Hormonal Regulation of Plant PCD

A well-studied PCD model in plants is camptothecin-mediated cell death in tomato cell suspensions (see De Jong et al., 2002 and references therein). Camptothecin, a topo isomerase-I inhibitor and inducer of PCD in animals (Kaufmann, 1998; Simizu et al., 1998), causes cell death in tomato suspension in a manner reminiscent of animal apoptosis—chromatin condensation, DNA and nuclear fragmentation. Inhibitors that inhibit generation of reactive oxygen species (ROS) (Lamb and Dixon, 1997), superoxide (O2-), hydroxy radicals (OH-) and hydrogen peroxide (H2O2), also inhibit camptothecin-mediated cell death (De Jong et al., 2002). This is quite interesting in light of the studies showing that oxidative stress induced by cupric ions generates oxygen free radicals, enhanced ethylene production and membrane fragmentation (Mattoo et al., 1986). In the latter system, scavengers of hydroxy radicals inhibited ethylene production as well as senescence-related protein degradation (Mattoo et al, 1986; Mehta et al, 1992).

Evidence is accumulating to indicate that plant cells share features of PCD characterized in animal cells (see Chapter 1). H2O2 activates protein kinase cascades as well as NF-kB transcription factor, which are components of defense signaling in animals. Earlier, hydroperoxide levels were suggested to be involved in ethylene evolution and the fruit ripening process (Frenkel and Eskin, 1977). Hypoxia-induced aerenchyma formation in maize roots (He et al., 1996; Gunawardena et al., 2001), maize endosperm development cell death (Young and Gallie, 2000), camptothecin-induced PCD in tomato cell suspensions (De Jong et al., 2002), and pea carpel senescence (Orzaez and Granell, 1997) are a few well-studied examples in plants where ethylene is directly involved in PCD.

Ozone-induced cell death in tomato leaf is preceded by a rapid increase in ethylene biosynthesis. Transcript levels for specific ACC synthase, ACC oxidase, and ethylene receptor genes are up regulated in the O3-treated leaves within 1 to 5 h (Moeder et al., 2002). These authors further produced transgenic plants containing an LE-ACO1 promoter-beta-glucuronidase fusion construct. In these plants, j-glucuronidase activity increased upon O3 exposure and the spatial distribution of GUS resembled the pattern of extracellular H2O2 production. These studies show that ethylene synthesis and perception are required for ROS production and spread of cell death.

Similarly, involvement of ethylene in PCD is exemplified by studies on host-plant interactions. Host defense during pathogenesis in plants involves HR, which culminates in the death of the infected cell and, in some instances, has been shown to involve ethylene (Dangl et al, 1996; Greenberg, 1996; Gilchrist, 1998; Podile and Sripriya, 2002). In recent years, ethylene's role in pathogen-mediated HR was investigated with tomato mutants that are defective in ethylene responsiveness. Never-ripe (NR) tomato is insensitive to ethylene and therefore its fruit do not ripen. When challenged with microbial pathogens, this mutant displays reduced disease symptoms compared to the wild type (Lund et al., 1997). Similarly, mycotoxin fumonisin causes cell death in wild type tomato but less so in the NR mutant (Moore et al., 1999). These studies show that ethylene plays a prominent role in PCD during pathogenesis. In addition to ethylene, salicylic acid has been implicated in disease-susceptible responses. Salicylic acid does not accumulate in the ethylene-insensitive plants (O'Donnell et al., 2001), perhaps suggesting cross talk between ethylene and salicylic acid during disease susceptibility. The cell death lesions in HR are mimicked in plants exposed to toxic levels of ozone (O3) and inhibitors of ethylene biosynthesis or perception prevent their development. O3 is known to induce ethylene biosynthesis, therefore, cell death both in pathogen attack or when plants are exposed to abiotic stresses involves ethylene action (Avni et al, 1994; Overmyer et al, 2000).

Ethylene regulates production of O- and cell death in carrot suspension cells, by activating NADPH oxidase (Chae and Lee, 2001). In other words, ethylene plays a role upstream of NADPH oxidase and other systems that produce ROS. De Jong et al. (2002) working with camptothecin-mediated cell death in tomato suspension cells also arrived at a similar conclusion. These authors proposed two partly overlapping cell-death pathways. One pathway involves caspases or metacaspases (De Jong et al., 2000; Uren et al., 2000; Elbaz et al., 2002) that require low ethylene levels for activation. The other pathway is caspase independent and operates at high ethylene levels. This hypothesis is consistent with proposals that different plant responses to ethylene are mediated by independent downstream pathways that have differing thresholds for ethylene levels (Chen and Bleecker, 1995) and/or respond to hormonal cross talk (Whitelaw et al, 2002).

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