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TaMDAR6 acts as a negative regulator of plant cell death and participates indirectly in stomatal regulation during the wheat stripe rust–fungus interaction
We identified a new monodehydroascorbate reductase (MDAR) gene from wheat, designated TaMDAR6, which is differentially affected by wheat–Puccinia striiformis f. sp. tritici (Pst) interactions. TaMDAR6 is a negative regulator of plant cell death (PCD) triggered by the Bax gene and Pst. Transcript lev...
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Published in: | Physiologia plantarum 2016-03, Vol.156 (3), p.262-277 |
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Main Authors: | , , , , , |
Format: | Article |
Language: | English |
Subjects: | |
Citations: | Items that this one cites Items that cite this one |
Online Access: | Get full text |
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Summary: | We identified a new monodehydroascorbate reductase (MDAR) gene from wheat, designated TaMDAR6, which is differentially affected by wheat–Puccinia striiformis f. sp. tritici (Pst) interactions. TaMDAR6 is a negative regulator of plant cell death (PCD) triggered by the Bax gene and Pst. Transcript levels of TaMDAR6 are significantly upregulated during a compatible wheat–Pst interaction, indicating that TaMDAR6 may contribute to plant susceptibility. In addition, H₂O₂ production and PCD are significantly induced and initial pathogen development is significantly reduced in the TaMDAR6 knocked‐down plants upon Pst infection. Thus, the suppression of TaMDAR6 enhances wheat resistance to Pst. Besides, the suppression of TaMDAR6 during an incompatible interaction induces a change in the morphology of stomata, which leads to poor stoma recognition and as a consequence to reduced infection efficiency. The percentage of infection sites that develop substomatal vesicles decreases in the TaMDAR6 knocked‐down plants during the incompatible interaction presumably due to the increase in ROS accumulation, which is likely to activate other resistance mechanisms that have a negative effect on substomatal vesicle formation. TaMDAR6 can therefore be considered a negative regulator of PCD and of wheat defense to Pst. |
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ISSN: | 0031-9317 1399-3054 |
DOI: | 10.1111/ppl.12355 |