Poster: Vegetative Development
Abs #
443: Evidence for the lack of evolutionary conservation of cell death pathways between plants and animals
Programmed cell death (PCD) is a genetically regulated process that rids plants and animals of unneeded or damaged cells during development, disease and homeostasis. It is believed that PCD mechanisms have evolved from unicellular organisms a view supported by the existence of similar molecular elements of PCD in both plants and animals. The best-studied PCD models in animals are the nematode Caenorhabditis elegans and the fruit fly Drosophila melanogaster. Several genes in these organisms have been identified that are responsible for inducing cell death in a caspase-dependent pathway, i.e. grim, rpr, and hid in the fly and ced3, ced4, and egl1 in the nematode. We reason that if animal PCD genes are able to induce PCD in plant cells, this indicates the presence of evolutionarily conserved factors shared by these two groups. We expressed rpr, hid, ced3, and ced4 in Nicotiana tabacum (tobacco) cells using an Agrobacterium-mediated transient expression system to deliver the genes into fully expanded leaves. Transient expression of rpr, hid, ced3, and ced4 in tobacco leaves did not elicit a PCD response after 72 hours post-inoculation. We confirmed expression in plant cells of the introduced genes using RT-PCR. Although transgenic tobacco plants containing ced3 and ced4 appeared normal we detect high mRNA levels of the introduced genes. These results indicate that the rpr and hid genes from D. melanogaster, and ced3 and ced4 from C. elegans are unable to induce PCD in N. tabacum. This suggests that similar caspase-dependent PCD pathways are not shared by plants and animals.
