L-proline (Pro) catabolism takes place in mitochondria involving two consecutive steps catalyzed by Pro-dehydrogenase (ProDH) and Ä1-Pyrroline-5-carboxylate (P5C) dehydrogenase (P5CDH). Pro accumulates to high levels upon exposure to environmental stresses, and its catabolism is an excellent source of nitrogen and energy during recovery from stress. In contrast, external Pro results toxic and causes cell death, effect proposed to be due to accumulation of the toxic intermediate P5C.
We are studying alterations in the Pro metabolism occurring in Arabidopsis tissues treated with Pseudomonas syringae pv. tomato (Pst). We previously reported that Pro levels and Pro biosynthetic genes activity are enhanced in tissues responding to avirulent, but not virulent, Pst and that these changes follow the initiation of the Hypersensitive Response (HR). We here characterize features of Pro degradation at early stages of HR in wild type plants. We evaluate as well contributions of ProDH and P5CDH to the HR lesion by monitoring HR components in transgenic/mutant lines impaired in these enzymes. Our results point out a relevant role of Pro degradation in HR development.
