exam 1 Flashcards
location+ purpose of poly-a-tail?
is placed onto mRNA end + acts as signal for translation + stability
aminoacyl tRNA synthetases + location
links aa to tRNA + cytoplasm
what complex binds to 40s?
eIF2-tRNA^aa
what does eIF4F do?
binds eIF2-tRNA^aa-40s to 5’ end of mRNA
once eIF4F has binded what it needs to, what happens next?
40s is on, next comes 60s to complete the ribosome. powered by GTP hydrolysis
EF-Tu and EF-T purposes? location?
help bring in next tRNA to the ribosome + cytoplasm
EF-G purpose? location?
translocation, moves empty tRNA from P to E site + inside ribosome
how is the translation process stopped?
RF factors come in and put a water molecule in place of the aa. they are summoned by the stop codon on the mRNA.
How does NMD work?
NMD (nonsense mediated decay) is activated when an EJC (exon junction complex) is sensed on the mRNA. the EJC was supposed to be cut off along the introns, but wasnt due to premature stop codon.
how does nonstop decay work?
no stop codon found, so ski7 goes into effect. it ejects the ribosome off and its presence triggers the arrival of an exosome.
how does no go decay work? what causes it?
secondary structure! builds up in ribosome and stalls the ribosome. This causes an RNA degrading enzyme to come in and bind to the A site and degrades defective mRNA via nonstop decay! with exosome.
why do free ribosomes exist?
they synthesize proteins that dont need ANY mods and can go directly to where they need to go
how does the newly formed pp get to the ER? what recognizes it?
the new pp has a SS (signal sequence). it is recognized by SRP (signal recog. particle). the SS-SRP complex is then recog. by the SRP receptor on the exterior of the rER membrane.
if a protein is misfolded in the ___, what does this lead to?
rER. leads to UPR, unfolded protein response
!what is PERK? what does it inhibit?
a UPR. it inhibits eIF2 in the ribosome. this pauses translation.
what is ERAD?
ER associated degradation, a UPR response. misfolded proteins are exported and degraded by proteasomes in cytosol.
why is co-translational translocation good?
limits time that protein can misfold whilst getting to the rER
rER vs sER in function?
rER folds proteins and deals with misfolded proteins, while sER produces lipids and steroids and does sarcoplasmic reticulum.
!what are sarcoplasmic reticulum cells?
these cells are abundant in skeletal and cardiac tissues.
Ca+ ions are pumped into sER by ATP-dependent calcium ATPases during muscle contraction.
what is the most important function of the golgi? why is it important?
to glycosylate. this helps prevent proteins from being degraded when outside the golgi/vesicle.
what does the golgi consist of?
CGN and TGN
how does a secretory protein vesicle get to its destination?
it gets to the outside of the cell by tethering and fusion. T-SNARE is a target on the plasma membrane and V-SNARE is the tag on the vesicle. They recog. each other and fuse.
how does a protein go to the ER from the TGN?
it is put into a COPI vesicle with a retrieval tag KDEL on it
how does a protein get to the CGN from the ER?
it is placed into a COPII coated vesicle
what are the 3 things a mature lysosome contains?
H+ ATPase pump, transporters/exporters, and glycosylated proteins on the membrane
what is a lysosomal hydrolase?
the characterizing enzyme inside an endosome and lysosome.
where are lysosomal hydrolases made?
rER
what is M6P? where is the receptor?
M6P is a tag + receptor for lysosomal hydrolase. the M6P tag goes on the pp, then the receptor on the rER membrane recognizes it to specially put it in a clathrin covered vesicle.
what affects the M6P bond?
pH, when high it will dissociate
how does a lysosome become a lysosome?
endosome + foreign thing in a clathrin vesicle + phagocytosis = lysosome
what is PTS-1 and PEX-5/7?
receptors that bind to each other to bring it thru the peroxisome translocon
what is the peroxisome translocon?
the entryway into the peroxisome
what is a tRNA suppressor?
tRNA recognizes a wrongly placed stop codon (a nonsense mutation (no, we cant stop the show now! Its nonsense)) and insert a functional aa in its place, suppressing the nonsense mutation.
