Abiotic stresses, especially cold, salinity and drought, are the primary causes of crop loss worldwide. Plant adaptation to environmental stresses is dependent upon the activation of cascades of molecular networks involved in stress perception, signal transduction, and the expression of specific stress-related genes and metabolites. Plants have stress-specific adaptive responses as well as responses which protect the plants from more than one environmental stress. There are multiple stress perception and signaling pathways, some of which are specific, but others may cross-talk at various steps. In this review article, we first expound the general stress signal transduction pathways, and then highlight various aspects of biotic stresses signal transduction networks. On the genetic analysis, many cold induced pathways are activated to protect plants from deleterious effects of cold stress, but till date, most studied pathway is ICE-CBF-COR signaling pathway. The Salt-Overly-Sensitive (SOS) pathway, identified through isolation and study of the sos1, sos2, and sos3 mutants, is essential for maintaining favorable ion ratios in the cytoplasm and for tolerance of salt stress. Both ABA-dependent and -independent signaling pathways appear to be involved in osmotic stress tolerance. ROS play a dual role in the response of plants to abiotic stresses functioning as toxic by-products of stress metabolism, as well as important signal transduction molecules and the ROS signaling networks can control growth, development, and stress response. Finally, we talk about the common regulatory system and cross-talk among biotic stresses, with particular emphasis on the MAPK cascades and the cross-talk between ABA signaling and biotic signaling.

Chemotaxis-competent cells respond to a variety of ligands by activating second messenger pathways leading to changes in the actin/myosin cytoskeleton and directed cell movement. We demonstrate that Dictyostelium Akt/PKB, a homologue of mammalian Akt/ PKB, is very rapidly and transiently activated by the chemoattractant cAMP. This activation takes place through G protein-coupled chemoattractant receptors via a pathway that requires homologues of mammalian p110 phosphoinositide-3 kinase. pkbA null cells exhibit aggregation-stage defects that include aberrant chemotaxis, a failure to polarize properly in a chemoattractant gradient and aggregation at low densities. Mechanistically, we demonstrate that the PH domain of Akt/ PKB fused to GFP transiently translocates to the plasma membrane in response to cAMP with kinetics similar to those of Akt/PKB kinase activation and is localized to the leading edge of chemotaxing cells in vivo. Our results indicate Akt/PKB is part of the regulatory network required for sensing and responding to the chemoattractant gradient that mediates chemotaxis and aggregation.

Insulin/IGF-1 signaling (IIS) regulates aging in worms, flies, and mice through a well-characterized, highly conserved core set of components. IIS also regulates early developmental decisions, the reproductive status of the animal, innate immunity, and stress-resistance functions. In C. elegans, the sole insulin/IGF-1 receptor, DAF-2, negatively regulates the FOXO transcription factor, DAF-16. We report here on a new component of the IIS longevity pathway, SMK-1, which specifically influences DAF-16-dependent regulation of the aging process in C. elegans by regulating the transcriptional specificity of DAF-16 activity. Localization analysis of DAF-16 places SMK-1 downstream of DAF-16's phosphorylation-dependent relocation to the nucleus. Physiological and transcription analyses indicate that smk-1 is required for the innate immune, UV, and oxidative stress but not the thermal stress functions of DAF-16. SMK-1 therefore plays a role in longevity by modulating DAF-16 transcriptional specificity without affecting other processes regulated by IIS.

The plant-specific GRAS/SCL transcription factors play diverse roles in plant development and stress responses. In this study, a poplar SCL gene, PeSCL7, was functionally characterized in Arabidopsis thaliana, especially with regard to its role in abiotic stress resistance. Expression analysis in poplar revealed that PeSCL7 was induced by drought and high salt stresses, but was repressed by gibberellic acid (GA) treatment in leaves. Transient expression of GFP-PeSCL7 in onion epidermal cells revealed that the PeSCL7 protein was localized in the nucleus. Transgenic Arabidopsis plants overexpressing PeSCL7 showed enhanced tolerance to drought and salt treatments. The activity of two stress-responsive enzymes was increased in transgenic seedlings. Taken together, these results suggest that PeSCL7 encodes a member of the stress-responsive GRAS/SCL transcription factors that is potentially useful for engineering drought- and salt-tolerant trees.

CD4 + CD25 + regulatory T cells (Treg cells) are important in maintenance of peripheral tolerance. The direct effect of CD4 + CD25 + Treg cells on macrophages was studied using a mouse model in which syngeneic CD4 + CD25 + Treg cells were adoptively transferred into the peritoneal cavity of SCID mice. Peritoneal macrophages in mice transferred with CD4 + CD25 + Treg cells expressed significantly higher levels of CD23, CD47 and CD206 and less CD80 and major histocompatibility complex class II molecules as compared with those mice that received either CD4 + CD25 À T cells or no cells. Macrophages of mice injected with CD4 + CD25 + Treg cells displayed a remarkably enhanced phagocytosis of chicken red blood cells, and arginase activity together with an increased interleukin-10 (IL-10) production, whereas they showed a decreased antigen-presenting ability and nitric oxide production. Keywords: alternatively activated macrophages; classically activated macrophages; immune tolerance; mouse; arginase Mononuclear phagocytes, an important part of innate immunity, have pivotal roles in pathogen and tissue debris clearance, antigen capture and presentation as well as in shaping the development of adaptive immune response. Macrophages are a highly heterogeneous cell population that adapt and respond to a large variety of microenvironmental signals. 1 Distinct macrophage subsets expressing different patterns of chemokines, surface markers and metabolic enzymes and showing diversity of functions can be induced in inflammatory and noninflammatory settings. 2-4 M1 (classically activated) macrophages, after induction by proinflammatory mediators, such as lipopolysaccharide (LPS), interleukin-1b (IL-1b) and interferon-g (IFN-g), produce significant amounts of proinflammatory cytokines (TNF-a, IFN-g, IL-6 and IL-12) and generate reactive oxygen species such as nitric oxide (NO) by activation of inducible nitric oxide synthase (Nos2). [2][3][4] In contrast, M2 (alternatively activated) macrophages, which are induced by exposure to IL-4, IL-13, IL-10, transforming growth factor-b (TGF-b) and glucocorticoids, produce less proinflammatory cytokines and instead, simultaneously also show more production of anti-inflammatory cytokines IL-10, TGF-b and IL-1 receptor antagonist as well as enzyme arginase. 2,5,6 Furthermore, M2 macrophages express high levels of CD206 and CD163. Overall, M2 macrophages are believed to participate in the blockade of inflammatory responses and promotion of tissue repair and type II immunity. 7,8 Importantly, recent studies have shown that M2 macrophages, which are different from M1 macrophages, have been implicated in controlling CD4 + T-cell hyporesponsiveness by inducing CD4 + CD25 + Treg cells or inhibiting IL-17-producing CD4 + T cells (Th17) in autoimmunity, transplant immunity or pathogenic infections. 9-11 These studies indicate that different macrophage subsets have distinguished roles in modulating immune response or tolerance.It is now known that CD4 + CD25 + regulatory T cells (Treg cells), which e...