Flashcards in Lectures 2+3 Deck (15):
It's an aminoglycoside that binds the 30s ribosomal subunit, causing a conformational change. This works to inhibit initiation by disrupting the complementartiy of the 16s rRNA component of the 30s ribosomal subunit, and can lead to misreading.
Tetracycline affects the _____ ribosomal subunit by inhibiting binding of _____ to the _____ site.
Affects the 30s ribosomal subunit by inhibiting the binding of AA-tRNA to the A-site.
Affects the 50s ribosomal subunit by binding the 23s rRNA component and inhibits peptidyl transferase.
It is a macrolide that affects the 50s ribosomal subunit and inhibits translocation.
Imitates Tyrosinyl-tRNA and is resistant to hydrolysis. It causes chain termination and is nonspecific (works on both 50s and 60s.)
Diptheria toxin has two subunits, ___ and ___. ___ allows the toxin to be integrated into the cell, and ___ poisons translation by inactivating _____ via _____.
Toxin that is released in 2 fragments:
B --> allows toxin to be integrated into cell
A --> an enzyme that poisons translation by inactivating eEF2 via ADP-ribosylation (the transfer of ADP-ribose from NAD+ onto dipthamide.)
A protein toxin comprised of 2 polypeptide cahins:
B --> binds cell surface receptors for uptake
A --> enzyme that depurinates 28s subunit rRNA at specific A residue.
What are the 2 modes of Translation Initiation in Eukaryotes
1. Cap-dependent binding - eIF4E binds the 5' cap and recruits the 40s ribosomal subunit. Then the 40s subunit scans for AUG in "good context." (90% of translation initiated this way in eukaryotes.)
2. Internal Ribosome Entry (no scanning and occurs is about 5-10% of eukaryotic translation.)
What is the Prokaryotic mode of Translation Initiation?
16s rRNA of 30s Subunit complements with Shine-Dalgarno sequence.
Mupirocin is an antibiotic that inhibits ______ synthetase --> no ____ can bind the OH at the 3' C-C-A end of the tRNA.
It's an antibiotic that inhibits Ile-tRNA synthetase --> no Ile binding to the OH of the C-C-A sequence at the 3' end of tRNA.
What's an example of Specific translational control and what's an example of a syndrome that disrupts this control?
Control of Ferritin. Low levels of Fe2+ allow IRE-BP to bind the IRE of Ferritin mRNA, inhibiting translation. High Fe2+ levels --> IRE-BP does NOT bind IRE.
Hereditary hyperferritinemia cataract syndrome --> mutation in the IRE --> IRE-BP can't bind --> increase in [Ferritin]
What's a example of general translational control?
Down-reg of supply of initiator Met-tRNAi via eIF2 kinases. eIF2 kinases phosphorylate eIF2 which sequester the eIF2B (guanysine nucleotide exchange factor), so there no GDP-GTP exchange. eIF2 needs GTP in order to "drop off" Met-tRNAi at 40s ribosomal subunit to initiate protein synth.
There are 4 kinases that phosphorylate eIF2. ___ is activated in reticulocytes in response to low levels of ____. ____ is activated in cells where ____ has been detected, which confers protection again viruses. ____ is activated in response to ER stress. ____ is activated by ___ starvation and subsequent buildup of uncharged ____.
1. HRI --> activated in reticulocytes in response to low levels of heme.
2. PKR --> activated in cells in which ds-RNA has been detected so as to prohibit synthesis of viral proteins.
3. PERK --> activated by ER stress
4. GCN2 --> activated by AA starvation (buildup of uncharged tRNA.)
What is "Vanishing White Matter" caused by?
A mutation in any one of the 5 subunits of eIF2B --> no GDP-GTP exchange --> no eIF2 initiation.