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ABSTRACTSugar signaling forms the basis of metabolic activities crucial for an organism to perform essential life activities. In plants, sugars like glucose, mediate a wide range of physiological responses ranging from seed germination to cell senescence. This has led to the elucidation of cell signaling pathways involving glucose and its counterparts and the mechanism of how these sugars take control over major hormonal pathways such as auxin, ethylene, abscisic acid and cytokinin in Arabidopsis. Plants use HXK1(Hexokinase) as a glucose sensor to modulate changes in photosynthetic gene expression in response to high glucose levels. Other proteins such as SIZ1, a major SUMO E3 ligase have recently been implicated in controlling sugar responses via transcriptional and translational regulation of a wide array of sugar metabolic genes. Here, we show that these two genes work antagonistically and are epistatic in controlling responsiveness toward high glucose conditions.

TOR kinase is a central coordinator of nutrient-dependent growth in eukaryotes. Maintaining optimal TOR signaling is critical for the normal development of organisms. In this study, we describe a negative feedback loop of TOR signaling helping in the adaptability of plants in changing environmental conditions. Using an interdisciplinary approach, we show that the plant-specific zinc finger protein FLZ8 acts as a regulator of TOR signaling in Arabidopsis. In sugar sufficiency, TOR-dependent and -independent histone modifications upregulate the expression of FLZ8. FLZ8 negatively regulates TOR signaling by promoting antagonistic SnRK1α1 signaling and bridging the interaction of SnRK1α1 with RAPTOR1B, a crucial accessory protein of TOR. This negative feedback loop moderates the TOR-growth signaling axis in the favorable condition and helps in the activation of stress signaling in unfavorable conditions, establishing its importance in the adaptability of plants.

Based upon the phenotype of young, dark-grown seedlings, a cytokinin-resistant mutant, cnr1, has been isolated, which displays altered cytokinin- and auxin-induced responses. The mutant seedlings possess short hypocotyls and open apical hooks (in dark), and display agravitropism, hyponastic cotyledons, reduced shoot growth, compact rosettes and short roots with increased adventitious branching and reduced number of root hairs. A number of these features invariably depend upon auxin/cytokinin ratio but the cnr1mutant retains normal sensitivity towards auxin as well as auxin polar transport inhibitor, TIBA, although upregulation of primary auxin-responsive Aux/IAAgenes is reduced. The mutant shows resistance towards cytokinin in hypocotyl/root growth inhibition assays, displays reduced regeneration in tissue cultures (cytokinin response) and decreased sensitivity to cytokinin for anthocyanin accumulation. It is thus conceivable that due to reduced sensitivity to cytokinin, the cnr1mutant also shows altered auxin response. Surprisingly, the mutant retains normal sensitivity to cytokinin for induction of primary response genes, the type-A Arabidopsisresponse regulators, although the basal level of their expression was considerably reduced as compared to the wild-type. The zeatin and zeatin riboside levels, as estimated by HPLC, and the cytokinin oxidase activity were comparable in the cnr1mutant and the wild-type. The hypersensitivity to red light (in hypocotyl growth inhibition assay), partial photomorphogenesis in dark, and hypersensitivity to sugars, are some other features displayed by the cnr1mutant. The lesion in the cnr1mutant has been mapped to the top of chromosome 1 where no other previously known cytokinin-resistant mutant has been mapped, indicating that the cnr1mutant defines a novel locus involved in hormone, light and sugar signalling.Based upon the phenotype of young, dark-grown seedlings, a cytokinin-resistant mutant, cnr1, has been isolated, which displays altered cytokinin- and auxin-induced responses. The mutant seedlings possess short hypocotyls and open apical hooks (in dark), and display agravitropism, hyponastic cotyledons, reduced shoot growth, compact rosettes and short roots with increased adventitious branching and reduced number of root hairs. A number of these features invariably depend upon auxin/cytokinin ratio but the cnr1mutant retains normal sensitivity towards auxin as well as auxin polar transport inhibitor, TIBA, although upregulation of primary auxin-responsive Aux/IAAgenes is reduced. The mutant shows resistance towards cytokinin in hypocotyl/root growth inhibition assays, displays reduced regeneration in tissue cultures (cytokinin response) and decreased sensitivity to cytokinin for anthocyanin accumulation. It is thus conceivable that due to reduced sensitivity to cytokinin, the cnr1mutant also shows altered auxin response. Surprisingly, the mutant retains normal sensitivity to cytokinin for induction of primary response genes, the type-A Arabidopsisresponse regulators, although the basal level of their expression was considerably reduced as compared to the wild-type. The zeatin and zeatin riboside levels, as estimated by HPLC, and the cytokinin oxidase activity were comparable in the cnr1mutant and the wild-type. The hypersensitivity to red light (in hypocotyl growth inhibition assay), partial photomorphogenesis in dark, and hypersensitivity to sugars, are some other features displayed by the cnr1mutant. The lesion in the cnr1mutant has been mapped to the top of chromosome 1 where no other previously known cytokinin-resistant mutant has been mapped, indicating that the cnr1mutant defines a novel locus involved in hormone, light and sugar signalling.

We have isolated an Arabidopsis mutant impaired in light- and brassinosteroid (BR) induced responses, as well as in sugar signalling. The bls1 (brassinosteroid, light and sugar1) mutant displays short hypocotyl, expanded cotyledons, and de-repression of light-regulated genes in young seedlings, and leaf differentiation and silique formation on prolonged growth in dark. In light, the bls1 mutant is dwarf and develops a short root, compact rosette, with reduced trichome number, and exhibits delayed bolting. The activity of the BR inducible TCH4 and auxin inducible SAUR promoters, fused with GUS gene, is also altered in seedlings harbouring bls1 mutant background. In addition, the bls1 mutant is hypersensitive to metabolizable sugars. The short hypocotyl phenotype in dark, short root phenotype in light and sugar hypersensitivity could be rescued with BR application. Moreover, the bls1 mutant also showed higher expression of a BR biosynthetic pathway gene CPD, which is known to be feedback-regulated by BR. Using a genome-wide AFLP mapping strategy, the bls1 mutant has been mapped to a 1.4?Mb region of chromosome 5. Since no other mutant with essentially a similar phenotype has been assigned to this region, we suggest that the bls1 mutant defines a novel locus involved in regulating endogenous BR levels, with possible ramifications in integrating light, hormone and sugar signalling.

Root architecture is developmentally plastic and affected by many intrinsic factors (e.g. plant hormones) and extrinsic factors (e.g. touch, gravity) in order to maximize nutrient and water acquisition. We have recently shown that asymmetrical exposure of cytokinin (CK) at the root tip causes root growth directional changes that is dependent on ethylene signaling and is potentiated by glucose signaling. Auxin homeostasis as maintained by auxin signaling and transport is also involved in CK-induced root cell elongation and differential growth. The signaling pathways eventually converge at actin filament organization since actin filament organization inhibitor latrunculin B (Lat B) can also induce similar growth. We, show that CK can actually alter actin filament organization as seen in actin binding protein 35S::GFP-ABD2-GFP transgenic lines as is also altered by auxin polar transport inhibitor 1-N-naphthylphthalamic acid (NPA) and Lat B in different manners.

In our recent publication,1we have shown that a T-DNA insertion in Arabidopsis CIPK6gene encoding a CBL-interacting protein kinase caused reduction in expression of the gene and emergence of lateral roots. The change in phenotype in the mutant line was likely due to reduction in shoot-to-root acropetal and the the root tip basipetal auxin transport. Here we report identification of a homozygous knockout line of AtCIPK6(atcipk6) with no detectable expression of the gene in normal growth condition. The knockout line exhibited considerable decrease in growth rate of the taproot as well as in emergence of lateral roots. The mutant line also showed reduction in the root tip basipetal and shoot-to-root acropetal polar auxin transport. Relative rate of auxin transport and the root phenotype of the atcipk6closely matched with those of pgp4-1, an Arabidopsis line mutated in PGP4. This gene encodes an ABC integral membrane transporter, which functions in polar auxin transport. These observations strengthen our earlier proposalt that CIPK6 is probably involved in polar auxin transport and indicate that it may function through the PGP4 auxin transporter.

ABSTRACTThe TARGET OF RAPAMYCIN-SNF1-RELATED PROTEIN KINASE 1 (TOR-SnRK1) arms race is a key regulator of plant growth in response to energy fluctuations and stress. Recently, we have identified that two members of the FCS-LIKE ZINC FINGER (FLZ) protein family, FLZ6 and 10, repress SnRK1 signaling and thereby involved in the activation of the TARGET OF RAPAMYCIN (TOR) signaling. In this study, we demonstrate that FLZ6 and 10 are also involved in the regulation of osmotic stress responses. Downregulation of FLZ6and 10results in enhanced expression of stress-responsive genes and better resilience towards osmotic stress at the seedling stage. These results indicate that FLZ6 and 10 are involved in the regulation of stress mitigation in plants through directly affecting SnRK1 signaling.

ABSTRACTCytokinin (CK) and glucose (GLC) control several common responses in plants. There is an extensive overlap between CK and GLC signal transduction pathways in Arabidopsis. Physiologically, both GLC and CK could regulate root length in light. CK interacts with GLC via HXK1 dependent pathway for root length control. Wild-type (WT) roots cannot elongate in the GLC free medium while CK-receptor mutant ARABIDOPSIS HISTIDINE KINASE4(ahk4) and type B ARR triple mutant ARABIDOPSIS RESPONSE REGULATOR1, 10,11(arr1, 10,11) roots could elongate even in the absence of GLC as compared with the WT. The root hair initiation was also found defective in CK signaling mutants ahk4, arr1,10,11and arr3,4,5,6,8,9on increasing GLC concentration (up to 3%); and lesser number of root hairs were visible even at 5% GLC as compared with the WT. Out of 941 BAP regulated genes, 103 (11%) genes were involved in root growth and development. Out of these 103 genes, 60 (58%) genes were also regulated by GLC. GLC could regulate 5736 genes, which include 327 (6%) genes involved in root growth and development. Out of these 327 genes, 60 (18%) genes were also regulated by BAP. Both GLC and CK signaling cannot alter root length in light in auxin signaling mutant AUXIN RESPONSE3/INDOLE-3-ACETIC ACID17(axr3/iaa17) suggesting that they may involve auxin signaling component as a nodal point. Therefore CK- and GLC- signaling are involved in controlling different aspects of root growth and development such as root length, with auxin signaling components working as downstream target.

Plants have the ability to adjust its physiology and metabolism to the changes of nutrient availability in the environment. Since a number of common responses are regulated by sugar and auxin, the obvious question arises is whether sugar and auxin act interdependently to bring about changes in plant morphology. In the February issue of the PloS ONE,1 we presented detailed investigation of glucose and auxin signaling interaction in controlling root growth and development in Arabidopsis thalianaseedlings. Further analysis of tissue specific regulation of glucose auxin signaling interaction may provide some insight as to how these two signaling molecules interact to control the morphogenic changes during seedling development.

Plants, being sessile organisms, are more exposed to the hazards of constantly changing environmental conditions globally. During the lifetime of a plant, the root system encounters various challenges such as obstacles, pathogens, high salinity, water logging, nutrient scarcity etc. The developmental plasticity of the root system provides brilliant adaptability to plants to counter the changes exerted by both external as well as internal cues and achieve an optimized growth status. Phytohormones are one of the major intrinsic factors regulating all aspects of plant growth and development both independently as well as through complex signal integrations at multiple levels. We have previously shown that glucose (Glc) and brassinosteroid (BR) signalings interact extensively to regulate lateral root (LR) development in Arabidopsis.1Auxin efflux as well as influx and downstream signaling components are also involved in Glc-BR regulation of LR emergence. Here, we provide evidence for involvement of ethylene signaling machinery downstream to Glc and BR in regulation of LR emergence.

Sensing and responding toward gravity vector is a complicated and multistep process. Gravity is a constant factor feeding plants with reliable information for the spatial orientation of their organs. Auxin, cytokinin, ethylene and BRs have been the most explored hormones in relation to gravitropism. We have previously shown that glucose (Glc) could promote brassinosteroid (BR) signaling thereby inducing changes in root directional growth. Auxin signaling and polar transport components are also involved in Glc induced changes in root directional growth. Here, we provide evidence for involvement of cytokinin and ethylene signaling components in regulation of root directional growth downstream to Glc and BR. Altogether, Glc mediated change in root direction is an adaptive feature which is a result of a collaborative effort integrating phytohormonal signaling cues.