Proline synthesis and degradation: a model system for elucidating stress-related signal transduction

Open Access
Publisher Website
Google Scholar
Abstract
A causal relationship between increased proline synthesis and plant tolerance of hyperosmotic stresses has been demonstrated. Nonetheless, the molecular basis of this effect is not yet established. Proline accumulation appears to be mediated by both ABA-dependent and ABA-independent signalling pathways, although the events that occur between the perception of stress and the induction of proline biosynthetic genes are poorly characterized. Recent evidence supports an important role for post-transcriptional events in dehydration- and ABA-induced proline synthesis. Further research concerning the factors that regulate the expression of enzymes involved in proline synthesis and degradation will not only be of value in attempts to increase plant stress tolerance, but may contribute to an improved understanding of at least certain stress-related aspects of the regulatory network which controls plant responses to the environment. In Arabidopsis thaliana, synthesis of the immediate precursor of proline, Δ1-pyrroline-5-carboxylate (P5C), is apparently regulated by a pathway disrupted by mutation of ABI1, a protein serine/threonine phosphatase of the 2C class. Similarities and differences between the signalling events upstream of the regulation of the gene encoding P5C synthetase and model stress-inducible Arabidopsis genes such as RD29A, KIN2, and RAB18 are reviewed. Further analysis of the factors that induce these genes may assist in elucidating the mechanisms involved in stress-induced proline accumulation. Putative stress-regulated promoter elements in the AtP5CS1, AtP5CS2 and AtP5CR genes are identified. Recent evidence that a signal related to proline synthesis and/or degradation selectively increases the expression of stress-related genes underscores the importance of elucidating the signalling events associated with proline accumulation under adverse conditions.

This publication has 0 references indexed in Scilit: