Blue light effects on rose photosynthesis and photomorphogenesis.

Through its impact on photosynthesis and morphogenesis, light is the environmental factor that most affects plant architecture. Using light rather than chemicals to manage plant architecture could reduce the impact on the environment. However, the understanding of how light modulates plant architecture is still poor and further research is needed. To address this question, we examined the development of two rose cultivars, Rosa hybrida'Radrazz' and Rosa chinensis'Old Blush', cultivated under two light qualities. Plants were grown from one-node cuttings for 6 weeks under white or blue light at equal photosynthetic efficiencies. While plant development was totally inhibited in darkness, blue light could sustain full development from bud burst until flowering. Blue light reduced the net CO(2) assimilation rate of fully expanded leaves in both cultivars, despite increasing stomatal conductance and intercellular CO(2) concentrations. In 'Radrazz', the reduction in CO(2) assimilation under blue light was related to a decrease in photosynthetic pigment content, while in both cultivars, the chl a/b ratio increased. Surprisingly, blue light could induce the same organogenetic activity of the shoot apical meristem, growth of the metamers and flower development as white light. The normal development of rose plants under blue light reveals the strong adaptive properties of rose plants to their light environment. It also indicates that photomorphogenetic processes can all be triggered by blue wavelengths and that despite a lower assimilation rate, blue light can provide sufficient energy via photosynthesis to sustain normal growth and development in roses.

Activation of the transcription factor carbohydrate-responsive element-binding protein by glucose leads to increased pancreatic beta cell differentiation in rats.

AIMS/HYPOTHESIS: Pancreatic cell development is a tightly controlled process. Although information is available regarding the mesodermal signals that control pancreatic development, little is known about the role of environmental factors such as nutrients, including glucose, on pancreatic development. We previously showed that glucose and its metabolism through the hexosamine biosynthesis pathway (HBP) promote pancreatic endocrine cell differentiation. Here, we analysed the role of the transcription factor carbohydrate-responsive element-binding protein (ChREBP) in this process. This transcription factor is activated by glucose, and has been recently described as a target of the HBP. METHODS: We used an in vitro bioassay in which pancreatic endocrine and exocrine cells develop from rat embryonic pancreas in a way that mimics in vivo pancreatic development. Using this model, gain-of-function and loss-of-function experiments were undertaken. RESULTS: ChREBP was produced in the endocrine lineage during pancreatic development, its abundance increasing with differentiation. When rat embryonic pancreases were cultured in the presence of glucose or xylitol, the production of ChREBP targets was induced. Concomitantly, beta cell differentiation was enhanced. On the other hand, when embryonic pancreases were cultured with inhibitors decreasing ChREBP activity or an adenovirus producing a dominant-negative ChREBP, beta cell differentiation was reduced, indicating that ChREBP activity was necessary for proper beta cell differentiation. Interestingly, adenovirus producing a dominant-negative ChREBP also reduced the positive effect of N-acetylglucosamine, a substrate of the HBP acting on beta cell differentiation. CONCLUSIONS/INTERPRETATION: Our work supports the idea that glucose, through the transcription factor ChREBP, controls beta cell differentiation from pancreatic progenitors.

Beta-cell development: the role of intercellular signals.

Understanding in detail how pancreatic endocrine cells develop is important for many reasons. From a scientific point of view, elucidation of such a complex process is a major challenge. From a more applied point of view, this may help us to better understand and treat specific forms of diabetes. Although a variety of therapeutic approaches are well validated, no cure for diabetes is available. Many arguments indicate that the development of new strategies to cure diabetic patients will require precise understanding of the way beta-cells form during development. This is obvious for a future cell therapy using beta-cells produced from embryonic stem cells. This also holds true for therapeutic approaches based on regenerative medicine. In this review, we summarize our current knowledge concerning pancreatic development and focus on the role of extracellular signals implicated in beta-cell development from pancreatic progenitors.

A novel cytosolic dual specificity phosphatase, interacting with glucokinase, increases glucose phosphorylation rate.

A novel protein was cloned from a rat liver cDNA library by interaction with the liver glucokinase. This protein contained 339 residues and possessed a canonical consensus sequence for a dual specificity phosphatase. The recombinant protein was able to dephosphorylate phosphotyrosyl and phosphoseryl/threonyl substrates. We called this protein the glucokinase-associated phosphatase (GKAP). The GKAP partially dephosphorylated the recombinant glucokinase previously phosphorylated, in vitro, by protein kinase A. The GKAP fused with green fluorescent protein was located in the cytosol, where glucokinase phosphorylates glucose, and not in the nucleus where the glucokinase is retained inactive by the glucokinase regulatory protein. More importantly, the GKAP accelerated the glucokinase activity in a dose-dependent manner and with a stoichiometry compatible with a physiological mechanism. This strongly suggested that the interaction between GKAP and glucokinase had a functional significance. The cloning of this novel protein with a dual specificity phosphatase activity allows the description of a possible new regulatory step in controlling the glycolysis flux.

The large intracytoplasmic loop of the glucose transporter GLUT2 is involved in glucose signaling in hepatic cells.

The hypothesis that the glucose transporter GLUT2 can function as a protein mediating transcriptional glucose signaling was addressed. To divert the putative interacting proteins from a glucose signaling pathway, two intracytoplasmic domains of GLUT2, the C terminus and the large loop located between transmembrane domains 6 and 7, were transfected into mhAT3F hepatoma cells. Glucose-induced accumulation of two hepatic gene mRNAs (GLUT2 and L-pyruvate kinase) was specifically inhibited in cells transfected with the GLUT2 loop and not with the GLUT2 C terminus. The dual effects of glucose were dissociated in cells expressing the GLUT2 loop; in fact a normal glucose metabolism into glycogen occurred concomitantly with the inhibition of the glucose-induced transcription. This inhibition by the GLUT2 loop could be due to competitive binding of a protein that normally interacts with endogenous GLUT2. In addition, the GLUT2 loop, tagged with green fluorescent protein (GFP), was located within the nucleus, whereas the GFP and GFP-GLUT2 C-terminal proteins remained in the cytoplasm. In living cells, a fraction (50%) of the expressed GFP-GLUT2 loop translocated rapidly from the cytoplasm to the nucleus in response to high glucose concentration and conversely in the absence of glucose. We conclude that, via protein interactions with its large loop, GLUT2 may transduce a glucose signal from the plasma membrane to the nucleus.

[Effectiveness of cicletanine on lesions in spontaneously hypertensive rats. Curative study--dose-effect relationship]. / Efficacité du ciclétanine sur les lésions du rat spontanément hypertendu. Etude curative--relation dose-effet.

Genetically hypertensive rats receiving a high sodium content diet develop, within weeks of their birth, major alterations of tissues and blood vessels. The purpose of this study was to evaluate the effects of cicletanine, a synthetic antihypertensive drug, on the progress of genetic hypertension. Iffa Credo SHR-SP male rats aged 11 weeks were divided into 4 groups. One group was used as control and 3 groups were treated with oral cicletanine in doses of 10, 30 and 90 mg/kg/day respectively. The control group showed a high mortality rate due to a significant decrease of weight gain and a highly significant increase of blood pressure, these changes being associated with lesions of tissues and vessels in the brain, heart and kidneys. A curative treatment with cicletanine improved these parameters and was accompanied by good tissue preservation. The curative effect of cicletanine seems to be due to an increase in endogenous prostaglandin synthesis.