Is the onset of senescence in leaf cells of intact plants due to low or high sugar levels?

This review examines the hypotheses that developmental programmed cell death in leaves is mediated (i) by sugar starvation in the leaf cells or (ii) by sugar accumulation in these cells. Experimental evidence for both hypotheses is critically discussed and found to be lacking. For example, some papers show that sugars prevent senescence of cut leaves placed in darkness, and prevent low sugar levels in the leaves. In these tests, the sugars seem to replace photosynthesis, hence the results have little relevance to leaf senescence in intact plants in the light. Low nitrogen nutrition and high light results in earlier senescence than the low nitrogen treatment alone. This is accompanied by high sugar levels in the leaves. The results have led to the idea that accumulation of sugars is the cause of the additional effect, or more generally, that sugar accumulation is always the direct cause of leaf senescence. Results from over-expressing, or knocking out, hexokinase genes tend to support the high sugar hypothesis, but pleiotropic effects confound this conclusion. In addition, several experiments show the effects of treatments on senescence without the increase in leaf sugar levels. Nonetheless, sugar levels are usually measured in whole leaves. Such an overall level does not reflect the differences in the onset of senescence between tissues and cells, and can therefore not be used as an argument for or against either of the two hypotheses. It is argued that future work should determine the time line of the concentrations of various sugars in various cells and cellular compartments, in relation to senescence processes in the same cells. Taken together, the data are not decisive. It is possible that neither of the two hypotheses is correct.     

Tomato strigolactones are derived from carotenoids and their biosynthesis is promoted by phosphate starvation

* Strigolactones are rhizosphere signalling compounds that mediate host location in arbuscular mycorrhizal (AM) fungi and parasitic plants. Here, the regulation of the biosynthesis of strigolactones is studied in tomato (Solanum lycopersicum). * Strigolactone production under phosphate starvation, in the presence of the carotenoid biosynthesis inhibitor fluridone and in the abscisic acid (ABA) mutant notabilis were assessed using a germination bioassay with seeds of Orobanche ramosa; a hyphal branching assay with Gigaspora spp; and by liquid chromatography coupled to tandem mass spectrometry (LC-MS/MS) analysis. * The root exudates of tomato cv. MoneyMaker induced O. ramosa seed germination and hyphal branching in AM fungi. Phosphate starvation markedly increased, and fluridone strongly decreased, this activity. Exudates of notabilis induced approx. 40% less germination than the wild-type. The LC-MS/MS analysis confirmed that the biological activity and changes therein were due to the presence of several strigolactones; orobanchol, solanacol and two or three didehydro-orobanchol isomers. * These results show that the AM branching factors and parasitic plant germination stimulants in tomato root exudate are strigolactones and that they are biosynthetically derived from carotenoids. The dual activity of these signalling compounds in attracting beneficial AM fungi and detrimental parasitic plants is further strengthened by environmental conditions such as phosphate availability.     

Response of anaerobic ammonium-oxidizing bacteria to hydroxylamine

Anaerobic ammonium oxidation is a recent addition to the microbial nitrogen cycle, and its metabolic pathway, including the production and conversion of its intermediate hydrazine, is not well understood. Therefore, the effect of hydroxylamine addition on the hydrazine metabolism of anaerobic ammonium-oxidizing (anammox) bacteria was studied both experimentally and by mathematical modeling. It was observed that hydroxylamine was disproportionated biologically in the absence of nitrite into dinitrogen gas and ammonium. Little hydrazine accumulated during this process; however, rapid hydrazine production was observed when nearly all hydroxylamine was consumed. A mechanistic model is proposed in which hydrazine is suggested to be continuously produced from ammonium and hydroxylamine (possibly via nitric oxide) and subsequently oxidized to N(2). The electron acceptor for hydrazine oxidation is hydroxylamine, which is reduced to ammonium. A decrease in the hydroxylamine reduction rate, therefore, leads to a decrease in the hydrazine oxidation rate, resulting in the observed hydrazine accumulation. The proposed mechanism was verified by a mathematical model which could explain and predict most of the experimental data.     

Stress-relaxation of human patellar articular cartilage in unconfined compression: prediction of mechanical response by tissue composition and structure

Mechanical properties of articular cartilage are controlled by tissue composition and structure. Cartilage function is sensitively altered during tissue degeneration, in osteoarthritis (OA). However, mechanical properties of the tissue cannot be determined non-invasively. In the present study, we evaluate the feasibility to predict, without mechanical testing, the stress-relaxation response of human articular cartilage under unconfined compression. This is carried out by combining microscopic and biochemical analyses with composition-based mathematical modeling. Cartilage samples from five cadaver patellae were mechanically tested under unconfined compression. Depth-dependent collagen content and fibril orientation, as well as proteoglycan and water content were derived by combining Fourier transform infrared imaging, biochemical analyses and polarized light microscopy. Finite element models were constructed for each sample in unconfined compression geometry. First, composition-based fibril-reinforced poroviscoelastic swelling models, including composition and structure obtained from microscopical and biochemical analyses were fitted to experimental stress-relaxation responses of three samples. Subsequently, optimized values of model constants, as well as compositional and structural parameters were implemented in the models of two additional samples to validate the optimization. Theoretical stress-relaxation curves agreed with the experimental tests (R=0.95-0.99). Using the optimized values of mechanical parameters, as well as composition and structure of additional samples, we were able to predict their mechanical behavior in unconfined compression, without mechanical testing (R=0.98). Our results suggest that specific information on tissue composition and structure might enable assessment of cartilage mechanics without mechanical testing.     

Relationship between low magnesium status and TRPM6 expression in the kidney and large intestine

The body maintains Mg(2+) homeostasis by renal and intestinal (re)absorption. However, the molecular mechanisms that mediate transepithelial Mg(2+) transport are largely unknown. Transient receptor potential melastatin 6 (TRPM6) was recently identified and shown to function in active epithelial Mg(2+) transport in intestine and kidney. To define the relationship between Mg(2+) status and TRPM6 expression, we used two models of hypomagnesemia: 1) C57BL/6J mice fed a mildly or severely Mg(2+)-deficient diet, and 2) mice selected for either low (MgL) or high (MgH) erythrocyte and plasma Mg(2+) status. In addition, the mice were subjected to a severely Mg(2+)-deficient diet. Our results show that C57BL/6J mice fed a severely Mg(2+)-deficient diet developed hypomagnesemia and hypomagnesuria and showed increased TRPM6 expression in kidney and intestine. When fed a Mg(2+)-adequate diet, MgL mice presented hypomagnesemia and hypermagnesuria, and lower kidney and intestinal TRPM6 expression, compared with MgH mice. A severely Mg(2+)-deficient diet led to hypomagnesemia and hypomagnesuria in both strains. Furthermore, this diet induced kidney TRPM6 expression in MgL mice, but not in MgH mice. In conclusion, as shown in C57BL/6J mice, dietary Mg(2+)-restriction results in increased Mg(2+) (re)absorption, which is correlated with increased TRPM6 expression. In MgL and MgH mice, the inherited Mg(2+) status is linked to different TRPM6 expression. The MgL and MgH mice respond differently to a low-Mg(2+) diet with regard to TRPM6 expression in the kidney, consistent with genetic factors contributing to the regulation of cellular Mg(2+) levels. Further studies of these mice strains could improve our understanding of the genetics of Mg(2+) homeostasis.     

Response of zooplankton to nutrient enrichment and fish in shallow lakes: a pan-European mesocosm experiment

1. Responses of zooplankton to nutrient enrichment and fish predation were studied in 1998 and 1999 by carrying out parallel mesocosm experiments in six lakes across Europe. 2. Zooplankton community structure, biomass and responses to nutrient and fish manipulation showed geographical and year‐to‐year differences. Fish had a greater influence than nutrients in regulating zooplankton biomass and especially the relative abundances of different functional groups of zooplankton. When fish reduced the biomass of large crustaceans, there was a complementary increase in the biomasses of smaller crustacean species and rotifers. 3. High abundance of submerged macrophytes provided refuge for zooplankton against fish predation but this refuge effect differed notably in magnitude among sites. 4. Large crustacean grazers (Daphnia, Diaphanosoma, Sida and Simocephalus) were crucial in controlling algal biomass, while smaller crustacean grazers and rotifers were of minor importance. Large grazers were able to control phytoplankton biomass even under hypereutrophic conditions (up to 1600 μg TP L^?1) when grazer biomass was high (>80–90 μg dry mass L^?1) or accounted for >30% of the grazer community. 5. The littoral zooplankton community was less resistant to change following nutrient enrichment in southern Spain, at high temperatures (close to 30 °C), than at lower temperatures (17–23 °C) characterising the other sites. This lower resistance was because of a greater importance of nutrients than zooplankton in controlling algal biomass. 6. Apart from the reduced role of large crustacean grazers at the lowest latitude, no consistent geographical patterns were observed in the responses of zooplankton communities to nutrient and fish manipulation.     

Expression of defender against apoptotic death (DAD-1) in Iris and Dianthus petals

The gene defender against apoptotic death ( DAD-1 ) prevents programmed cell death in animal cells. We investigated the expression pattern of DAD-1 in petals of iris ( Iris  ×  hollandica cv. Blue Magic) and carnation ( Dianthus caryophyllus cv. Etarro). DAD-1 expression in Iris petals was strongly reduced by the time of visible senescence, which occurs 4 days after flower opening. Microscopic analysis showed that most mesophyll cells had died prior to a clear decrease in DAD-1 expression and that epidermis cells started to die by that time. In carnation petals DAD-1 expression also decreased by the time of massive cell death. After ethylene treatment, DAD-1 expression in carnation again decreased concomitant with the advance in massive cell death. In conclusion, DAD-1 is not an early regulator of petal cell death. Its expression may be required for the programmed dismantling of cells, as it ceases only just prior to, or concomitant with, cell death.     

Potential Conflicts of Interest of Editorial Board Members from Five Leading Spine Journals

Conflicts of interest arising from ties between pharmaceutical industry and physicians are common and may bias research. The extent to which these ties exist among editorial board members of medical journals is not known. This study aims to determine the prevalence and financial magnitude of potential conflicts of interest among editorial board members of five leading spine journals. The editorial boards of: The Spine Journal; Spine; European Spine Journal; Journal of Neurosurgery: Spine; and Journal of Spinal Disorders & Techniques were extracted on January 2013 from the journals’ websites. Disclosure statements were retrieved from the 2013 disclosure index of the North American Spine Society; the program of the 20th International Meeting on Advanced Spine Techniques; the program of the 48th Annual Meeting of the Scoliosis Research Society; the program of the AOSpine global spine congress; the presentations of the 2013 Annual Eurospine meeting; and the disclosure index of the American Academy of Orthopaedic Surgeons. Names of the editorial board members were compared with the individuals who completed a disclosure for one of these indexes. Disclosures were extracted when full names matched. Two hundred and ten (29%) of the 716 identified editorial board members reported a potential conflict of interest and 154 (22%) reported nothing to disclose. The remaining 352 (49%) editorial board members had no disclosure statement listed for one of the indexes. Eighty-nine (42%) of the 210 editorial board members with a potential conflict of interest reported a financial relationship of more than $10,000 during the prior year. This finding confirms that potential conflicts of interest exist in editorial boards which might influence the peer review process and can result in bias. Academia and medical journals in particular should be aware of this and strive to improve transparency of the review process. We emphasize recommendations that contribute to achieving this goal.