An ethylene-induced cDNA encoding a lipase expressed at the onset of senescence

Abstract

M embrane deterioration is an early and characteristic feature of plant senescence engendering increased permeability, loss of ionic gradients, and decreased function of key membrane proteins such as ion pumps (1). One of the clearest manifestations of this is the onset of membrane leakiness measurable as increased conductivity of diffusates from intact tissue. This is detectable in carnation petals, for example, well before petal inrolling, the first morphological manifestation of senescence in this tissue, and also before the climacteric-like rise in ethylene production (2). The decline in membrane structural integrity at the onset of senescence appears to be largely attributable to accelerated metabolism of membrane lipids and ensuing change in the molecular organization of the bilayer. Indeed, loss of membrane phospholipid is one of the best documented indices of membrane lipid metabolism during senescence and has been demonstrated for senescing flower petals, leaves, cotyledons and ripening fruit (3, 4).The selective depletion of phospholipid fatty acids from the membranes of senescing tissues results in an increase in the sterol:fatty acid ratio in the bilayer and a consequent decrease in bulk lipid fluidity. This has been demonstrated by fluorescence depolarization and electron spin resonance for microsomal membranes from senescing cotyledons, flowers, leaves, and ripening fruit (5-8) and for plasmalemma of ripening fruit and senescing flowers (5). The decrease in lipid fluidity is engendered by an enrichment of free sterols relative to fatty acids in the bilayer as fatty acids are cleaved from the membrane lipids and selectively removed, reflecting the fact that free sterols are known to restrict the mobility of phospholipid fatty acids (9). As well, in some senescing tissues, the decrease in bulk lipid fluidity appears to be caused in part by a selective depletion of polyunsaturated fatty acids from membranes and an ensuing increase in the saturated-to-unsaturated fatty acid ratio (6). There are also reports that the large changes in bulk membrane lipid fluidity accompanying senescence may alter the conformation of membrane proteins, rendering them prone to proteolysis (10, 11).Recent data suggest that free fatty acids arising from the metabolism of membrane lipids may be removed from the bilayer by blebbing of lipid particles highly enriched in free fatty acids from the membrane surface into the cytosol (12-14). These lipid particles appear to be structurally analogous to oil bodies. Indeed, there is growing evidence that the free fatty acids released from senescing membranes are metabolized by glyoxylate cycle enzymes also induced at the onset of senescence (15). However, it is also clear that free fatty acids accumulate in senescing membranes and induce lipid-phase separations. The resulting mixture of liquid-crystalline and gel phase lipid domains in the bilayer contributes to the leakiness of senescing membranes because of packing imperfections at the phase boundaries (16).Deesterification of membr...

Glycerophosphocholine Metabolism in Higher Plant Cells. Evidence of a New Glyceryl-Phosphodiester Phosphodiesterase

“…The vacuole GPC-PDE may also participate in membrane degradation in different physiological situations of programmed cell death: In tracheary element differentiation (Fukuda, 1997), tonoplast rupture is considered as a critical event in cell death. In senescence, lipolytic acyl hydrolases, which release glycerophosphodiesters from phospholipids, seem to play an important role in membrane disruption (Hong et al, 2000). Thus, the modification of vacuoles during different senescence processes could release different hydrolases from the vacuole sap.…”

Expression and Regulation of Senescence-related Genes in Carnation Flowers with Low Ethylene Production during Senescence

“…Wilting may be caused by the degradation of cell components, which prompts cell death mediated by hydrolytic enzymes such as cysteine proteinase (CPase) (Jones et al, 1995) and lipase (Lip) (Hong et al, 2000;Kim et al, 1999a). Cysteine proteinase inhibitor (CPIn) seems to suppress CPase and to regulate petal wilting (Kim et al, 1999b;Sugawara et al, 2002).…”

Flower senescence: some molecular aspects

“…Some of the genes have been found to be upregulated while others downregulated during flower senescence. The genes upregulated during normal developmental petal senescence relate to remobilization of nutrients, and include proteases, nucleases, lipases and transporters (Hong et al 2000;wagstaff et al 2002;Langston et al 2005;Price et al 2008). A general overview of some of the important genes or transcripts isolated from various flower systems is provided in Table 1.…”