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Phospholipase D

Phospholipase D (PLD) is an anesthetic-sensitive and mechanosensitive enzyme of the phospholipase protein superfamily that catalyzes the hydrolysis of membrane phospholipids.

Discovery
PLD-type activity was first reported in 1947 by Donald J. Hanahan and I.L. Chaikoff. More than half a century of biochemical studies have implicated phospholipase D and PA activity in a wide range of physiological processes and diseases, including inflammation, diabetes, phagocytosis, neuronal & cardiac signaling, and oncogenesis. == Physiological function ==
Physiological function
Strictly speaking, phospholipase D is a transphosphatidylase: it mediates the exchange of polar headgroups covalently attached to membrane-bound lipids. Utilizing water as a nucleophile, this enzyme catalyzes the cleavage of the phosphodiester bond in structural phospholipids such as phosphatidylcholine and phosphatidylethanolamine. PA is heavily involved in intracellular signal transduction. In addition, some members of the PLD superfamily may employ primary alcohols such as ethanol or 1-butanol in the cleavage of the phospholipid, effectively catalyzing the exchange the polar lipid headgroup. As choline is very abundant in the cell, PLD activity does not significantly affect choline levels, and choline is unlikely to play any role in signalling. Phosphatidic acid, as a signal molecule, acts to recruit SK1 to membranes. PA is extremely short lived and is rapidly hydrolysed by the enzyme phosphatidate phosphatase to form diacylglycerol (DAG). DAG may also be converted to PA by DAG kinase. Although PA and DAG are interconvertible, they do not act in the same pathways. Stimuli that activate PLD do not activate enzymes downstream of DAG and vice versa. It is possible that, though PA and DAG are interconvertible, separate pools of signalling and non-signalling lipids may be maintained. Studies have suggested that DAG signalling is mediated by polyunsaturated DAG while PLD derived PA is monounsaturated or saturated. Thus functional saturated/monounsaturated PA can be degraded by hydrolysing it to form non-functional saturated/monounsaturated DAG while functional polyunsaturated DAG can be degraded by converting it into non-functional polyunsaturated PA. A lysophospholipase D called autotaxin was recently identified as having an important role in cell-proliferation through its product, lysophosphatidic acid (LPA). == Structure and mechanism ==
Structure and mechanism
Plant and animal PLDs have a consistent molecular structure, characterized by sites of catalysis surrounded by an assortment of regulatory sequences. phosphatidylserine synthase, bacterial PLDs, and viral proteins. Each of these appears to possess a domain duplication which is apparent by the presence of two HKD motifs containing well-conserved histidine, lysine, and asparagine residues which may contribute to the active site aspartic acid. An Escherichia coli endonuclease (nuc) and similar proteins appear to be PLD homologues but possess only one of these motifs. PLD genes additionally encode highly conserved regulatory domains: the phox consensus sequence (PX), the pleckstrin homology domain (PH), and a binding site for phosphatidylinositol 4,5-bisphosphate (PIP2). A local increase in PIP2 or decrease in cholesterol causes the enzyme to translocate to PIP2 micro domains near its substrate PC. PLD is thus primarily activated by localization within the plasma membrane rather than conformational change. These lipids domains may be disrupted by anesthetics each encoded by distinct genes. PLD activity appears to be present in most cell types, with the possible exceptions of peripheral leukocytes and other lymphocytes. Both PLD isoforms require PIP2 as a cofactor for activity. PLD1 and PLD2 exhibit different subcellular localizations that dynamically change in the course of signal transduction. PLD activity has been observed within the plasma membrane, cytosol, ER, and Golgi complex. PLD1 PLD1 is a 120 kDa protein that is mainly located on the inner membranes of cells. It is primarily present at the Golgi complex, endosomes, lysosomes, and secretory granules. Upon the binding of an extracellular stimulus, PLD1 is transported to the plasma membrane. Basal PLD1 activity is low however, and in order to transduce the extracellular signal, it must first be activated by proteins such as Arf, Rho, Rac, and protein kinase C. ==Regulation==
Regulation
In addition to diverging in intrinsic activity with its differing isoforms, PLD is extensively regulated by hormones, neurotransmitters, lipids, small monomeric GTPases, and other small molecules that bind to their corresponding domains on the enzyme. PLDs regulated by these phospholipids are commonly involved in intracellular signal transduction. Their activity is dependent upon the binding of these phosphoinositides near the active site. In plants and animals, this binding site is characterized by the presence of a conserved sequence of basic and aromatic amino acids. In plants such as Arabidopsis thaliana, this sequence is constituted by a RxxxxxKxR motif together with its inverted repeat, where R is arginine and K is lysine. Its proximity to the active site ensures high level of PLD1 and PLD2 activity, and promotes the translocation of PLD1 to target membranes in response to extracellular signals. Basal regulation The intrinsic activity of PLD differs between its known isoforms. Mammalian PLD1 and PLD2, for example, exhibit different basal activities despite high sequence conservation. PLD1 requires activation by protein factors such as Arf, Rho, or protein kinase C, whereas PLD2 is constitutively active. Structural differences near the active site tunnel account for this disparity: in PLD2, a segment corresponding to residues 687–696 folds into an alpha helix, widening the substrate entrance; in PLD1, the homologous residues form a flexible loop occluding the tunnel. The displacement of a partially conserved adjacent loop by the PLD2 helix may further contribute to isoform-specific regulation. In plants (e.g. PLDα), similar conformational gating of the active site by an autoinhibitory helix is observed. C2 domain Calcium acts as a cofactor in PLD isoforms that contain the C2 domain. Binding of Ca2+ to the C2 domain leads to conformational changes in the enzyme that strengthen enzyme-substrate binding, while weakening the association with phosphoinositides. In some plant isoenzymes, such as PLDβ, Ca2+ may bind directly to the active site, indirectly increasing its affinity for the substrate by strengthening the binding of the activator PIP2. PX domain The pbox consensus sequence (PX) is thought to mediate the binding of additional phosphatidylinositol phosphates, in particular, phosphatidylinositol 5-phosphate (PtdIns5P), a lipid thought to be required for endocytosis, may help facilitate the reinternalization of PLD1 from the plasma membrane. PH domain The highly conserved Pleckstrin homology domain (PH) is a structural domain approximately 120 amino acids in length. It binds phosphatidylinositides such as phosphatidylinositol (3,4,5)-trisphosphate (PIP3) and phosphatidylinositol (4,5)-bisphosphate (PIP2). It may also bind heterotrimeric G proteins via their βγ-subunit. Binding to this domain is also thought to facilitate the re-internalization of the protein by increasing its affinity to endocytotic lipid rafts. Interactions with small GTPases In animal cells, small protein factors are important additional regulators of PLD activity. These small monomeric GTPases are members of the Rho and ARF families of the Ras superfamily. Some of these proteins, such as Rac1, Cdc42, and RhoA, allosterically activate mammalian PLD1, directly increasing its activity. In particular, the translocation of cytosolic ADP-ribosylation factor (ARF) to the plasma membrane is essential for PLD activation. ==Physiological and pathophysiological roles==
Physiological and pathophysiological roles
Alcohol Intoxication Phospholipase D metabolizes ethanol into phosphatidylethanol (PEtOH) in a process termed transphosphatidylation. Using fly genetics the PEtOH was shown to mediates alcohol's hyperactive response in fruit flies. And ethanol transphosphatidylation was shown to be up-regulated in alcoholics and the family members of alcoholics. This ethanol transphosphatidylation mechanism recently emerged as an alternative theory for alcohol's effect on ion channels. Many ion channels are regulated by anionic lipids. and the competition of PEtOH with endogenous signaling lipids is thought to mediate the effect of ethanol on ion channels in some instances and not direct binding of the free ethanol to the channel. PLD2 is upstream of Piezo2 and inhibits the channel. Piezo2 is an excitatory channel, ence PLD inhibits an excitatory channel and activates TREK-1 which is an inhibitory channel. The channels combine to reduce neuronal excitability. In cancer Phospholipase D is a regulator of several critical cellular processes, including vesicle transport, endocytosis, exocytosis, cell migration, and mitosis. == Gallery ==
Gallery
Image:Phosphatidyl-Choline.svg|Phosphatidyl choline Image:Phosphatidate_skeletal.svg|Phosphatidate Image:Choline-skeletal.svg|Choline == References ==
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