The physiological and molecular mechanisms of tolerance to osmotic and ionic components of salinity stress are reviewed at the cellular, organ, and whole-plant level. Plant growth responds to salinity in two phases: a rapid, osmotic phase that inhibits growth of young leaves, and a slower, ionic phase that accelerates senescence of mature leaves. Plant adaptations to salinity are of three distinct types: osmotic stress tolerance, Na + or Cl − exclusion, and the tolerance of tissue to accumulated Na + or Cl − . Our understanding of the role of the HKT gene family in Na + exclusion from leaves is increasing, as is the understanding of the molecular bases for many other transport processes at the cellular level. However, we have a limited molecular understanding of the overall control of Na + accumulation and of osmotic stress tolerance at the whole-plant level. Molecular genetics and functional genomics provide a new opportunity to synthesize molecular and physiological knowledge to improve the salinity tolerance of plants relevant to food production and environmental sustainability.

https://rodas5.us.es/file/c2a700e9-8b4a-1970-d343-4a269c302970/1/estres_salino_bibliografia_scorm.zip/files/estres_salino_bibliografia.pdf

Mechanisms of salinity tolerance

Plant responses to salt and water stress have much in common. Salinity reduces the ability of plants to take up water, and this quickly causes reductions in growth rate, along with a suite of metabolic changes identical to those caused by water stress. The initial reduction in shoot growth is probably due to hormonal signals generated by the roots. There may be salt-specific effects that later have an impact on growth; if excessive amounts of salt enter the plant, salt will eventually rise to toxic levels in the older transpiring leaves, causing premature senescence, and reduce the photosynthetic leaf area of the plant to a level that cannot sustain growth. These effects take time to develop. Salttolerant plants differ from salt-sensitive ones in having a low rate of Na + and Cl ‐ transport to leaves, and the ability to compartmentalize these ions in vacuoles to prevent their build-up in cytoplasm or cell walls and thus avoid salt toxicity. In order to understand the processes that give rise to tolerance of salt, as distinct from tolerance of osmotic stress, and to identify genes that control the transport of salt across membranes, it is important to avoid treatments that induce cell plasmolysis, and to design experiments that distinguish between tolerance of salt and tolerance of water stress.

https://onlinelibrary.wiley.com/doi/pdf/10.1046/j.0016-8025.2001.00808.x

Comparative physiology of salt and water stress

Salt and drought stress signal transduction consists of ionic and osmotic homeostasis signaling pathways, detoxification (i.e., damage control and repair) response pathways, and pathways for growth regulation. The ionic aspect of salt stress is signaled via the SOS pathway where a calcium-responsive SOS3-SOS2 protein kinase complex controls the expression and activity of ion transporters such as SOS1. Osmotic stress activates several protein kinases including mitogen-activated kinases, which may mediate osmotic homeostasis and/or detoxification responses. A number of phospholipid systems are activated by osmotic stress, generating a diverse array of messenger molecules, some of which may function upstream of the osmotic stress-activated protein kinases. Abscisic acid biosynthesis is regulated by osmotic stress at multiple steps. Both ABA-dependent and -independent osmotic stress signaling first modify constitutively expressed transcription factors, leading to the expression of early response transcriptional activators, which then activate downstream stress tolerance effector genes.

/pdf/salt-and-drought-stress-signal-transduction-in-plants-4bj87ki2ww.pdf

Salt and drought stress signal transduction in plants

▪ Abstract Plant responses to salinity stress are reviewed with emphasis on molecular mechanisms of signal transduction and on the physiological consequences of altered gene expression that affect biochemical reactions downstream of stress sensing. We make extensive use of comparisons with model organisms, halophytic plants, and yeast, which provide a paradigm for many responses to salinity exhibited by stress-sensitive plants. Among biochemical responses, we emphasize osmolyte biosynthesis and function, water flux control, and membrane transport of ions for maintenance and re-establishment of homeostasis. The advances in understanding the effectiveness of stress responses, and distinctions between pathology and adaptive advantage, are increasingly based on transgenic plant and mutant analyses, in particular the analysis of Arabidopsis mutants defective in elements of stress signal transduction pathways. We summarize evidence for plant stress signaling systems, some of which have components analogous to t...

Plant cellular and molecular responses to high salinity.

Roles of glycine betaine and proline in improving plant abiotic stress resistance

Heterochromatin is a tightly packed form of chromatin that is associated with DNA methylation and histone 3 lysine 9 methylation (H3K9me). Here, we identify an H3K9me2-binding protein, Agenet domain (AGD)-containing p1 (AGDP1), in Arabidopsis thaliana. Here we find that AGDP1 can specifically recognize the H3K9me2 mark by its three pairs of tandem AGDs. We determine the crystal structure of the Agenet domain 1 and 2 cassette (AGD12) of Raphanus sativus AGDP1 in complex with an H3K9me2 peptide. In the complex, the histone peptide adopts a unique helical conformation. AGD12 specifically recognizes the H3K4me0 and H3K9me2 marks by hydrogen bonding and hydrophobic interactions. In addition, we find that AGDP1 is required for transcriptional silencing, non-CG DNA methylation, and H3K9 dimethylation at some loci. ChIP-seq data show that AGDP1 preferentially occupies long transposons and is associated with heterochromatin marks. Our findings suggest that, as a heterochromatin-binding protein, AGDP1 links H3K9me2 to DNA methylation in heterochromatin regions. DNA methylation and H3K9 dimethylation are two linked epigenetic marks of silenced chromatin in plants that depend on the activity of CMT3/2 and SUVH4/5/6. Here the authors identify AGDP1 as an H3K9me2-binding protein required for heterochromatic non-CG DNA methylation, H3K9 dimethylation, and transcriptional silencing.

/pdf/arabidopsis-agdp1-links-h3k9me2-to-dna-methylation-in-205qee50d6.pdf

Arabidopsis AGDP1 links H3K9me2 to DNA methylation in heterochromatin

Protease inhibitors from several classes work synergistically against Callosobruchus maculatus

The gene encoding the antifungal protein osmotin is induced by several hormonal and environmental signals In this study, tissue-specific and inducer-mediated expression of the reporter gene beta-glucuronidase (uidA) fused to different fragment lengths of the osmotin promoter was evaluated in transgenic tobacco (Nicotiana tabacum) The region of the promoter between -248 to -108 (Fragment A) was found to be essential and sufficient for inducer (abscisic acid (ABA), C2H4 and NaCl)-mediated expression of the reporter gene Expression of the reporter gene was developmentally regulated and increased with maturity of leaves, stem and flowers Expression also was tissue-specific being most highly expressed in epidermis and vascular parenchyma of the stem The regulators ABA, C2H4 and NaCl exhibited tissue-specific induction of this promoter The promoter was specifically responsive to C2H4 in flowers at virtually all stages of development, but not responsive in these tissues to ABA or NaCl Conversely, ABA and NaCl were able to induce reporter gene activity using promoter Fragment A in specific tissues of root where C2H4 was unable to induce activity Further dissection of the promoter Fragment A into fragments containing either the conserved GCC element (PR); PR/AT; or G/AT sequences, and subsequent testing of these fragments fused to GUS in transgenic plants was performed These experiments revealed that the promoter fragment containing PR element alone, although required, was barely able to allow responsiveness to C2H4 However, significant C2H4-induced activity was obtained with a promoter fragment containing the AT and PR elements together

Tissue-specific activation of the osmotin gene by ABA, C2H4 and NaCl involves the same promoter region.

Reduced cell expansion and changes in cell walls of plant cells adapted to NaCl

Fusarium oxysporum f. sp. nicotianae is a causal agent for vascular wilt disease in tobacco. It is sensitive to osmotin, a tobacco pathogenesis-related protein (PR-5) that is implicated in plant defense against phytopathogenic fungi. We show that osmotin susceptibility of F. oxysporum f. sp. nicotianae was reduced by overexpression of the heterologous cell wall glycoprotein Saccharomyces cerevisiae protein containing inverted repeats (PIR2), a member of the PIR family of fungal cell wall glycoproteins that protect S. cerevisiae from the toxic action of osmotin. S. cerevisiae PIR2 was targeted to the cell wall of F. oxysporum. Disease severity and fungal growth were increased in tobacco seedlings inoculated with F. oxysporum transformed with PIR2 compared to seedlings infected with untransformed F. oxysporum or that transformed with vector, although accumulation of transcript and protein of defense genes was similar. The results show that fungal cell wall components can increase resistance to plant defense proteins and affect virulence.

Ray A. Bressan

Papers

Arabidopsis AGDP1 links H3K9me2 to DNA methylation in heterochromatin

Protease inhibitors from several classes work synergistically against Callosobruchus maculatus

Tissue-specific activation of the osmotin gene by ABA, C2H4 and NaCl involves the same promoter region.

Reduced cell expansion and changes in cell walls of plant cells adapted to NaCl

Overexpression of a cell wall glycoprotein in Fusarium oxysporum increases virulence and resistance to a plant PR-5 protein.