Translation occurs in three stages...
1) In initiation, the components of the translational apparatus come
together with the mRNA molecule (A tRNA carrying the first amino acid binds
to the start codon).
2) In elongation, amino acids are brought to the mRNA as amino-acyl
tRNAs and are added one at a time to a growing polypeptide chain.
3) In termination, a stop codon in the mRNA is recognized by a protein
release factor and the translational apparatus comes apart to release a
completed polypeptide.
tRNA molecules contain...
1) three major loops,
2) four base-paired regions,
3) an anticodon triplet and
4) a 3 prime terminal sequence of CCA (where the appropriate amino
acid can be attached by an ester bond).
During maturation of the tRNA molecule a number of nucleotides are
modified in tRNA specific ways.
The modified nucleotides in the tRNA structure are inosine (I), methylinosine
(mI), dihydrouridine (D), ribothymidine (T), pseudouridine (¥) and
methylguanosine (Gm).
The 3D structure of tRNA molecules is similar to a hockey stick (the
L shaped tertiary structure of tRNA) which has the amino acid attachment
site is at one end (tip of the handle) and the anticodon at the other (blade
of the stick).
Twenty different aminoacyl-tRNA synthetases link amino acids to the
correct tRNAs.
Some recognize only one tRNA, some recognize a few because of the redundancy
in the genetic code.
Although there are 61 possible codons, there are far fewer tRNAs.
A number of codons that encode the same amino acid differ only in the
third position of the codon.
A slight shift or "wobble" in the position
of the base guanine in a tRNA anticodon would permit it to pair with uracil
instead of its normal complementary base (cytosine).
The base pairs permitted at the third position of a codon by the wobble
hypothesis are as follows:
| Bases recognized in codon | |
| (third position only) | Base in anticodon |
| U | A |
| G | C |
| A or G | U |
| C or U | G |
| U, C or A | I (inosine) |
In two chemical steps, aminoacyl-tRNA synthetases
catalyzes the formation of an ester bond between the carboxyl group of
an amino acid and the 3 prime hydroxyl (OH) group of the appropriate tRNA.
Step 1) The amino acid and a molecule of ATP enter the active site
of the enzyme.
The ATP loses pyrophosphate and the resulting AMP bonds covalently to the
amino acid.
The pyrophosphate is hydrolyzed into two phosphate groups.
Step 2) The tRNA covalently bonds to the amino acid to displace the
AMP and the aminoacyl tRNA is then released from the enzyme.
The formation of the 70S translation initiation
complex (in prokaryotes) occurs in three steps.
1) Three initiation factors (IF) and GTP bind to the small ribosomal
subunit.
2) The initiator aminoacyl tRNA and mRNA are attached.
The mRNA-binding site is composed, at least in part, of a portion of
the 16S rRNA of the small ribosomal subunit.
The 3 prime end of the 16S rRNA bears a pyrimidine-rich stretch that
base pairs with the Shine-Dalgarno sequence of the mRNA (in prokaryotes).
3) The large ribosomal subunit joins the complex.
The resulting 70S initiation complex has fMet-tRNAfMet residing
in the ribosome's P site.
In eukaryotes, translation includes a different set of initiation factors
(eIFs), a slightly different assembly pathway and a non-formylated tRNA
met.
eIF2 binds the initiator tRNA met before the small ribosomal
subunit.
This complex can attach to the 5 prime cap structure of the mRNA.
As there is no Shine-Dalgarno sequence, the ribosome begins translation
at a AUG that is located within the Kozak consensus sequence (often a good
match to CAAAAUG).
Chain elongation during protein synthesis requires
the presence of a peptidyl tRNA or, in the first elongation cycle, an fMet-tRNAfMet
at
the peptidyl (P) site.
1) Elongation begins with the binding of the second aminoacyl tRNA
at the ribosomal aminoacyl (A) site.
The tRNA is escorted to the A site by the elongation factor EF-Tu,
which also carries two bound GTPs.
As the tRNA binds, the GTPs are hydrolyzed and EF-Tu is released. EF-Ts
helps recycle the EF-Tu.
2) A peptide bond is formed between the carboxyl group of the terminal
amino acid (or fMet in the first cycle) at the P site and the amino group
of the newly arrived amino acid at the A site.
This reaction is catalyzed by the peptidyl transferase activity of
the 23S rRNA molecule in the large ribosomal subunit.
3) After EF-G-GTP binds to the ribosome and GTP is hydrolyzed, the
tRNA carrying the elongated polypeptide translocates from the A site to
the P site.
The discharged tRNA moves from the P site to the E (exit) site and
leaves the ribosome.
As the peptidyl tRNA translocates, it takes the mRNA along with it.
Consequently, the next mRNA codon is moved into the A site, which is
open for the next aminoacyl tRNA.
These events are repeated for each additional amino acid.
Termination of protein synthesis depends on
release factors that recognize the three stop codons.
When a stop codon (UAG, UAA, or UGA) arrives at the A site, it is recognized
and bound by a protein release factor.
This protein causes the polypeptide to be transferred to a molecule
of water to cause its release from the tRNA and the dissociation of the
other components of the elongation complex.
Proteins have to be folded into the proper three dimensional conformation
to work properly.
A number of diseases, including Alzheimer's disease, may be considered
to be protein-folding diseases.
Sometimes the primary sequence of amino acids is sufficient to spontaneously
direct the folding of proteins into their proper shape.
However, often newly-made proteins require the help of molecular chaperones
to attain their final shape.
The heatshock proteins, Hsp70 and Hsp60, are molecular chaperones.
Heat-denatured proteins can be renatured through the activity of molecular
chaperones and heatshock proteins are made during times of stress.
Prion diseases, such as "mad cow" disease, may "self-propagate" based
upon a misfolded protein that can, in turn, misfold other versions of the
same protein.
After the amino chain is made, many proteins undergo posttranslational
processing (including removal of stretches of amino acids).
1) In prokaryotes, the N-formyl group is always removed in the
mature protein and often the methionine and, sometimes, a number of N-terminal
amino acids are cleaved away from the final protein product.
2) The protein hormone insulin provides an example of posttranslational
processing.
Proinsulin is converted to the active hormone by the enzymatic removal
of a long internal section of polypeptide.
The two remaining chains continue to be covalently connected by disulfide
bonds connecting cysteine residues in insulin.
3) Recently discovered, the process of protein splicing
(analagous
to RNA splicing) removes inteins and splices the exteins together to make
a mature protein.
2) If the polypeptide is destined for the cytosol or for import
into the nucleus, mitochondria, chloroplasts, or peroxisomes, its synthesis
continues in the cytosol.
When the polypeptide is complete, it is released from the ribosome
and either remains in the cytosol or is transported into the appropriate
organelle by posttranslational import.
Polypeptide uptake by the nucleus occurs via the nuclear pores, using a mechanism different from that involved in posttranslational uptake by other organelles.
In cotranslational import, proteins to be targeted
to the endoplasmic reticulum initially have an N-terminal peptide, the
ER signal sequence, translated by a cytosolic ribosome.
The ER signal sequence is bound by a signal-recognition particle (SRP),
a ribonucleoprotein complex composed of 6 peptides and a 300 nucleotide
RNA molecule.
The SRP binds to the SRP receptor to dock the ribosome on the ER membrane.
When the SRP receptor binds GTP, the nascent polypeptide enters the
pore.
The SRP is released with hydrolysis of the GTP.
The growing polypeptide translocates through a hydrophilic pore created
by one or more membrane proteins called the translocon.
The most recent evidence suggests that the ribosome fits tightly across
the cytoplasmic side of the pore and that the ER-lumen side is somehow
closed off until the polypeptide is about 70 amino acids long.
When the polypepide is complete, the signal peptidase cleave the signal
to release the protein into the ER lumen while retaining the signal peptide,
for a time, in the membrane.
Afterwards the ribosome is released and the pore closes completely.
In the endoplasmic reticulum, folding of the newly-made proteins may
also require molecular chaperones and other proteins involved in protein
folding.
Bip (binding protein), a member of the Hsp70 chaperone family, briefly
binds to and stabilizes hydrophobic regions of proteins (especially rich
in Trp, Phe, Leu) allowing proper folding instead of aggregation with other
inmature proteins.
Protein disulfide isomerase catalyses the formation and breakage of
disulfide bonds between cysteine residues to produce a stable conformation.
There are two possible mechanisms for the insertion
of integral membrane proteins having a single transmembrane segment.
1) Type I: Insertion of a polypeptide with both a terminal ER signal
sequence and an internal stop-transfer sequence.
The terminal peptide is eventually cut off, leaving a transmembrane
protein with its N-terminus in the ER lumen and its C-terminus in the cytosol.
2) Type II: Insertion of a polypeptide with only a single, internal
start transfer sequence, which both starts polypeptide transfer and anchors
itself permanently in the membrane.
The amino-carboxyl orientation of the completed protein depends on
the orientation of the start-transfer sequence when it first inserts into
the translocation apparatus.
Posttranslational import allows some polypeptides to enter organelles
after protein synthesis.
Like cotranslational import into the ER, posttranslational import
into a mitochondrion (and chloroplast) involves a signal sequence (called
a transit sequence), a membrane receptor, pore-forming membrane proteins,
and a peptidase.
Polypeptides being imported into the mitochondrion
span
both membranes at the same time.
This was demonstrated in a cell-free import system
incubated on ice
in which the polypeptides begin to penetrate the mitochondrion but then
stall.
The transit sequence is cleaved by the transit peptidase present in
the matrix, indicating that the N-terminus of the polypeptide is within
the mitochondrion.
At the same time, most of the polypeptide molecule is can be attacked
by exogenously added proteolytic enzymes on the outside of the mitochondrion.
Therefore, the polypeptide must span both membranes transiently during
import at a contact site between the two membranes.
However, in the mitochondrion, the membrane receptor recognizes the
signal sequence directly without the intervention of a cytosolic SRP.
Furthermore, chaperone proteins play several crucial roles in the mitochondrial
process:
1) Chaperones keep the polypeptide partially unfolded after synthesis
in the cytosol so that binding of the transit sequence and translocation
can occur.
2) Chaperones drive the translocation itself by binding to and releasing
from the polypeptide within the matrix, an ATP-requiring process and
3) Chaperones often help the polypeptide fold into its final conformation.
Polypeptides synthesized on cytosolic ribosomes but destined for either
the intermembrane space or the inner membrane of the mitochondrion require
two separate targeting sequences (both located at the N-terminus).
1) The polypeptide is directed to a contact (translocation) site on
the mitochondrion by a positively charged or amphipathic transit sequence.
2) Cleavage of the transit sequence by a peptidase in the mitochondrial
matrix uncovers a highly hydrophobic second signal sequence.
3) This second signal sequence causes the polypeptide to be inserted
into the inner membrane in the same way that mitochondrially encoded polypeptides
are targeted to this membrane.
4) The remainder of the polypeptide is then moved across the membrane
into the intermembrane space (or into the inner membrane for integral inner
membrane proteins).
5) Cleavage by a second peptidase can release the polypeptide into
the intermembrane space leaving the signal sequence behind in the inner
membrane.
Notes prepared from Becker's World of the Cell, 8th edition
Hardin, Bertoni & Kleinsmith, 2012
Figures copyright of Pearson Education Inc.
email me at bestave@mun.ca