Nutrients shape the growth, maturation, and aging of plants and animals. In plants, the juvenile to adult transition (vegetative phase change) is initiated by a decrease in miR156. In Arabidopsis, we found that exogenous sugar decreased the abundance of miR156, whereas reduced photosynthesis increased the level of this miRNA. This effect was correlated with a change in the timing of vegetative phase change, and was primarily attributable to a change in the expression of two genes, MIR156A and MIR156C, which were found to play dominant roles in this transition. The glucose-induced repression of miR156 was dependent on the signaling activity of HEXOKINASE1. We also show that the defoliation-induced increase in miR156 levels can be suppressed by exogenous glucose. These results provide a molecular link between nutrient availability and developmental timing in plants, and suggest that sugar is a component of the leaf signal that mediates vegetative phase change.DOI: http://dx.doi.org/10.7554/eLife.00260.001

Vegetative phase change is regulated by a decrease in the abundance of the miRNAs, miR156 and miR157, and the resulting increase in the expression of their targets, SQUAMOSA PROMOTER BINDING PROTEIN-LIKE (SPL) transcription factors. To determine how miR156/miR157 specify the quantitative and qualitative changes in leaf morphology that occur during vegetative phase change, we measured their abundance in successive leaves and characterized the phenotype of mutations in different MIR156 and MIR157 genes. miR156/miR157 decline rapidly between leaf 1&2 and leaf 3 and decrease more slowly after this point. The amount of miR156/miR157 in leaves 1&2 greatly exceeds the threshold required to specify their identity. Subsequent leaves have relatively low levels of miR156/miR157 and are sensitive to small changes in their abundance. In these later-formed leaves, the amount of miR156/miR157 is close to the threshold required to specify juvenile vs. adult identity; a relatively small decrease in the abundance of miR156/157 in these leaves produces a disproportionately large increase in SPL proteins and a significant change in leaf morphology. miR157 is more abundant than miR156 but has a smaller effect on shoot morphology and SPL gene expression than miR156. This may be attributable to the inefficiency with which miR157 is loaded onto AGO1, as well as to the presence of an extra nucleotide at the 5' end of miR157 that is mis-paired in the miR157:SPL13 duplex. miR156 represses different targets by different mechanisms: it regulates SPL9 by a combination of transcript cleavage and translational repression and regulates SPL13 primarily by translational repression. Our results offer a molecular explanation for the changes in leaf morphology that occur during shoot development in Arabidopsis and provide new insights into the mechanism by which miR156 and miR157 regulate gene expression.

Two hundred 1-day-old male commercial Arbor Acres broiler birds were randomly distributed to a control group and a polysavone group (5 replicates of 20 birds each) to investigate the influence of polysavone, a natural extract from alfalfa, on abdominal fat deposition and immunity in broiler chickens. Birds in the control group were supplied with a basal diet, and 0.06% polysavone was added to the basal diet of birds in the polysavone group. Body weight and feed consumption for each replicate were recorded weekly. At 3, 4, 5, and 6 wk of age, 4 birds from each replicate were randomly selected for blood and organ sampling. Polysavone had no significant effect on feed intake, BW, or feed:gain ratio in the experimental period, and it decreased the abdominal fat weights at 5 and 6 wk of age. Polysavone improved (P <0.05) the relative thymus and spleen weights at 6 wk of age and the bursa weights at 4 and 5 wk of age compared with the control group. At 4 and 6 wk of age, the proliferation of T and B lymphocytes in the polysavone group was significantly greater (P <0.05) than that in the control group. When birds were 4 and 5 wk of age, polysavone resulted in a significant increase (P <0.05) in serum anti-Newcastle disease virus hemagglutination inhibition antibody titer. These results showed that polysavone may decrease abdominal fat deposition and enhance immunity without an adverse effect on the performance of broiler chickens.

Porphyromonas gingivalis, a gram-negative anaerobic bacterium, is a recognized periodontopathogen. It exhibits a high degree of aerotolerance and is able to survive in host cells, indicating that efficient oxidative stress protection mechanisms must be present in this organism. Manganese homeostasis plays a major role in oxidative stress protection in a variety of organisms; however, the transport and role of this metal in P. gingivalis is not well understood. Analysis of the genome of P. gingivalis W83 revealed the presence of two genes encoding homologs of a ferrous iron transport protein, FeoB1 and FeoB2. FeoB2 has been implicated in manganese accumulation in P. gingivalis. We sought to determine the role of the FeoB2 protein in metal transport as well as its contribution to resistance to oxygen radicals. Quantitative reverse transcriptase PCR analyses demonstrated that expression of feoB2 is induced in the presence of oxygen. The role of FeoB2 was investigated using an isogenic mutant strain deficient in the putative transporter. We characterized the FeoB2-mediated metal transport using 55 Fe 2؉ and 54 Mn 2؉ . The FeoB2-deficient mutant had dramatically reduced rates of manganese uptake (0.028 pmol/min/10 7 bacteria) compared with the parental strain (0.33 pmol/min/10 7 bacteria) (after 20 min of uptake using 50 nM of 54 Mn 2؉ ). The iron uptake rates, however, were higher in the mutant strain (0.75 pmol/min/10 7 bacteria) than in the wild type (0.39 pmol/min/10 7 bacteria). Interestingly, reduced survival rates were also noted for the mutant strain after exposure to H 2 O 2 and to atmospheric oxygen compared to the parental strain cultured under the same conditions. In addition, in vitro infection of host cells with the wild type, the FeoB2-deficient mutant, and the same-site revertant revealed that the mutant had a significantly decreased capability for intracellular survival in the host cells compared to the wild-type strain. Our results demonstrate that feoB2 encodes a major manganese transporter required for protection of the bacterium from oxidative stress generated by atmospheric oxygen and H 2 O 2 . Furthermore, we show that FeoB2 and acquisition of manganese are required for intracellular survival of P. gingivalis in host cells.

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