Abstract
We have identified an Arabidopsis mutant, wat1 (wall and tryptophan1), with increased tolerance to Ralstonia solanacearum, a soil-borne vascular pathogen that causes bacterial wilt in numerous plant species. Our study of WAT1,
an Arabidopsis homolog of Medicago truncatula Nodulin21, provides the first functional characterization of a member of the Plant-Drug/Metabolite Exporter family. From a developmental standpoint, WAT1 encodes a novel tonoplast-localized transporter that is required for auxin homeostasis and secondary wall formation. To characterize wat1 tolerance to Ralstonia, several approaches are being employed. We are performing cell wall phenotyping of wat1 vs. wild-type roots using cytology and immunocytochemistry. Experiments with pectin antibodies revealed that wat1 roots contain constitutively higher amounts of pectin, mainly localized in the stele, than in the wild-type. We have also
determined the effect of the wat1 mutation on pathogen multiplication. Bacterial density in the aerial portion of the plant is significantly reduced in wat1. To test if wat1 tolerance is specific to Ralstonia, we tested a battery of vascular (X.
campestris pv. campestris, P. cucumerina, V. dahliae) and non-vascular (P. syringae pv. tomato, C. higginsianum) pathogens. The systematic tolerance to vascular pathogens and the sensitivity to non-vascular pathogens suggest that
mechanisms involved in wat1 tolerance might be localized within the vascular system. To determine if ethylene, jasmonic acid, and/or salicylic acid signaling pathways are involved in wat1 tolerance, double mutants were generated by crossing wat1 with ein2, coi1, jar1-1, sid2, and NahG transgene.
Finally, comparative transcriptomic analyses of wat1 vs. wild-type have been performed to identify novel constitutive mechanisms associated with wat1 tolerance.
an Arabidopsis homolog of Medicago truncatula Nodulin21, provides the first functional characterization of a member of the Plant-Drug/Metabolite Exporter family. From a developmental standpoint, WAT1 encodes a novel tonoplast-localized transporter that is required for auxin homeostasis and secondary wall formation. To characterize wat1 tolerance to Ralstonia, several approaches are being employed. We are performing cell wall phenotyping of wat1 vs. wild-type roots using cytology and immunocytochemistry. Experiments with pectin antibodies revealed that wat1 roots contain constitutively higher amounts of pectin, mainly localized in the stele, than in the wild-type. We have also
determined the effect of the wat1 mutation on pathogen multiplication. Bacterial density in the aerial portion of the plant is significantly reduced in wat1. To test if wat1 tolerance is specific to Ralstonia, we tested a battery of vascular (X.
campestris pv. campestris, P. cucumerina, V. dahliae) and non-vascular (P. syringae pv. tomato, C. higginsianum) pathogens. The systematic tolerance to vascular pathogens and the sensitivity to non-vascular pathogens suggest that
mechanisms involved in wat1 tolerance might be localized within the vascular system. To determine if ethylene, jasmonic acid, and/or salicylic acid signaling pathways are involved in wat1 tolerance, double mutants were generated by crossing wat1 with ein2, coi1, jar1-1, sid2, and NahG transgene.
Finally, comparative transcriptomic analyses of wat1 vs. wild-type have been performed to identify novel constitutive mechanisms associated with wat1 tolerance.
| Original language | English |
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| Title of host publication | ISMPMI International Congress abstracts, Quebec City, Canada, 19-23 July 2009 |
| Publisher | International Society for Molecular Plant-Microbe Interactions |
| Pages | 56 |
| Publication status | Published - 2009 |
| Event | XIV Congress on Molecular Plant-Microbe Interactions, Quebec City, Canada - Duration: 19 Jul 2009 → 23 Jul 2009 |
Conference
| Conference | XIV Congress on Molecular Plant-Microbe Interactions, Quebec City, Canada |
|---|---|
| Period | 19/07/09 → 23/07/09 |