Proline and abiotic stresses: Responses and adaptation

Abstract

Abiotic stresses are major threats influencing crop growth and production globally. Abiotic stresses can cause several cellular dysfunctions, and some of them are beneficial and required for stress tolerance enhancement. Compatible solute accumulation is one of these changes, and among them proline (Pro) overproduction is a physiological response commonly found in plants exposed to various abiotic stresses. Pro overproduction has been proposed to correlate with stress resistance in many plants. Pro implication in stress tolerance mechanism is supported by the observations that exogenous supply and genetic manipulation of metabolic pathways associated with Pro biosynthesis have been beneficial in enhancing stress tolerance in many plant species under different stresses. Pro improves stress tolerance via acting as a stress-related signal influencing adaptive responses, osmotic adjustment mediator, and molecular chaperone to stabilize subcellular structures, scavenging reactive oxygen species (ROS), acting as a metal chelator, serving as a nitrogen/carbon source for cells under stress conditions and after stress relief, maintaining cytoplasmic pH and hence alleviating its acidosis, triggering gene expression, and buffering cellular redox potential. Pro actual role in conferring stress tolerance is, however, still a matter of debate because there are several inconsistencies among published data. Also, Pro biosynthesis is dependent on a high diversity of regulation mechanisms, and even several of them are still largely obscure, which might exacerbate these discrepancies. Furthermore, the broad natural variation in Pro overproduction and its true role in metabolism of plants under stress conditions necessitate further research for better understanding of the reported variations. Despite the Pro beneficial roles observed under stress conditions, we believe that the often proposed relationship between Pro production and stress resistance may not be universal.