Posttranslational modifications of proteins by small ubiquitin-like modifiers (SUMOs) regulate protein degradation and localization, protein–protein interaction, and transcriptional activity. SUMO E3 ligase functions are executed by SIZ1/SIZ2 and Mms21 in yeast, the PIAS family members RanBP2, and Pc2 in human. The Arabidopsis thaliana genome contains only one gene, SIZ1, that is orthologous to the yeast SIZ1/SIZ2. Here, we show that Arabidopsis SIZ1 is expressed in all plant tissues. Compared with the wild type, the null mutant siz1-3 is smaller in stature because of reduced expression of genes involved in brassinosteroid biosynthesis and signaling. Drought stress induces the accumulation of SUMO-protein conjugates, which is in part dependent on SIZ1 but not on abscisic acid (ABA). Mutant plants of siz1-3 have significantly lower tolerance to drought stress. A genome-wide expression analysis identified ∼1700 Arabidopsis genes that are induced by drought, with SIZ1 mediating the expression of 300 of them by a pathway independent of DREB2A and ABA. SIZ1-dependent, drought-responsive genes include those encoding enzymes of the anthocyanin synthesis pathway and jasmonate response. From these results, we conclude that SIZ1 regulates Arabidopsis growth and that this SUMO E3 ligase plays a role in drought stress response likely through the regulation of gene expression.

One-fifth of irrigated agriculture is negatively affected by high soil salinity. The expected population growth, over 9 billion by 2050, enhances the pressure for agricultural production in marginal saline lands. Rice (Oryza sativa L.), the staple food for more than half of the world's population, is the most salt-sensitive cereal. The need for salt-tolerant rice varieties able to cope with several other stress conditions obviously puts a lot of pressure on breeders who must better comprehend the physiology and genetic control of salt tolerance. In spite of several good reviews recently published, an integrated vision of current information on rice tolerance to salt stress has been lacking. Here we present the most recent data on the salinity effect on rice physiology and stress adaptation, including implications on growth regulation and reproductive development. We have included an inventory of salt tolerance donors available for breeding programs and a comprehensive survey of current work on QTL detection and cloning as well as marker-assisted selection to introgress favorable alleles into elite rice lines. A schematic view of the rice chromosomes on which salt tolerance QTLs and candidate genes are positioned is also included. Finally, we focus on the most promising candidate genes involved in salt stress response. There, we discuss the available knowledge on salt stress signaling and ion homeostasis, LEAs and other stress-induced proteins, genes with unknown function and transcription regulators as well as the present knowledge on the role of post-translational modifications on the modulation of the response to salinity in rice. We conclude by highlighting still missing clues that could help to design better salt tolerant varieties, and we evaluate the significance of the data presented for the future of rice breeding and sustainability of the culture in marginal saline soils.

Summary: Salt stress is a complex physiological trait affecting plants by limiting growth and productivity. Rice, one of the most important food crops, is rated as salt‐sensitive. High‐throughput screening methods are required to exploit novel sources of genetic variation in rice and further improve salinity tolerance in breeding programmes. To search for genotypic differences related to salt stress, we genotyped 392 rice accessions by EcoTILLING. We targeted five key salt‐related genes involved in mechanisms such as Na⁺/K⁺ ratio equilibrium, signalling cascade and stress protection, and we found 40 new allelic variants in coding sequences. By performing association analyses using both general and mixed linear models, we identified 11 significant SNPs related to salinity. We further evaluated the putative consequences of these SNPs at the protein level using bioinformatic tools. Amongst the five nonsynonymous SNPs significantly associated with salt‐stress traits, we found a T67K mutation that may cause the destabilization of one transmembrane domain in OsHKT1;5, and a P140A alteration that significantly increases the probability of OsHKT1;5 phosphorylation. The K24E mutation can putatively affect SalT interaction with other proteins thus impacting its function. Our results have uncovered allelic variants affecting salinity tolerance that may be important in breeding.