Genetic analysis of osmotic and cold stress signal transduction in Arabidopsis: interactions and convergence of abscisic acid-dependent and abscisic acid-independent pathways.

Chilling and freezing temperatures adversely affect the productivity and quality of crops. Hence improving the cold hardiness of crop plants is an important goal in agriculture, which demands a clear understanding of cold stress signal perception and transduction. Pharmacological and biochemical evidence shows that membrane rigidification followed by cytoskeleton rearrangement, Ca 2+ influx and Ca 2+ –dependent phosphorylation are involved in cold stress signal transduction. Cold–responsive genes are regulated through C–repeat/dehydration–responsive elements (CRT/DRE) and abscisic acid (ABA)–responsive element cis elements by transacting factors C–repeat binding factors/dehydration–responsive element binding proteins (CBFs/DREBs) and basic leucine zippers (bZIPs) (SGBF1), respectively. We have carried out a forward genetic analysis using chemically mutagenized Arabidopsis plants expressing cold–responsive RD29A promoter–driven luciferase to dissect cold signal transduction. We have isolated the fiery1 ( fry1 ) mutant and cloned the FRY1 gene, which encodes an inositol polyphosphate 1–phosphatase. The fry1 plants showed enhanced induction of stress genes in response to cold, ABA, salt and dehydration due to higher accumulation of the second messenger, inositol (1,4,5)– triphosphate (IP 3 ). Thus our study provides genetic evidence suggesting that cold signal is transduced through changes in IP 3 levels. We have also identified the hos1 mutation, which showed super induction of cold–responsive genes and their transcriptional activators. Molecular cloning and characterization revealed that HOS1 encodes a ring finger protein, which has been implicated as an E3 ubiquitin conjugating enzyme. HOS1 is present in the cytoplasm at normal growth temperatures but accumulates in the nucleus upon cold stress. HOS1 appears to regulate temperature sensing by the cell as cold–responsive gene expression occurs in the hos1 mutant at relatively warm temperatures. Thus HOS1 is a negative regulator, which may be functionally linked to cellular thermosensors to modulate cold–responsive gene transcription.

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Sugar/osmoticum levels modulate differential abscisic acid-independent expression of two stress-responsive sucrose synthase genes in Arabidopsis

Biochemical Journal ◽

10.1042/bj3440503 ◽

1999 ◽

Vol 344 (2) ◽

pp. 503-509 ◽

Cited By ~ 47

Author(s):

Annabelle DÉJARDIN ◽

Lubomir N. SOKOLOV ◽

Leszek A. KLECZKOWSKI

Keyword(s):

Signal Transduction ◽

Abscisic Acid ◽

Cold Stress ◽

Osmotic Potential ◽

Sucrose Synthase ◽

Cellular Response ◽

Expression Profiles ◽

Soluble Sugars ◽

Leaf Osmotic Potential ◽

Detached Leaves

Sucrose synthase (Sus) is a key enzyme of sucrose metabolism. Two Sus-encoding genes (Sus1 and Sus2) from Arabidopsis thaliana were found to be profoundly and differentially regulated in leaves exposed to environmental stresses (cold stress, drought or O2 deficiency). Transcript levels of Sus1 increased on exposure to cold and drought, whereas Sus2 mRNA was induced specifically by O2 deficiency. Both cold and drought exposures induced the accumulation of soluble sugars and caused a decrease in leaf osmotic potential, whereas O2 deficiency was characterized by a nearly complete depletion in sugars. Feeding abscisic acid (ABA) to detached leaves or subjecting Arabidopsis ABA-deficient mutants to cold stress conditions had no effect on the expression profiles of Sus1 or Sus2, whereas feeding metabolizable sugars (sucrose or glucose) or non-metabolizable osmotica [poly(ethylene glycol), sorbitol or mannitol] mimicked the effects of osmotic stress on Sus1 expression in detached leaves. By using various sucrose/mannitol solutions, we demonstrated that Sus1 was up-regulated by a decrease in leaf osmotic potential rather than an increase in sucrose concentration itself. We suggest that Sus1 expression is regulated via an ABA-independent signal transduction pathway that is related to the perception of a decrease in leaf osmotic potential during stresses. In contrast, the expression of Sus2 was independent of sugar/osmoticum effects, suggesting the involvement of a signal transduction mechanism distinct from that regulating Sus1 expression. The differential stress-responsive regulation of Sus genes in leaves might represent part of a general cellular response to the allocation of carbohydrates during acclimation processes.

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MAP3Kinase-dependent SnRK2-kinase activation is required for abscisic acid signal transduction and rapid osmotic stress response

Nature Communications ◽

10.1038/s41467-019-13875-y ◽

2020 ◽

Vol 11 (1) ◽

Cited By ~ 24

Author(s):

Yohei Takahashi ◽

Jingbo Zhang ◽

Po-Kai Hsu ◽

Paulo H. O. Ceciliato ◽

Li Zhang ◽

...

Keyword(s):

Signal Transduction ◽

Abscisic Acid ◽

Osmotic Stress ◽

Knock Out ◽

Kinase Activation ◽

Aba Signal Transduction ◽

Osmotic Stress Response ◽

Stress Signal ◽

Biochemical Analyses

AbstractAbiotic stresses, including drought and salinity, trigger a complex osmotic-stress and abscisic acid (ABA) signal transduction network. The core ABA signalling components are snf1-related protein kinase2s (SnRK2s), which are activated by ABA-triggered inhibition of type-2C protein-phosphatases (PP2Cs). SnRK2 kinases are also activated by a rapid, largely unknown, ABA-independent osmotic-stress signalling pathway. Here, through a combination of a redundancy-circumventing genetic screen and biochemical analyses, we have identified functionally-redundant MAPKK-kinases (M3Ks) that are necessary for activation of SnRK2 kinases. These M3Ks phosphorylate a specific SnRK2/OST1 site, which is indispensable for ABA-induced reactivation of PP2C-dephosphorylated SnRK2 kinases. ABA-triggered SnRK2 activation, transcription factor phosphorylation and SLAC1 activation require these M3Ks in vitro and in plants. M3K triple knock-out plants show reduced ABA sensitivity and strongly impaired rapid osmotic-stress-induced SnRK2 activation. These findings demonstrate that this M3K clade is required for ABA- and osmotic-stress-activation of SnRK2 kinases, enabling robust ABA and osmotic stress signal transduction.

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