x-shaped chromosomes, joined by centromere,sisterchromatids are identical
centrioles (bundles of protein) move to poles of cell
network of spindlefibres form across the cell
PROMETAPHASE: nuclear envelope starts to break down to releasechromosomes into cytoplasm
2. METAPHASE (MITOSIS)
chromosomes line up along the centre / equator of the cell
attached to the mitotic spindle by their centromeres
arranged sideways and neatly
CHECKPOINT: to make sure all chromosomes are on the metaphase plate which is important to ensure each daughter cell gets the same number of chromosomes
3. ANAPHASE (MITOSIS)
spindle fibres contract
pulling the sister chromatidsaway from each other, towards the poles
centromeres are pulled first causing them to look v-shaped
2separate groups of chromatids
4. TELOPHASE (MITOSIS)
chromatids each the poles
uncoil and become long and thin again
new nuclear envelope forms around the two new full sets of chromosomes
forms two new nuclei, daughternuclei
geneticallyidentical
CYTOKINESIS
when the cell physicallyseparates / divides and the cytoplasmsplits
contractile ring forms at the centre
makes an indentation called a cleavage furrow
pinches in and the cell divides into 2identicaldaughter cells
starts in telophase
MITOSIS: controlled process of celldivision
CANCER: uncontrolled cell division
when there’s a mutation in a gene that controls cell division, cells grow out of control, forming a tumour.
MUTATION: a change in the basesequence of DNA
MALIGNANT TUMOUR: grows rapidly and can invadehealthy neighbouring tissues.
BENIGN TUMOUR: grows slowly and doesn’t spread
CANCER TREATMENT
some treatments control the rate of cell division in tumour cells by disrupting the cell cycle and killingtumour cells.
however these treatments don’tdistinguish between cancer cells and normal cells that are dividing.
but it is morelikely to killtumour cells as they dividemorefrequently.
CANCER TREATMENT
CHEMOTHERAPY: preventssynthesis of enzymes that are needed for DNA replication in gap phase 1, meaning the cell cannot enter the synthesis phase, disrupting the cell cycle and causing the cell to kill itself.
CANCER TREATMENT
RADIATION THERAPY: radiation damagesDNA in the synthesis phase. This meant at the next checkpoint, if severe damage was detected, the cell kills itself, preventing further tumour growth.
CELL DIVISION IN PROKARYOTES - BINARY FISSION
circular DNA and plasmidsreplicate (once for circular, more for plasmids)
cell gets bigger and DNA loopsmove to opposite poles of the cell
cytoplasm begins to divide and new cell walls begin to form
cytoplasm fully splits and 2daughter cells are made, each with one identicalloop of circular DNA and with variableplasmids.
VIRAL REPLICATION
attach to host cell using their attachment proteins which bind to complementaryreceptor proteins on the surface membrane of the host cell.
genetic material from virus is released into host cell.
use host cells ‘machinery’ like enzymes and ribosomes to replicated the genetic material and proteins.
viral components assembleinsidehost cell. Replicated viruses released from the host cell.
different viruses have differentattachment proteins so attach to differentreceptors so therefore can only infectone kind of cell.