Regulação coordenada da mobilização de lipídios e proteínas por hormônios, fontes de carbono e nitrogênio durante o crescimento pós-germinativo em Girassol

The mobilization of food reserves in storage tissues and allocation of their hydrolysis products in the growing axis are critical processes for the establishment of seedlings after germination. Therefore, it is crucial for mobilization of reserves to be synchronized with the growing axis, so that photosynthetic activity can be started before depletion of reserves. For this, integrative approaches involving different reserves, different hydrolysis products and interaction between storage and growing axis tissues, either through hormones or metabolites with signaling role, can contribute greatly to the elucidation of the regulation mechanisms for reserve mobilization. In this study, was hypothesized that hormones and metabolites have different actions on reserve mobilization, and there must be a crossed effect of sugars on the mobilization of proteins and amino acids on lipids and starch mobilization in sunflower seedlings. This study was conducted with seeds of sunflower (Helianthus annuus L.) hybrid Helio 253 using in vitro culture system. Seeds were germinated on Germitest® paper and grown on agar-water 4 g/L without addition of nutrients during 9 days after imbibition (DAI) for growth curve. To verify the effect of metabolites and hormones, seedlings were transferred in the 2nd DAI to agar-water 4 g/L supplemented with increasing concentrations of sucrose or L-glutamine, abscisic acid, gibberellic acid or indolebutyric acid. The results of this study confirm that the mobilization of lipids and storage proteins occurs in a coordinated manner during post-germination growth in sunflower, corroborating the hypothesis that the application of external carbon (sucrose) and nitrogen (L-glutamine) sources can delay the mobilization of these reserves in a crossed way. Moreover, considering the changes in the patterns of reserve mobilization and partition of their products in seedlings treated with different growth regulators, it is evident that the effects of metabolites and hormones must involve, at least in part, distinct mechanisms of action

Improved production of chlorogenic acid from cell suspension cultures of Lonicera macranthoids

Purpose: To evaluate the potential of Lonicera macranthoids Hand. -Mazz. Yulei1 suspension culture system for enhanced production of the main secondary metabolite, chlorogenic acid. Methods: The callus of L. macranthoides Hand.-Mazz. “Yulei1” was suspension cultured in B5 liquid medium supplemented with different plant growth regulators. Biomass accumulation was calculated by weight method and chlorogenic acid production was measured using high performance liquid chromatography (HPLC). HPLC was carried out on C18 analytical column at 35 °C and the detection wavelength was set at 324 nm. Results: The results showed that maximum accumulation of biomass and chlorogenic acid were achieved 15 days after culture growth. The optimized conditions for biomass accumulation and chlorogenic acid production were 50 g/L of inoculum on fresh weight basis, B5 medium supplemented with plant growth regulators, 30 - 40 g/L sucrose and initial medium pH of 5.5. Maximum accumulation of chlorogenic acid and biomass were observed when the culture medium was supplemented with 2.0 mg/L6-BA. Optimal accumulation of chlorogenic acid was observed using combination of hormones 2.0 mg/L 6-Benzyladenine (BA) + 0.5 mg/L2, 4-Dichlorophenoxyacetic acid (2,4-D), while optimal accumulation of biomass was observed with 2.0 mg/L 6-BA + 2.0 mg/L2, 4-D. In addition, phenylalanine also contributed to the synthesis of chlorogenic acid at a concentration > 50 mg/L. Conclusion: Cell suspension cultures of L. macranthoides Hand.-Mazz. “Yulei1” have successfully been established. The findings provide a potential basis for large scale production of chlorogenic acid using cell suspension cultures of L. macranthoides.

Lactofem e etefom como reguladores de crescimento de cultivares de soja.

2016

Regeneração in vitro de cultivares de Sorghum bicolor via embriogênese somática.

2016

Negative regulators of a growth factor-mediated signaling pathway in the nematode Caenorhabditis elegans

Vulval differentiation in C. elegans is mediated by an Epidermal growth factor (EGF)- EGF receptor (EGFR) signaling pathway. I have cloned unc-101, a negative regulator of vulval differentiation of the nematode C. elegans. unc-101 encodes a homolog of AP47, the medium chain of the trans-Golgi clathrin-associated protein complex. This identity was confirmed by cloning and comparing sequence of a C. elegans homolog of AP50, the medium chain of the plasma membrane clathrin-associated protein complex. I provided the first genetic evidence that the trans-Golgi clathrin-coated vesicles are involved in regulation of an EGF signaling pathway. Most of the unc-101 alleles are deletions or nonsense mutations, suggesting that these alleles severely reduce the unc-101 activity. A hybrid gene that contains parts of unc-101 and mouse AP4 7 rescued at least two phenotypes of unc-101 mutations, the Unc and the suppression of vulvaless phenotype of let-23(sy1) mutation. Therefore, the functions of AP47 are conserved between nematodes and mammals.

unc-101 mutations can cause a greater than wild-type vulval differentiation in combination with certain mutations in sli-1, another negative regulator of the vulval induction pathway. A mutation in a new gene, rok-1, causes no defect by itself, but causes a greater than wild-type vulval differentiation in the presence of a sli-1 mutation. The unc-101; rok-1; sli-1 triple mutants display a greater extent of vulval differentiation than any double mutant combinations of unc-101, rok-1 and sli-1. Therefore, rok-1 locus defines another negative regulator of the vulval induction pathway.

I analyzed a second gene encoding an AP47 homolog in C. elegans. This gene, CEAP47, encodes a protein 72% identical to both unc-101 and mammalian AP47. A hybrid gene containing parts of unc-101 and CEAP47 sequences can rescue phenotypes of unc-101 mutants, indicating that UNC- 101 and CEAP47 proteins can be redundant if expressed in the same set of cells.

Effect of plant regulators on growth and flowering of 'Meyer' zoysiagrass

This trial aimed to evaluate the effect of sequential applications of different plant regulators over growth and flower rachis emission of 'Meyer' zoysiagrass (Zoysia japonica). The study was conducted on 15-month old green turfgrass under a randomized complete block design with four replications. The following plant regulator and doses were tested: trinexapac-ethyl (113+113, 226+113, 226+226, 452+113, 452+226, 452+452, 678+339 e 904+452 g a.i./ha-1), prohexadione-calcium (100+100 e 200+200 g a.i. ha-1) and bispyribac-sodium (40+40 e 60+60 g a.i. ha-1), as well as an untreated control. The turfgrass was mowed again at 3.0 cm aboveground and the second plant regulator was applied when 'Meyer' zoysiagrass was between 5.0 and 6.0 cm high. The effect of the treatments was visually rated for visual injury, plant height, height and number of flower rachis, and total dry mass production of clippings. Only bispyribac-sodium had visual symptoms of injury on 'Meyer' zoysiagrass, and no intoxication was observed at 28 days after the second application (DAAB). The sequential applications of trinexapac-ethyl, prohexadione-calcium and bispyribac-sodium reduced by more than 80% the total clipping dry mass produced by 'Meyer' zoysiagrass. All the plant regulators tested also showed promising results in reducing the height and emission of rachis, especially when trinexapac-ethyl was applied at the doses 452+452, 678+339 and 904+452 g a.i. ha-1. 'Meyer' zoysiagrass turfgrass can be handled with the sequential application of a plant regulator, which reduces the need for mowing over a period up to 110 days after the application of the second plant regulator, and it also avoids deleterious visual effects over turfgrass.

Effects of plant regulators on the growth and flowering of Saint Augustine grass plants

The objective of this work was to evaluate the effects of three plant growth inhibitors on the development and emission of floral rachis of Saint Augustine grass [Stenotaphrum secundatum (Walt.) Kuntzel] plants. The study was carried out in a 15 month old lawn with the experimental plots being distributed in accordance with a complete randomized block design with four replications. The treatments consisted of sole application of trinexapac-ethyl (113, 226, 452, 678, and 904 g ai ha(-1)), prohexadione-calcium (100 and 200 g ai ha(-1)), and bispyribac-sodium (40 and 60 g ai ha(-1)) plus a check treatment in which the plants were not submitted to any of the plant growth inhibitors. The effects of those products were evaluated in terms of visual signs of plant intoxication, plant height, emission and height of floral rachises, and chip total dry matter production. All the plant growth inhibitors resulted in visible injury to the plants but these intoxication signs practically disappeared 28 days after the application. Trinexapac-ethyl at the dose of 904 g ai ha(-1) reduced plant height by 59.7%, the emission of floral rachis by 96.4%, and the amount of chip dry matter production by 87.7%. Plant growth inhibitors may reduce the number of times of lawn plants cutting up to 119 days after their application with no harmful effects on the plants visual aspect.

Brivanib alaninate, a dual inhibitor of vascular endothelial growth factor receptor and fibroblast growth factor receptor tyrosine kinases, induces growth inhibition in mouse models of human hepatocellular carcinoma

PURPOSE: Hreceptor (VEGFR) and FGF receptor (FGFR) signaling pathways. EXPERIMENTAL DESIGN: Six different s.c. patient-derived HCC xenografts were implanted into mice. Tumor growth was evaluated in mice treated with brivanib compared with control. The effects of brivanib on apoptosis and cell proliferation were evaluated by immunohistochemistry. The SK-HEP1 and HepG2 cells were used to investigate the effects of brivanib on the VEGFR-2 and FGFR-1 signaling pathways in vitro. Western blotting was used to determine changes in proteins in these xenografts and cell lines. RESULTS: Brivanib significantly suppressed tumor growth in five of six xenograft lines. Furthermore, brivanib-induced growth inhibition was associated with a decrease in phosphorylated VEGFR-2 at Tyr(1054/1059), increased apoptosis, reduced microvessel density, inhibition of cell proliferation, and down-regulation of cell cycle regulators. The levels of FGFR-1 and FGFR-2 expression in these xenograft lines were positively correlated with its sensitivity to brivanib-induced growth inhibition. In VEGF-stimulated and basic FGF stimulated SK-HEP1 cells, brivanib significantly inhibited VEGFR-2, FGFR-1, extracellular signal-regulated kinase 1/2, and Akt phosphorylation. CONCLUSION: This study provides a strong rationale for clinical investigation of brivanib in patients with HCC.

Targeting aurora kinases : a novel approach to curb the growth and chemoresistance of androgen refractory prostate cancer

Aurora Kinase (AK) based therapy targeting AK-A & B is effective against some cancers. We have explored its potential against previously unreported incurable, metastatic androgen depletion independent Prostate Cancer (ADIPC). We used androgen sensitive (AS) and ADI lines derived from Transgenic Adenocarcinoma of the Mouse Prostate (TRAMP) mice. The relevance of this model was unequivocally established through focussed array, quantitative PCR and western blotting studies; significantly greater alteration of genes (fold change and number) representing major cancer pathways was shown in ADI cells compared to AS lines. A marked enhancement of in vivo growth of the ADI subline showing the greatest degree of gene modulations [TRAMP C1 (TC1)-T5: TC1-T5] reflected this. In contrast to the parental AS TC1 line, TC1-T5 cells grew with 100% incidence in the prostate, as lung pseudometastases and migrated to the bone and other soft tissues. The potential involvement of AKs in this transition was indicated by the significant upregulation of AK-A/B and their downstream regulators, survivin and phosphorylated-histone H3 in TC1-T5 cells compared to TC1 cells. This led to enhanced sensitivity of TC1-T5 cells to the pan-AK inhibitor, VX680 and to significant reduction in in vivo tumour growth rates when AK-A and/or B were downregulated in TC1-T5 cells. This cell growth inhibition was markedly enhanced when both AKs were downregulated and also led to substantially greater sensitivity of these cells to docetaxel, the only chemotherapeutic with activity against ADI PC. Finally, use of VX680 with docetaxel led to impressive synergies suggesting promise for treating clinical ADI metastatic PC.

Signal transduction mechanisms underlying growth hormone receptor action

Our understanding of the mechanisms of action of GH and its receptor, the GHR, has advanced significantly in the last decade and has provided some important surprises. It is now clear that the GH-GHR axis activates a number of inter-related signalling pathways, not all of which are dependent on the intracellular tyrosine kinase, JAK2 as originally postulated. JAK2-independent pathways, mediated via the Src family kinases, together with a number of negative regulators of GH signalling and emerging cross-talk mechanisms with other growth factor receptors, provide a complex array of mechanisms that are capable of fine-tuning responses to GH in a cell context dependent manner. Additionally, it is also now clear that GH and the GHR can translocate to the nucleus of target cells and initiate, as yet not well defined, nuclear responses. Continued emphasis on elucidation of these complex mechanisms is critical to provide further insights into the diverse physiological and pathophysiological effects of GH.

Aberrant fibroblast growth factor receptor signaling in bladder and other cancers

Fibroblast growth factors (FGFs) are potent mitogens, morphogens, and inducers of angiogenesis, and FGF signaling governs the genesis of diverse tissues and organs from the earliest stages. With such fundamental embryonic and homeostatic roles, it follows that aberrant FGF signaling underlies a variety of diseases. Pathological modifications to FGF expression are known to cause salivary gland aplasia and autosomal dominant hypophosphatemic rickets, while mutations in FGF receptors (FGFRs) result in a range of skeletal dysplasias. Anomalous FGF signaling is also associated with cancer development and progression. Examples include the overexpression of FGF2 and FGF6 in prostate cancer, and FGF8 overexpression in breast and prostate cancers. Alterations in FGF signaling regulators also impact tumorigenesis, which is exemplified by the down-regulation of Sprouty 1, a negative regulator of FGF signaling, in prostate cancer. In addition, several FGFRs are mutated in human cancers (including FGFR2 in gastric cancer and FGFR3 in bladder cancer). We recently identified intriguing alterations in the FGF pathway in a novel model of bladder carcinoma that consists of a parental cell line (TSU-Pr1/T24) and two sublines with increasing metastatic potential (TSU-Pr1-B1 and TSU-Pr1-B2), which were derived successively through in vivo cycling. It was found that the increasingly metastatic sublines (TSU-Pr1-B1 and TSU-Pr1-B2) had undergone a mesenchymal to epithelial transition. FGFR2IIIc expression, which is normally expressed in mesenchymal cells, was increased in the epithelial-like TSU-Pr1-B1 and TSU-Pr1-B2 sublines and FGFR2 knock-down was associated with the reversion of cells from an epithelial to a mesenchymal phenotype. These observations suggest that modified FGF pathway signaling should be considered when studying other cancer types.

NADPH oxidases as regulators of tumor angiogenesis : current and emerging concepts

Significance Reactive oxygen species (ROS) such as superoxide, hydrogen peroxide, and peroxynitrite are generated ubiquitously by all mammalian cells and have been understood for many decades as inflicting cell damage and as causing cancer by oxidation and nitration of macromolecules, including DNA, RNA, proteins, and lipids. Recent Advances A current concept suggests that ROS can also promote cell signaling pathways triggered by growth factors and transcription factors that ultimately regulate cell proliferation, differentiation, and apoptosis, all of which are important hallmarks of tumor cell proliferation and angiogenesis. Moreover, an emerging concept indicates that ROS regulate the functions of immune cells that infiltrate the tumor environment and stimulate angiogenesis, such as macrophages and specific regulatory T cells. Critical Issues In this article, we highlight that the NADPH oxidase family of ROS-generating enzymes are the key sources of ROS and, thus, play an important role in redox signaling within tumor, endothelial, and immune cells thereby promoting tumor angiogenesis. Future Directions Knowledge of these intricate ROS signaling pathways and identification of the culprit NADPH oxidases is likely to reveal novel therapeutic opportunities to prevent angiogenesis that occurs during cancer and which is responsible for the revascularization after current antiangiogenic treatment.

Status assessment of water use research in turf growth and maintenance.

The strategic objectives of Turf Australia (formerly the Turf Producers Association (TPA)) relating to water use in turf are to: • Source and collate information to support the case for adequate access to water for the Turf production and maintenance sectors and • Compile information generated into a convincing communication package that can be readily used by the industry in its advocacy programs (to government, regulators, media etc) More specifically, the turfgrass industry needs unbiased scientific evidence of the value of healthy grass in our environment. It needs to promote the use of adequate water even during drought periods to maintain quality turfgrass, which provides many benefits to the broader community including cooling the environment, saving energy and encouraging healthy lifestyles. The many environmental, social and health benefits of living turfgrass have been the subject of numerous investigations beyond the scope of this review. However further research is needed to fully understand the economic returns achievable by the judicious use of water for the maintenance of healthy turfgrass. Consumer education, backed by scientific evidence will highlight the “false economy” in allowing turfgrass to wither and die during conditions which require high level water restrictions. This report presents a review of the literature pertaining to research in the field of turf water use. The purpose of the review was to better understand the scope and nature of existing research results on turf water relations so that knowledge gaps could be identified in achieving the above strategic objectives of the TPA. Research to date has been found to be insufficient to compile a convincing communication package as described. However, identified knowledge gaps can now be addressed through targeted research. Information derived from targeted research will provide valuable material for education of the end user of turfgrass. Recommendations have been developed, based on the results of this desktop review. It was determined that future research in the field of turf irrigation needs to focus on a number of key factors which directly or indirectly affect the relationship between turfgrass and water use. These factors are: • Climate • Cultivar • Quality • Site use requirements • Establishment and management The overarching recommendation is to develop a strategic plan for turfgrass water relations research based around the five determinants of turf water use listed above. This plan should ensure research under these five categories is integrated into a holistic approach by which the consumer can be guided in species and/or cultivar choices as well as best management practices with respect to turfgrass water relations. Worsening drought cycles and limited supply of water for irrigation were the key factors driving every research project reviewed in this report. Subsidence of the most recent (or current) drought conditions in Australia should not be viewed by the turf industry as a reason to withdraw support or funding for research in this area. Drought conditions, limited domestic water availability and urban water restrictions will return in Australia albeit in 5, 10 or 20 years time and the turf industry has an opportunity to prepare for that time.