Remorins (REMs) are proteins of unknown function specific to vascular plants. We have used imaging and biochemical approaches and in situ labeling to demonstrate that REM clusters at plasmodesmata and in ;70-nm membrane domains, similar to lipid rafts, in the cytosolic leaflet of the plasma membrane. From a manipulation of REM levels in transgenic tomato (Solanum lycopersicum) plants, we show that Potato virus X (PVX) movement is inversely related to REM accumulation. We show that REM can interact physically with the movement protein TRIPLE GENE BLOCK PROTEIN1 from PVX. Based on the localization of REM and its impact on virus macromolecular trafficking, we discuss the potential for lipid rafts to act as functional components in plasmodesmata and the plasma membrane.

Lipid peroxidation was investigated in relation with the hypersensitive reaction in cryptogein-elicited tobacco leaves. A massive production of free polyunsaturated fatty acid (PUFA) hydroperoxides dependent on a 9-lipoxygenase (LOX) activity was characterized during the development of leaf necrosis. The process occurred after a lag phase of 12 h, was accompanied by the concomitant increase of 9-LOX activity, and preceded by a transient accumulation of LOX transcripts. Free radical-mediated lipid peroxidation represented 10% of the process. Inhibition and activation of the LOX pathway was shown to inhibit or to activate cell death, and evidence was provided that fatty acid hydroperoxides are able to mimic leaf necrotic symptoms. Within 24 h, about 50% of leaf PUFAs were consumed, chloroplast lipids being the major source of PUFAs. The results minimize the direct participation of active oxygen species from the oxidative burst in membrane lipid peroxidation. They suggest, furthermore, the involvement of lipase activity to provide the free PUFA substrates for LOX. The LOX-dependent peroxidative pathway, responsible for tissue necrosis, appears as being one of the features of hypersensitive programmed cell death.In plant-pathogen interactions, a typical feature of plant resistance is hypersensitive reaction (HR), 1 characterized by the induction of rapid cell death at the site of an attempted attack by either an avirulent strain of a pathogen or a nonpathogen. The collapse of challenged cells, occurring during incompatible interactions, was shown in most cases to be dependent on a gene for gene plant pathogen interaction (1, 2). HR is accompanied by a battery of defense mechanisms including de novo synthesis of antimicrobial enzymes and metabolites, strengthening of the cell wall, and the onset of systemic acquired resistance dependent on salicylic acid accumulation (3, 4). HR often leads to dry lesions that are supposed to limit pathogen growth. Other proposed roles is the release in apoplasm of defense-related proteins and toxic metabolites, as well as of signals that activate the defenses of both neighboring and distant cells. Hypersensitive cell death appears to not be the result of the direct action of released pathogenic factors but is rather under the genetic control of the host. Indeed, several observations underline that HR is an example of PCD in plants (1, 2). Furthermore, hypersensitive cell death has morphological and molecular features similar to the mammalian PCD, called apoptosis. These include cytoplasm and chromatin condensation followed by their fragmentation, activation of calciumdependent endonucleases (5-8) and of cysteine proteases (9 -11), and involvement of similar regulation factors (2). Some differences between HR and mammalian apoptosis were observed, however, such as changes in DNA laddering (5,8) and the lack in HR of the repressor role of Bcl-x L (12). One ultimate characteristic of HR is the loss of membrane integrity, and thus HR is often characterized by an associated electrolyte le...

Several studies have provided new insights into the role of sphingolipid/sterol-rich domains so-called lipid rafts of the plasma membrane (PM) from mammalian cells, and more recently from leaves, cell cultures, and seedlings of higher plants. Here we show that lipid raft domains, defined as Triton X-100-insoluble membranes, can also be prepared from Medicago truncatula root PMs. These domains have been extensively characterized by ultrastructural studies as well as by analysis of their content in lipids and proteins. M. truncatula lipid domains are shown to be enriched in sphingolipids and D 7 -sterols, with spinasterol as the major compound, but also in steryl glycosides and acyl-steryl glycosides. A large number of proteins (i.e. 270) have been identified. Among them, receptor kinases and proteins related to signaling, cellular trafficking, and cell wall functioning were well represented whereas those involved in transport and metabolism were poorly represented. Evidence is also given for the presence of a complete PM redox system in the lipid rafts.