Reproductive Cell Death A Floral Organs

Before gametes are produced by plants, reproductive structures must be differentiated. PCD plays a role in these processes. Most plants produce perfect or hermaphroditic flowers, but a few produce flowers with only pistils or only anthers. The flowers are initially perfect, but development of either pistils or anthers is arrested and PCD follows resulting in a single sex, mature flower (Irish and Nelson 1989; Dellaporta and Calderon-Urrea, 1993).

The initial bisexuality of both male and female flowers of monoecious Zea mays was noted early and described in detail later (Bonnett, 1948). More recently scanning electron microscopy (SEM) and TEM studies revealed that the initially bisexual tassel flowers abort gynoecium tissue in succession in both flowers of each spikelet leaving only anthers to develop (Cheng et al., 1983). Cells in the aborting tissue become increasingly vacuolated and the content of ribosomes and other organelles decreases as degeneration progresses. The process initiates in and spreads from the subepidermal region (Calderon-Urrea and Dellaporta, 1999). Slightly later, abortion of anthers begins in ear flowers, occurring first in the upper and later in the lower flower of each paired spikelet (Cheng et al., 1983). In maize the cellular phenotype of anther abortion was similar to that occurring in the gynoecium cells (Cheng et al., 1983; Cheng and Pareddy, 1994), but it varies somewhat in several other grasses (Le Roux and Kellogg, 1999).

Silene latifolia, white campion, illustrates regulation of PCD by sex chromosomes (Grant et al., 1994a). Both male and female plants begin reproductive development with perfect flowers (Grant et al., 1994b), but the gynoecium primordium emerges as a small, undif-ferentiated rod on male plants. Two developmental stages later in female plants, stamens first stop developing and later they degenerate. The timing of failure of female versus male flower parts plus genetic evidence indicate that the mechanism suppressing development of gynoecium is independent of the one leading to cell death in anthers (Grant et al, 1994b). Genes are present on the Y chromosome which determine male development by converting the female default program to male (Grant et al., 1994a). Presumably the Y chromosome suppresses genes on the X chromosome responsible for PCD of anthers on female plants.

Sex-linked gene loci rather than sex chromosomes activate PDC to achieve single-sex flowers on monoecious maize or dioecious Ecballium elaterium or Spinacia oleracea plants. In maize recessive mutations of several genes result in dwarf plants with perfect or male flowers in the normally female ear (Irish and Nelson, 1989). This condition is called "anther ear", a name applied to one of the mutants. Biochemical evidence has shown that gibberellin biosynthesis is blocked at different steps in these mutants (di, d2, d3, d4, and an1) and application of gibberellin rescues the normal phenotype (Phinney, 1984). Anther ear 1 has been cloned (Bensen et al., 1995); its sequence is homologous to a plant cyclase and biochemical evidence indicates its product synthesizes ent-kaurene. The d3 gene has been shown to encode a cytochrome p450 enzyme involved in gibberellin biosynthesis (Winkler and Helentjaris, 1995). Thus some GA down stream from ent-kaurene, perhaps GA1, is needed to cause PCD of anthers in ear florets. Other evidence also links high or low levels of GA with female or male development, respectively (Irish and Nelson, 1989).

The sexual development of the normally male tassel of maize is influenced by tasselseed genes known to occur in five loci (Ts1, Ts2, Ts4, Ts5, Ts6) (DeLong et al., 1993; Dellaporta and Calderon-Urrea, 1993). Two genes, ts1 and ts2, cause production of female flowers in the tassel when they are homozygously recessive. In wild type tassels, both stamens and a carpel are initiated in each flower, but the carpel is aborted (Irish and Nelson, 1993). In tassel flowers of ts1 and ts2 mutants, the carpel does not abort, but the stamens do. Thus these genes appear to control a switch for execution of PCD in either the carpel or stamens. Ts5 is a dominant mutation which causes a base-to-tip gradient of pistillate to staminate flowers in the tassel (Irish and Nelson, 1989). This gene affects the abortion of gynoecium, and thus it also controls PCD in tassel floret development. Mutants for Ts4 (recessive) and Ts6 (dominant) block normal PCD of the gynoecium in tassel flowers (Dellaporta and Calderon-Urrea, 1993).

The gene encoding ts2 has been cloned and sequenced (DeLong et al., 1993). Ts2 mRNA was expressed subepidermally in the gynoecium of tassel flowers shortly before abortion. Restoration of Ts2 action and male development occurred when the transposon used to induce the ts2 allele was excised. The predicted amino acid sequence of the Ts2 protein is similar to bacterial hydroxysteroid dehydrogenases. Such an enzyme could be active in the synthesis of gibberellins or steroids (DeLong et al., 1993). GAs are known to regulate floral development based on the dwarf mutants mentioned above, and brassinosteroids have been implicated in flowering based on the phenotypes of deficient mutants (Li et al., 1996). Since the Ts2 message is expressed in the gynoecium of tassel flowers and the Ts2 gene product may synthesize a bioactive terpenoid, the Ts2 product may trigger PCD in pistils in tassel florets. The mutant gene (ts2) presumably fails to produce a functional product and, therefore, the female development program is not switched off. Ts2 also functions in ears to suppress development of the second floret in each spikelet; thus, in both tassel and ear Ts2 causes PCD in female organs. A cell death mechanism similar to that in maize appears to be present in a wild relative, Tripsacum dactyloides (Li et al., 1997).

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