SOS Signal Research Articles

Sodium (Na+) homeostasis and salt tolerance of plants

Soil and water salinity substantially constrain crop and biomass production. Research over the last two plus decades, facilitated by advances in molecular genetics and biotechnology, and with genetic model systems, has identified genes involved in salt acclimation or adaptation and linked these to critical mechanisms and processes. A case in point is present understanding of critical transport determinants that facilitate intra- and intercellular Na+ homeostasis of plants in saline environments predominated by NaCl. Pumps in the plasma membrane (H+-ATPase), and the tonoplast (H+-ATPase) and H+ pyrophosphatases (AVP1) generate proton electrochemical gradients necessary to energize Na+ efflux to the apoplast and influx into vacuoles, respectively. The plasma membrane Na+/H+ antiporter SOS1 is responsible for apoplastic efflux, and NHX type Na+/H+ antiporters for vacuolar and endosomal compartmentalization. Ca2+ext reduces passive intracellular Na+ influx cells by decreasing Na+ transport through high affinity K+ uptake systems and what are presumed to be nonselective cation channels, and activating, through the SOS signal pathway, the SOS1 plasma membrane Na+/H+ antiporter. Moreover, there is greater understanding about how cellular transport systems functionally integrate to facilitate tissue and organismal Na+ homeostasis. Notable in this process are HKT1 Na+ transporters, which regulate Na+ loading into the root xylem, limiting flux to and accumulation in the shoot. This review will summarize ion transport systems that facilitate plant Na+ homeostasis. Halophyte and glycophyte salinity responses and transport determinant function are compared and contrasted. The potential of halophytes as genetic resources for unique alleles or loci of transport protein genes and transcriptional and post-transcriptional regulation of transport protein function are discussed in the context of crop salt tolerance.

도난방지 및 구조신호 전송기능이 있는 저가형 농용트랙터 블랙박스 개발

Purpose: The inexpensive black box system was developed to acquire and save driving information, to give the slope information, and to transmit SOS and theft signal. Method: The device consists of a main micro controller to acquire and save data, a GPS sensor module, a CDMA module, a touch LCD module, a RF (Radio Frequency) ID module, a SD (Secure Digital) card module, an emergency electric power source, a theftproof circuit, and a sensing device. The sensing device consists of a 8 bit micro controller, a accelerometer to detect impulse, two slope sensors to detect roll and pitch angle and a circuit to detect operation of 6 lighting devices. Results: Test results are as follows: 1) a tractor can be start up only with an electronic key (password or RFID card), 2) theft signal was transmitted when a tractor moved without an electronic key, 3) SOS was transmitted at conditions that rollover or crash happened. 4) 5 more than per 1s data are recorded at 5 minute intervals as new file name in SD card. Conclusions: This system can be used to save travelling record, reduce accident, prevent theft and rescue life in the accidents.

ATM IN THE CYTOPLASM: ROS ACTING AS SOS SIGNALS

ATM IN THE CYTOPLASM: ROS ACTING AS SOS SIGNALS

Overexpression of SlSOS2 (SlCIPK24) confers salt tolerance to transgenic tomato

The Ca(2+)-dependent SOS pathway has emerged as a key mechanism in the homeostasis of Na(+) and K(+) under saline conditions. We have identified and functionally characterized the gene encoding the calcineurin-interacting protein kinase of the SOS pathway in tomato, SlSOS2. On the basis of protein sequence similarity and complementation studies in yeast and Arabidopsis, it can be concluded that SlSOS2 is the functional tomato homolog of Arabidopsis AtSOS2 and that SlSOS2 operates in a tomato SOS signal transduction pathway. The biotechnological potential of SlSOS2 to provide salt tolerance was evaluated by gene overexpression in tomato (Solanum lycopersicum L. cv. MicroTom). The better salt tolerance of transgenic plants relative to non-transformed tomato was shown by their faster relative growth rate, earlier flowering and higher fruit production when grown with NaCl. The increased salinity tolerance of SlSOS2-overexpressing plants was associated with higher sodium content in stems and leaves and with the induction and up-regulation of the plasma membrane Na(+)/H(+) (SlSOS1) and endosomal-vacuolar K(+), Na(+)/H(+) (LeNHX2 and LeNHX4) antiporters, responsible for Na(+) extrusion out of the root, active loading of Na(+) into the xylem, and Na(+) and K(+) compartmentalization.

Analysis of a salinity induced BjSOS3 protein from Brassica indicate it to be structurally and functionally related to its ortholog from Arabidopsis

Arabidopsis has been a favorite model system for plant biologist. It is anticipated that comparative analysis of this plant with other members of Brassicaceae may aid in identification of orthologs playing role as key genetic determinants for salinity response. In this endeavor, we have recently identified SOS family members from Brassica juncea in our laboratory and reported their salinity responsive transcriptional induction in seedlings of various diploid and amphidiploids species. In the present study, we have carried out detailed time kinetics for BjSOS3 expression in a salinity tolerant B.juncea var. CS52. Transcript analysis at the sensitive growth stages of plants viz. seedling and reproductive stage indicated clear differential transcriptional regulation of BjSOS3 under non-induced as well as salinity induced conditions in a time and organ specific manner, mirroring their respective tolerance physiology. Similar to its ortholog from Arabidopsis thaliana, the modeled BjSOS3 protein show typical features of a Ca(2+) binding protein with four conserved EF-hands. We have also attempted to study the binding of SOS3 protein with the modeled SOS2 protein. It has been established that SOS3 protein senses Ca(2+) though the binding is very weak; we show the down regulation of BjSOS3 mRNA in presence of calcium chelator - EGTA under the various stress conditions including ABA. In situ localization of BjSOS3-GFP fusion protein in onion peel has shown its presence strongly in plasma membrane as well as cytosol. The leads presented in the paper will assist in understanding and establishing the SOS signaling machinery in B.juncea.

SOS3 mediates lateral root development under low salt stress through regulation of auxin redistribution and maxima in Arabidopsis

• The SOS signaling pathway plays an important role in plant salt tolerance. However, little is known about how the SOS pathway modulates organ development in response to salt stress. Here, the involvement of SOS signaling in NaCl-induced lateral root (LR) development in Arabidopsis was assessed. • Wild-type and sos3-1 mutant seedlings on iso-osmotic concentrations of NaCl and mannitol were analyzed. The marker lines for auxin accumulation, auxin transport, cell division activity and stem cells were also examined. • The results showed that ionic effect alleviates the inhibitory effects of osmotic stress on LR development. LR development of the sos3-1 mutant showed increased sensitivity specifically to low salt. Under low-salt conditions, auxin in cotyledons and LR primordia (LRP) of the sos3-1 mutant was markedly reduced. Decreases in auxin polar transport of mutant roots may cause insufficient auxin supply, resulting in defects not only in LR initiation but also in cell division activity in LRP. • Our data uncover a novel role of the SOS3 gene in modulation of LR developmental plasticity and adaptation in response to low salt stress, and reveal a new mechanism for plants to sense and adapt to small changes of salt.

Making Cellular Memories

The induction of a protracted response to a brief stimulus is a form of cellular memory. Here we describe the role of transcriptional regulation in both natural and synthetic memory networks and discuss the potential applications of engineered memory networks in medicine and industrial biotechnology.

Hormetic Triggers for Intervention in Aging, Disease and Trauma

Hormesis refers to the ability of a chemical or physical agent to condition the physiological state of an organism to tolerate stress with low doses of otherwise harmful agents. Evolutionary evidence shows that the survival and longevity of species hinge on their optimal ability to resist stress challenge. Hormesis is a potent strategy to stimulate latent repair processes to tolerate a specific challenge. Examples of hormetic agent-mimetics, which induce at least partial physiological conditioning, activate known pathways of longevity determinants, i.e., genetic stability, altered metabolism, immunoregulation and stress resistance. Despite the diversity of age-related diseases, glucose and oxidation-mediated protein and DNA damage are common denominators. The associated physiological conditioning-benefits may trigger: 1) activation of latent stress resistance pathways of youthful DNA repair; 2) increased resistance to oxidizing pollutants; 3) improved protein structure and function; 4) improved immunity; 5) damaged tissue remodeling; 6) adjustments in central and peripheral nervous systems; 7) altered metabolism; and 8) delay or breaking of inappropriate protein cross-links. Hormetic mimetics have intervention potential in cancer, diabetes, age-related diseases, infectious diseases, heart and kidney failure, cardiovascular diseases and Alzheimer’s disease. Small nucleotide SOS signals, dipeptides, ethanol, thiols, and metals and conserved peptide sequences found in sharks, frogs, woodchucks, and bears, can regulate cytokines, cellular immunity, and central and peripheral neuronal regulatory pathways to promote healthy blood pressure maintenance, heart rate, and metabolic pathways. disease sensitivity. Conserved stress mimetics are highlighted here that rejuvenate DNA and proteins repair and thus may intervene in aging, disease, and trauma. Hibernation Induction Trigger mimetics, Deltorphins, emerge as novel hormetic agents, effective both as pre and post exposure to physiological conditioners to tolerate stress, and prevent damage, and delay possibly aging. Hormesis mimetics offer powerful survival strategies, with better control over the beneficial dose response. Combinations of several mimetics may more closely mimic environmental challenges, which stimulate multiple stress responses.

The Arabidopsis Kinase-Associated Protein Phosphatase Regulates Adaptation to Na+ Stress

The kinase-associated protein phosphatase (KAPP) is a regulator of the receptor-like kinase (RLK) signaling pathway. Loss-of-function mutations rag1-1 (root attenuated growth1-1) and rag1-2, in the locus encoding KAPP, cause NaCl hypersensitivity in Arabidopsis thaliana. The NaCl hypersensitive phenotype exhibited by rag1 seedlings includes reduced shoot and primary root growth, root tip swelling, and increased lateral root formation. The phenotype exhibited by rag1-1 seedlings is associated with a specific response to Na(+) toxicity. The sensitivity to Na(+) is Ca(2+) independent and is not due to altered intracellular K(+)/Na(+). Analysis of the genetic interaction between rag1-1 and salt overly sensitive1 (sos1-14) revealed that KAPP is not a component of the SOS signal transduction pathway, the only Na(+) homeostasis signaling pathway identified so far in plants. All together, these results implicate KAPP as a functional component of the RLK signaling pathway, which also mediates adaptation to Na(+) stress. RLK pathway components, known to be modulated by NaCl at the messenger RNA level, are constitutively down-regulated in rag1-1 mutant plants. The effect of NaCl on their expression is not altered by the rag1-1 mutation.

Salt Modulates Gravity Signaling Pathway to Regulate Growth Direction of Primary Roots in Arabidopsis

Plant root architecture is highly plastic during development and can adapt to many environmental stresses. The proper distribution of roots within the soil under various conditions such as salinity, water deficit, and nutrient deficiency greatly affects plant survival. Salinity profoundly affects the root system architecture of Arabidopsis (Arabidopsis thaliana). However, despite the inhibitory effects of salinity on root length and the number of roots, very little is known concerning influence of salinity on root growth direction and the underlying mechanisms. Here we show that salt modulates root growth direction by reducing the gravity response. Exposure to salt stress causes rapid degradation of amyloplasts in root columella cells of Arabidopsis. The altered root growth direction in response to salt was found to be correlated with PIN-FORMED2 (PIN2) messenger RNA abundance and expression and localization of the protein. Furthermore, responsiveness to gravity of salt overly sensitive (sos) mutants is substantially reduced, indicating that salt-induced altered gravitropism of root growth is mediated by ion disequilibrium. Mutation of SOS genes also leads to reduced amyloplast degradation in root tip columella cells and the defects in PIN2 gene expression in response to salt stress. These results indicate that the SOS pathway may mediate the decrease of PIN2 messenger RNA in salinity-induced modification of gravitropic response in Arabidopsis roots. Our findings provide new insights into the development of a root system necessary for plant adaptation to high salinity and implicate an important role of the SOS signaling pathway in this process.

SOS Regulation of the Type III Secretion System of EnteropathogenicEscherichia coli

Genomes of bacterial pathogens contain and coordinately regulate virulence-associated genes in order to cause disease. Enteropathogenic Escherichia coli (EPEC), a major cause of watery diarrhea in infants and a model gram-negative pathogen, expresses a type III secretion system (TTSS) that is encoded by the locus of enterocyte effacement (LEE) and is necessary for causing attaching and effacing intestinal lesions. Effector proteins encoded by the LEE and in cryptic prophage are injected into the host cell cytoplasm by the TTTS apparatus, ultimately leading to diarrhea. The LEE is comprised of multiple polycistronic operons, most of which are controlled by the global, positive regulator Ler. Here we demonstrated that the LEE2 and LEE3 operons also responded to SOS signaling and that this regulation was LexA dependent. As determined by a DNase I protection assay, purified LexA protein bound in vitro to a predicted SOS box located in the divergent, overlapping LEE2/LEE3 promoters. Expression of the lexA1 allele, encoding an uncleavable LexA protein in EPEC, resulted in reduced secretion, particularly in the absence of the Ler regulator. Finally, we obtained evidence that the cryptic phage-located nleA gene encoding an effector molecule is SOS regulated. Thus, we demonstrated, for the first time to our knowledge, that genes encoding components of a TTSS are regulated by the SOS response, and our data might explain how a subset of EPEC effector proteins, encoded in cryptic prophages, are coordinately regulated with the LEE-encoded TTSS necessary for their translocation into host cells.

Serotonin's SOS signal

Neurotransmitters relay signals within the brain and to peripheral tissues, allowing communication between nerve cells. New work from in this issue of Cell Metabolism reveals that, in C. elegans, serotonin functions during conditions of stress through the well-characterized insulin/IGF-1 signaling pathway, suggesting a mechanism for the stress response.

Stochastic models for regulatory networks of the genetic toggle switch

Bistability arises within a wide range of biological systems from the lambda phage switch in bacteria to cellular signal transduction pathways in mammalian cells. Changes in regulatory mechanisms may result in genetic switching in a bistable system. Recently, more and more experimental evidence in the form of bimodal population distributions indicates that noise plays a very important role in the switching of bistable systems. Although deterministic models have been used for studying the existence of bistability properties under various system conditions, these models cannot realize cell-to-cell fluctuations in genetic switching. However, there is a lag in the development of stochastic models for studying the impact of noise in bistable systems because of the lack of detailed knowledge of biochemical reactions, kinetic rates, and molecular numbers. In this work, we develop a previously undescribed general technique for developing quantitative stochastic models for large-scale genetic regulatory networks by introducing Poisson random variables into deterministic models described by ordinary differential equations. Two stochastic models have been proposed for the genetic toggle switch interfaced with either the SOS signaling pathway or a quorum-sensing signaling pathway, and we have successfully realized experimental results showing bimodal population distributions. Because the introduced stochastic models are based on widely used ordinary differential equation models, the success of this work suggests that this approach is a very promising one for studying noise in large-scale genetic regulatory networks.

Ca2+ sparks – SOS signals of struggling muscle

Ca2+ sparks – SOS signals of struggling muscle

The TAO-Gen Algorithm for Identifying Gene Interaction Networks with Application to SOS Repair in E. coli

One major unresolved issue in the analysis of gene expression data is the identification and quantification of gene regulatory networks. Several methods have been proposed for identifying gene regulatory networks, but these methods predominantly focus on the use of multiple pairwise comparisons to identify the network structure. In this article, we describe a method for analyzing gene expression data to determine a regulatory structure consistent with an observed set of expression profiles. Unlike other methods this method goes beyond pairwise evaluations by using likelihood-based statistical methods to obtain the network that is most consistent with the complete data set. The proposed algorithm performs accurately for moderate-sized networks with most errors being minor additions of linkages. However, the analysis also indicates that sample sizes may need to be increased to uniquely identify even moderate-sized networks. The method is used to evaluate interactions between genes in the SOS signaling pathway in Escherichia coli using gene expression data where each gene in the network is over-expressed using plasmids inserts.

Signal processing at the Ras circuit: what shapes Ras activation patterns?

A systems biology approach is applied to gain a quantitative understanding of the integration of signalling by the small GTPase Ras. The Ras protein acts as a critical switch in response to signals that determine the cell's fate. In unstimulated cells, Ras switching between an inactive GDP-binding and active GTP-binding state is controlled by the intrinsic catalytic activities of Ras. The calculated high sensitivity of the basal Ras-GTP fraction to changes in the rate constant of GTP-hydrolysis by Ras can account for the carcinogenic potential of Ras mutants with decreased GTPase activities. Extracelluar stimuli initiate Ras interactions with GDP/GTP exchange factors such as SOS, and GTP-hydrolysis activating proteins such as RasGAP. Our data on freshly isolated hepatocytes stimulated with epidermal growth factor (EGF) show transient SOS activation and sustained Ras-GTP patterns. We demonstrate that these dose-response data can only be explained by transient RasGAP activitation, and not by merely switching off the SOS signal, e.g. by inhibitory phosphorylation of SOS. A transient RasGAP activity can be brought about by a number of mechanisms. A comprehensive kinetic model of the EGF receptor (EGFR) network was developed to explore feasible molecular scenarios, including the receptor-mediated recruitment of SOS and RasGAP to the plasma membrane, phosphorylation of RasGAP and p190 RhoGAP by soluble tyrosine kinases, and RasGAP interactions with phosphoinositides and p190 RhoGAP. We show that a transient RasGAP association with EGFR followed by the capture of RasGAP through the formation of complexes with p190 RhoGAP can account for data on hepatocytes. In summary, our results demonstrate that a combination of experimental monitoring and integrated dynamic analysis is capable of dissecting regulatory mechanisms that govern cellular signal transduction.

Programmable cells: interfacing natural and engineered gene networks.

Novel cellular behaviors and characteristics can be obtained by coupling engineered gene networks to the cell's natural regulatory circuitry through appropriately designed input and output interfaces. Here, we demonstrate how an engineered genetic circuit can be used to construct cells that respond to biological signals in a predetermined and programmable fashion. We employ a modular design strategy to create Escherichia coli strains where a genetic toggle switch is interfaced with: (i) the SOS signaling pathway responding to DNA damage, and (ii) a transgenic quorum sensing signaling pathway from Vibrio fischeri. The genetic toggle switch endows these strains with binary response dynamics and an epigenetic inheritance that supports a persistent phenotypic alteration in response to transient signals. These features are exploited to engineer cells that form biofilms in response to DNA-damaging agents and cells that activate protein synthesis when the cell population reaches a critical density. Our work represents a step toward the development of "plug-and-play" genetic circuitry that can be used to create cells with programmable behaviors.

海中転落者のための救助システムについて-II : 特定小電力無線機を用いた救助システム

In the previous paper, we proposed and evaluated a worldwide usable rescue system, which was based on the use of the mobile device combining the GPS unit and the satellite communication unit. However, the system was not practically applicable because the problem of the size reduction of the mobile device remained unresolved. In this paper, we proposed a new rescue system, which was based on the use of a special low-power transmitter. According to the statistics by Japan Coast Guard, two thirds of man-overboard accidents occurred near by own vessels or in the inshore area. Therefore, we propose a relay system for indirect sending of the SOS signal from the victim through the vessel or the onshore equipment. Realization of the system ensures the size reduction of the mobile device, which performs only the startup function of the relay unit, while the GPS and the satellite communication unit are integrated into the relay unit. The experiments have been carried out at the lake area, inshore area and offshore area. As a result, the special low-power transmitter is able to activate the relay unit in the range of 1, 000m. The proposed rescue system is characterized with the high practical applicability due to the size reduction of the mobile device.

Genes that are uniquely stress regulated in salt overly sensitive (sos) mutants.

Repetitive rounds of differential subtraction screening, followed by nucleotide sequence determination and northern-blot analysis, identified 84 salt-regulated (160 mM NaCl for 4 h) genes in Arabidopsis wild-type (Col-0 gl1) seedlings. Probes corresponding to these 84 genes and ACP1, RD22BP1, MYB2, STZ, and PAL were included in an analysis of salt responsive gene expression profiles in gl1 and the salt-hypersensitive mutant sos3. Six of 89 genes were expressed differentially in wild-type and sos3 seedlings; steady-state mRNA abundance of five genes (AD06C08/unknown, AD05E05/vegetative storage protein 2 [VSP2], AD05B11/S-adenosyl-L-Met:salicylic acid carboxyl methyltransferase [SAMT], AD03D05/cold regulated 6.6/inducible2 [COR6.6/KIN2], and salt tolerance zinc finger [STZ]) was induced and the abundance of one gene (AD05C10/circadian rhythm-RNA binding1 [CCR1]) was reduced in wild-type plants after salt treatment. The expression of CCR1, SAMT, COR6.6/KIN2, and STZ was higher in sos3 than in wild type, and VSP2 and AD06C08/unknown was lower in the mutant. Salt-induced expression of VSP2 in sos1 was similar to wild type, and AD06C08/unknown, CCR1, SAMT, COR6.6/KIN2, and STZ were similar to sos3. VSP2 is regulated presumably by SOS2/3 independent of SOS1, whereas the expression of the others is SOS1 dependent. AD06C08/unknown and VSP2 are postulated to be effectors of salt tolerance whereas CCR1, SAMT, COR6.6/KIN2, and STZ are determinants that must be negatively regulated during salt adaptation. The pivotal function of the SOS signal pathway to mediate ion homeostasis and salt tolerance implicates AD06C08/unknown, VSP2, SAMT, 6.6/KIN2, STZ, and CCR1 as determinates that are involved in salt adaptation.

A model for the abrogation of the SOS response by an SOS protein: a negatively charged helix in DinI mimics DNA in its interaction with RecA.

DinI is a recently described negative regulator of the SOS response in Escherichia coli. Here we show that it physically interacts with RecA and prevents the binding of single-stranded DNA to RecA, which is required for the activation of the latter. DinI also displaces ssDNA from a stable RecA-DNA cofilament, thus eliminating the SOS signal. In addition, DinI inhibits RecA-mediated homologous DNA pairing, but has no effect on actively proceeding strand exchange. Biochemical data, together with the molecular structure, define the C-terminal alpha-helix in DinI as the active site of the protein. In an unusual example of molecular mimicry, a negatively charged surface on this alpha-helix, by imitating single-stranded DNA, interacts with the loop L2 homologous pairing region of RecA and interferes with the activation of RecA.