TOPIC 8.2 stem cells, regulating transcription & translation + cancer

Question 1

stem cells

Answer 1

replicate/ keep dividing
undifferentiated, can develop into other cells

Question 2

totipotent stem cells

Answer 2

toti=total
differentiate to ANY type of cell

Question 3

pluripotent stem cells

Answer 3

pluri=placenta
differentiate into any cell except placenta cells

Question 4

unipotent stem cells

Answer 4

uni=1
differentiate to 1 type of cell eg.cardiomyocytes

Question 5

multipotent stem cells

Answer 5

adult
differentiate to limited num specialised cells to replace/repair damaged tissues

Question 6

iPS cells

Answer 6

genetically altered in lab to act sd pluripotent. can divide to provide limitless supply

Question 7

how stem cells become specialised

Answer 7

all stem cells hv same genes. in development, some transcribed & translated (expressed/ switched on and off) - determines cell structure & controls processes

Question 8

transcriptional factor (TF)

Answer 8

protein controlling transcription of genes. bind to spec base seq - causes region to start transcription = activator
repressor = inhibit transcription rate

Question 9

eg. TF - steroid hormone oestrogen

Answer 9

activator
lipid soluble - diffuses thru phospholipid bilayer to cytoplasm -> binds to complementary TF oestrogen receptor = oestrogen receptor-oestrogen complex
binds to DNA -> stimulates transcription of gene that makes up DNA

Question 10

how genes switched off (epigenome)

Answer 10

inactive genes in tight packed (condensed) arrangement - ensures cant be read + not accessible

Question 11

how genes switched on (epigenome)

Answer 11

DNA-histone complex less condense (loosely packed) - DNA easily accessible by TF which can initiate mRNA production

Question 12

Inc methylation of DNA

Answer 12

CH3 added to C base = INHIBITS transcription
prevents binding of TF to DNA
actracts proteins that condense DNA-histone complex (DNA not acessible to TF)

Question 13

dec acetylation

Answer 13

DEC TRANSCRIPTION
acetyl grps removed from histones
chromatin condense - DNA not accessible by enzymes
inc +ve charge on histones -> inc attraction to DNA phosphate grp - condense tight packed - not accessible by TF

Question 14

malignant

Answer 14

cancerous
rapid growth to life threatening abnormally large size
larger darker nucleus
unspecialised cells
spread to other reigons of body by metastasis

Question 15

benign

Answer 15

grow slowly to large size - less life threateinng, can disrupt organ funct
cells produce adhesion - stick tog (localised)
specialised cells w normal nucleus

Question 16

oncogenes

Answer 16

mutated
stimuates cells to divide uncontrolably = tumor

Question 17

proto-oncogenes

Answer 17

non mutated
stimulate cell division by producing proteins that make cells divide

Question 18

tumor suppressor genes TSG

Answer 18

slow cell division by producing protein that stop cell division

mutation - gene off - proetin not coded for = cells divide uncontrollably = tumor

Question 19

hypermethylation of tumor supressor gene

Answer 19

methyl grps added to TSG transcription of TSG inhibited -> Protein that prevents cell division not produced = uncontrolled cell division = tumor

Question 20

hypomethylation of proto oncogene

Answer 20

act as oncogenes - inc protein production that encourages cell division = uncontrolled cell division = tumor

Question 21

gene therapy

Answer 21

faulty genes replaced - inactive TSG swapped w active

Question 22

epigenetics

Answer 22

Heritable changes in gene funct w/out changing DNA base seq

Question 23

RNAi

Answer 23

translation of mRNA from target genes inhibited
enzyme cuts double stranded RNA to SiRNA (still ds)
SiRNA unwinds - single strand binds w enzyme and binds to complementary base on mRNA (specific to 1 mRNA)
proteins associated w SiRNA destroy mRNA before translation