Protein targeting


Protein targeting or protein sorting is the biological mechanism by which proteins are transported to their appropriate destinations within or outside the cell. Proteins can be targeted to the inner space of an organelle, different intracellular membranes, the plasma membrane, or to the exterior of the cell via secretion. Information contained in the protein itself directs this delivery process. Correct sorting is crucial for the cell; errors or dysfunction in sorting have been linked to multiple diseases.

History

In 1970, Günter Blobel conducted experiments on protein translocation across membranes. Blobel, then an assistant professor at Rockefeller University, built upon the work of his colleague George Palade. Palade had previously demonstrated that non-secreted proteins were translated by free ribosomes in the cytosol, while secreted proteins were translated by ribosomes bound to the endoplasmic reticulum. Candidate explanations at the time postulated a processing difference between free and ER-bound ribosomes, but Blobel hypothesized that protein targeting relied on characteristics inherent to the proteins, rather than a difference in ribosomes. Supporting his hypothesis, Blobel discovered that many proteins have a short amino acid sequence at one end that functions like a postal code specifying an intracellular or extracellular destination. He described these short sequences as signal peptides or signal sequences and was awarded the 1999 Nobel prize in Physiology for the same.

Signal peptides

Signal peptides serve as targeting signals, enabling cellular transport machinery to direct proteins to specific intracellular or extracellular locations. While no consensus sequence has been identified for signal peptides, many nonetheless possess a characteristic tripartite structure:
  1. A positively charged, hydrophilic region near the N-terminal.
  2. A span of 10 to 15 hydrophobic amino acids near the middle of the signal peptide.
  3. A slightly polar region near the C-terminal, typically favoring amino acids with smaller side chains at positions approaching the cleavage site.
After a protein has reached its destination, the signal peptide is generally cleaved by a signal peptidase. Consequently, most mature proteins do not contain signal peptides. While most signal peptides are found at the N-terminal, in peroxisomes the targeting sequence is located on the C-terminal extension. Unlike signal peptides, signal patches are composed by amino acid residues that are discontinuous in the primary sequence but become functional when folding brings them together on the protein surface. Unlike most signal sequences, signal patches are not cleaved after sorting is complete. In addition to intrinsic signaling sequences, protein modifications like glycosylation can also induce targeting to specific intracellular or extracellular regions.

Protein translocation

Since the translation of mRNA into protein by a ribosome takes place within the cytosol, proteins destined for secretion or a specific organelle must be translocated. This process can occur during translation, known as co-translational translocation, or after translation is complete, known as post-translational translocation.

Co-translational translocation

Most secretory and membrane-bound proteins are co-translationally translocated. Proteins that reside in the endoplasmic reticulum, golgi or endosomes also use the co-translational translocation pathway. This process begins while the protein is being synthesized on the ribosome, when a signal recognition particle recognizes an N-terminal signal peptide of the nascent protein. Binding of the SRP temporarily pauses synthesis while the ribosome-protein complex is transferred to an SRP receptor on the ER in eukaryotes, and the plasma membrane in prokaryotes. There, the nascent protein is inserted into the translocon, a membrane-bound protein conducting channel composed of the Sec61 translocation complex in eukaryotes, and the homologous SecYEG complex in prokaryotes. In secretory proteins and type I transmembrane proteins, the signal sequence is immediately cleaved from the nascent polypeptide once it has been translocated into the membrane of the ER or plasma membrane by signal peptidase. The signal sequence of type II membrane proteins and some polytopic membrane proteins are not cleaved off and therefore are referred to as signal anchor sequences. Within the ER, the protein is first covered by a chaperone protein to protect it from the high concentration of other proteins in the ER, giving it time to fold correctly. Once folded, the protein is modified as needed, then transported to the Golgi for further processing and goes to its target organelles or is retained in the ER by various ER retention mechanisms.
The amino acid chain of transmembrane proteins, which often are transmembrane receptors, passes through a membrane one or several times. These proteins are inserted into the membrane by translocation, until the process is interrupted by a stop-transfer sequence, also called a membrane anchor or signal-anchor sequence. These complex membrane proteins are currently characterized using the same model of targeting that has been developed for secretory proteins. However, many complex multi-transmembrane proteins contain structural aspects that do not fit this model. Seven transmembrane G-protein coupled receptors mostly do not have an amino-terminal signal sequence. In contrast to secretory proteins, the first transmembrane domain acts as the first signal sequence, which targets them to the ER membrane. This also results in the translocation of the amino terminus of the protein into the ER membrane lumen. This translocation, which has been demonstrated with opsin with in vitro experiments, breaks the usual pattern of "co-translational" translocation which has always held for mammalian proteins targeted to the ER. A great deal of the mechanics of transmembrane topology and folding remains to be elucidated.

Post-translational translocation

Even though most secretory proteins are co-translationally translocated, some are translated in the cytosol and later transported to the ER/plasma membrane by a post-translational system. In prokaryotes this process requires certain cofactors such as SecA and SecB and is facilitated by Sec62 and Sec63, two membrane-bound proteins. The Sec63 complex, which is embedded in the ER membrane, causes hydrolysis of ATP, allowing chaperone proteins to bind to an exposed peptide chain and slide the polypeptide into the ER lumen. Once in the lumen the polypeptide chain can be folded properly. This process only occurs in unfolded proteins located in the cytosol.
In addition, proteins targeted to other cellular destinations, such as mitochondria, chloroplasts, or peroxisomes, use specialized post-translational pathways. Proteins targeted for the nucleus are also translocated post-translationally through the addition of a nuclear localization sequence that promotes passage through the nuclear envelope via nuclear pores.

Sorting of proteins

Mitochondria

While some proteins in the mitochondria originate from mitochondrial DNA within the organelle, most mitochondrial proteins are synthesized as cytosolic precursors containing uptake peptide signals. Unfolded proteins bound by cytosolic chaperone hsp70 that are targeted to the mitochondria may be localized to four different areas depending on their sequences. They may be targeted to the mitochondrial matrix, the outer membrane, the intermembrane space, or the inner membrane. Defects in any one or more of these processes has been linked to health and disease.

Mitochondrial matrix

Proteins destined for the mitochondrial matrix have specific signal sequences at their beginning that consist of a string of 20 to 50 amino acids. These sequences are designed to interact with receptors that guide the proteins to their correct location inside the mitochondria. The sequences have a unique structure with clusters of water-loving and water-avoiding amino acids, giving them a dual nature known as amphipathic. These amphipathic sequences typically form a spiral shape with the charged amino acids on one side and the hydrophobic ones on the opposite side. This structural feature is essential for the sequence to function correctly in directing proteins to the matrix. If mutations occur that mess with this dual nature, the protein often fails to reach its intended destination, although not all changes to the sequence have this effect. This indicates the importance of the amphipathic property for the protein to be correctly targeted to the mitochondrial matrix.Proteins targeted to the mitochondrial matrix first involves interactions between the matrix targeting sequence located at the N-terminus and the outer membrane import receptor complex TOM20/22. In addition to the docking of internal sequences and cytosolic chaperones to TOM70. Where TOM is an abbreviation for translocase of the outer membrane. Binding of the matrix targeting sequence to the import receptor triggers a handoff of the polypeptide to the general import core known as TOM40. The general import core then feeds the polypeptide chain through the intermembrane space and into another translocase complex TIM17/23/44 located on the inner mitochondrial membrane. This is accompanied by the necessary release of the cytosolic chaperones that maintain an unfolded state prior to entering the mitochondria. As the polypeptide enters the matrix, the signal sequence is cleaved by a processing peptidase and the remaining sequences are bound by mitochondrial chaperones to await proper folding and activity. The push and pull of the polypeptide from the cytosol to the intermembrane space and then the matrix is achieved by an electrochemical gradient that is established by the mitochondrion during oxidative phosphorylation. In which a mitochondrion active in metabolism has generated a negative potential inside the matrix and a positive potential in the intermembrane space. It is this negative potential inside the matrix that directs the positively charged regions of the targeting sequence into its desired location.