MOLECULAR AND GENETIC DISSECTION OF NEMATODE FEEDING SITES
Plant Nematode Genetics Group, Box 7616 NC State University, Raleigh NC 27695, USA
Background and objectives
Plant-parasitic nematodes are significant pathogens of many important crops, directly reducing yield and predisposing the host to other biotic and abiotic stresses. Annual worldwide yield losses are estimated at $US10m. For many nematode species, the key to parasitism is the induction of specialized feeding cells in the host, such as the giant cells (induced by Meloidogyne spp.) and the syncytia (induced by Heterodera and Globodera spp.). Disruption of feeding cells, mediated either by natural R-genes or transgenic approaches, effects nematode control. We have identified 220 tomato genes specifically unregulated in giant cells . To determine which of these are necessary and/or sufficient for feeding cell development, we have initiated a series of functional assays. Such genes will be good candidates for the construction of synthetic R-genes, and will elucidate the mechanisms of feeding cell ontogeny and function, and complement our molecular and genetic studies of the parasite .
Results and conclusions
Because giant cells exhibit karyokinesis uncoupled from cytokinesis, we are especially interested in genes in our bank we postulate to play a role in cell-cycle regulation. DB#103 encodes a ubiquitin conjugating enzyme (UBC) we named Leubc4. UBCs regulate protein degradation and thus control processes such as the Gl to S transition. In situ experiments localized Leubc4 transcripts to meristematic cells only, as well as to the non-dividing giant cells. Using antibodies raised to LEUBC4 synthetic peptides, we showed that this protein is localized in the nucleus. Together, these results implicate a role for DB#103 in regulation of nuclear proliferation, and this is being tested in transgenic plants. Consistent with this model is our finding that although abundantly expressed in giant cells, Leubc4 transcripts are barely detectable in syncytia; syncytial nuclei are non-dividing. We have undertaken similar analyses for several other giant cell, up-regulated genes. Based on our collective data, we propose a two-step model of feeding cell induction . In step one, a nematode-specified ligand (perhaps a cytokinin, or molecule active in this, or another hormone reception pathway) initiates vascular differentiation of a parenchyma cell selected by the parasite. Subsequently, the nematode initiates feeding, and this nutrient sink serves as a physiological cue to specify adoption of a transfer cell phenotype by the differentiating parenchyma cell. This simple model is consistent with the key morphological and physiological features of feeding cells, and we tentatively have identified a candidate 'receptor' of a nematode ligand.
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