Environmental stress activation of plant long-terminal repeat retrotransposons.

Genomic retrotransposons (RTs) are major components of most plant genomes. They spread throughout the genomes by a process termed retrotransposition, which consists of reverse transcription and reinsertion of the copied element into a new genomic location (a copy-and-paste system). Abiotic and biotic stresses activate long-terminal repeat (LTR) RTs in photosynthetic eukaryotes from algae to angiosperms. LTR RTs could represent a threat to the integrity of host genomes because of their activity and mutagenic potential by epigenetic regulation. Host genomes have developed mechanisms to control the activity of the retroelements and their mutagenic potential. Some LTR RTs escape these defense mechanisms, and maintain their ability to be activated and transpose as a result of biotic or abiotic stress stimuli. These stimuli include pathogen infection, mechanical damage, in vitro tissue culturing, heat, drought and salt stress, generation of doubled haploids, X-ray irradiation and many others. Reactivation of LTR RTs differs between different plant genomes. The expression levels of reactivated RTs are influenced by the transcriptional and post-transcriptional gene silencing mechanisms (e.g. DNA methylation, heterochromatin formation and RNA interference). Moreover, the insertion of RTs (e.g. Triticum aestivum L. Wis2-1A) into or next to coding regions of the host genome can generate changes in the expression of adjacent host genes of the host. In this paper, we review the ways that plant genomic LTR RTs are activated by environmental stimuli to affect restructuring and diversification of the host genome.

Control of glycerol biosynthesis under high salt stress in Arabidopsis.

Loss-of-function and gain-of-function approaches were utilised to detect the physiological importance of glycerol biosynthesis during salt stress and the role of glycerol in conferring salt tolerance in Arabidopsis. The salt stress experiment involved wild type (WT) and transgenic Arabidopsis overexpressing the yeast GPD1 gene (analogue of Arabidopsis GLY1 gene). The experiment also involved the Arabidopsis T-DNA insertion mutants gly1 (for suppression of glycerol 3-phosphate dehydrogenase or G3PDH), gli1 (for suppression of glycerol kinase or GK), and act1 (for suppression of G3P acyltransferase or GPAT). We evaluated salt tolerance levels, in conjunction with glycerol and glycerol 3-phosphate (G3P) levels and activities of six enzymes (G3PDH, ADH (alcohol dehydrogenase), ALDH (aldehyde dehydrogenase), GK, G3PP (G3P phosphatase) and GLYDH (glycerol dehydrogenase)) involved in the glycerol pathway. The GPD1 gene was used to overexpress G3PDH, a cytosolic NAD+-dependent key enzyme of cellular glycerol biosynthesis essential for growth of cells under abiotic stresses. T2 GPD1-transgenic plants and those of the two mutants gli1 and act1 showed enhanced salt tolerance during different growth stages as compared with the WT and gly1 mutant plants. These results indicate that the participation of glycerol, rather than G3P, in salt tolerance in Arabidopsis. The results also indicate that the gradual increase in glycerol levels in T2 GPD1-transgenic, and gli1 and act1 mutant plants as NaCl level increases whereas they dropped at 200mM NaCl. However, the activities of the G3PDH, GK, G3PP and GLYDH at 150 and 200mM NaCl were not significantly different. We hypothesise that mechanism(s) of glycerol retention/efflux in the cell are affected at 200mM NaCl in Arabidopsis.