Cell Reproduction
multicellular organisms
sexual
sexual involves meisosi
two parents
fusion of 2 gametes
produces variation
asexual
involes mitosis
one parent, no gametes
no variation
bacteria reproduce asexual through binarry fission
test question***: cells must be told to divide, they do not divide meaninglessly
if cell divides without being told that cancer
I - PMAT Cytokinesis
Interphase, promhase, metaphase, anaphase, telophase, cytokensis
mitosis
new nucleic
***actin cleave the furrows in cytokinesis
control fo the cell cycle
grwoth factors
GF binds to fibroblast and epithetical cells
tells the cells to divide, whicever cells were damaged to make new ones
MPF - mitosis promoting factor
active, kinase, phosphorylates and activates other things, activate the main “computer” that simulates other things
cyclin activates all the parts in DNA replication
Must know the diseases
turney syndrome
trisomy x syndrome
klinefelter syndrome
extra y
DO NOT LEARN ABOUT SALVARY GLANDS AND FRUIT FLIES in notes
should know about karyotypes
Meisos questions may show up on the test use the practice
said it whenthe 4 circles were on the screen part of mcq
cancer
metastisize
blood, or lymph
test question: in order for all cells to divice need a growth factor, someone recepts to it, but cancer does not need a growth factor
proto-oncogenes
like gas to a car,
normal
oncogenes
bad, abnormal
DO NOT NEED TO KNOW ABOUT
carcomas
sacrocomas
lymphomas
tumor suppressor genes
like a break to a car
p-53 - in 50% of cancer p-53 is mutated
on frq
**Page 7 under the tumor supressor genes the note in pink and the notes in green that whole section with the star
mutations to proto-oncogenes are dominant
meaning that if one is mutated it turns into an oncogene
only one bad alelle is enough to case damage
tumor supressor genes are recessive
must knock out both alles for their to actual be damage
you need two functioning protoconcogenes but only you need one tumor supressor gene
for the proteogene ras
left is protoconcogene,, right is tumor suppressor gene
proto oncogene
**tyrosine-kinase receptor
ras
g protein sends signal when growth factor binds, but when it is mutated it sends a signal even though it did not get the signal to send the signal
and if one of those g protein are mutated it can cause damage because it will constantly send signals, and unecessary cell division
tumor supressor gene
p53 - is to activate transcription of p21 which should inhibit the cell cycle but if p53 is mutated, then
if were missing p21
in active form rb portein, the gene is inactived in the regulator protein
if rb inactivated, then the active gene
normally when the cell is not divided, then the rb is active, if its time to divided then its phosphorylated releases the regulatory protein to start cell division
when there is a mutated, rb gets the signal to divide and unbind even though there is no grwoth factor
guardian of the genome
p53 found in cell 24/7 but is inactive
active p53 lands on the dna, heping transcription of p21
p53 always avaiable, and turned on when needed and turns on p21
p21 job is to hold the s-cyclin cdk complex
like puting handcuffs and stops cell division
three posibilities if it is damaged
fix it
apoptosis
go to g0 - no more dividing
****test question - recgonized dby cytotoxic t cells (cytotoxic t cells recognoize cancerous cells
even though it is tumor supressor gene, one p53 is still enough to cause damage
the p53 protein is a quatenary structure
made of more than one polypeptides
mutate one, the robot can’t form
so one mutation is enough
p53 even though its a tumor supressor gene and those mutations are receieive it is less resistant to mutations and even one is enough to lose its final shape (quaternary)
dna repair mechanisms prevent cancer
97% of dna are non coding anyway
DO NOT NEED TO KnOW
cancer treatment
chemo therpay
radiation
cyclic AMP - second messanger
phosphorylates somethig
turns something on
could also turn stop off