Impact of polyploidy on plant tolerance to abiotic and biotic stresses.

Polyploidy, defined as the coexistence of three or more complete sets of chromosomes in an organism's cells, is considered as a pivotal moving force in the evolutionary history of vascular plants and has played a major role in the domestication of several crops. In the last decades, improved cultivars of economically important species have been developed artificially by inducing autopolyploidy with chemical agents. Studies on diverse species have shown that the anatomical and physiological changes generated by either natural or artificial polyploidization can increase tolerance to abiotic and biotic stresses as well as disease resistance, which may positively impact on plant growth and net production. The aim of this work is to review the current literature regarding the link between plant ploidy level and tolerance to abiotic and biotic stressors, with an emphasis on the physiological and molecular mechanisms responsible for these effects, as well as their impact on the growth and development of both natural and artificially generated polyploids, during exposure to adverse environmental conditions. We focused on the analysis of those types of stressors in which more progress has been made in the knowledge of the putative morpho-physiological and/or molecular mechanisms involved, revealing both the factors in common, as well as those that need to be addressed in future research.

Autocrine abscisic acid mediates the UV-B-induced inflammatory response in human granulocytes and keratinocytes.

UV-B is an abiotic environmental stress in both plants and animals. Abscisic acid (ABA) is a phytohormone regulating fundamental physiological functions in plants, including response to abiotic stress. We previously demonstrated that ABA is an endogenous stress hormone also in animal cells. Here, we investigated whether autocrine ABA regulates the response to UV-B of human granulocytes and keratinocytes, the cells involved in UV-triggered skin inflammation. The intracellular ABA concentration increased in UV-B-exposed granulocytes and keratinocytes and ABA was released into the supernatant. The UV-B-induced production of NO and of reactive oxygen species (ROS), phagocytosis, and cell migration were strongly inhibited in granulocytes irradiated in the presence of a monoclonal antibody against ABA. Moreover, presence of the same antibody strongly inhibited release of NO, prostaglandin E2 (PGE(2)), and tumor necrosis factor-α (TNF-α) by UV-B irradiated keratinocytes. Lanthionine synthetase C-like protein 2 (LANCL2) is required for the activation of the ABA signaling pathway in human granulocytes. Silencing of LANCL2 in human keratinocytes by siRNA was accompanied by abrogation of the UV-B-triggered release of PGE(2), TNF-α, and NO and ROS production. These results indicate that UV-B irradiation induces ABA release from human granulocytes and keratinocytes and that autocrine ABA stimulates cell functions involved in skin inflammation.