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    Legume leaf senescence: a trascriptional analysis

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    Senescence is the last stage of development of a leaf, and is marked by a progressive degradation of cellular components and their recycling to other organs of a plant. We recently performed a transcriptomic analysis of leaf senescence in the legume model Medicago truncatula. Changes in gene expression reflected the profound physiological rearrangement and provided intriguing clues for the involvement of some of the members identified, which await future investigation. The resulting data also revealed similarities and differences with Arabidopsis leaf senescence

    KDC2, a functional homomeric channel expressed during carrot embryogenesis

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    In Daucus carota, the model system for embryogenesis, it has been demonstrated that potassium and K(+) selective channels are involved in embryo development. Here, we report the isolation and cloning of a new carrot Shaker-like potassium channel, potassium D. carota channel 2 (KDC2), whose expression pattern during somatic embryogenesis proceeds along with the establishment of the polar axes and the settlement of the hypocotyl region. In plants, KDC2 transcript is localized at the shoot level, in the epidermis and guard cells, similarly to its Arabidopsis homolog KAT1. Electrophysiological assays indicated KDC2 as the first carrot subunit able to form homomeric functional channels in Xenopus oocytes, with properties similar to those of Arabidopsis KAT1

    Nitric oxide affects plant mitochondrial functionality in vivo

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    In this report, we show that nitric oxide affects mitochondrial functionality in plant cells and reduces total cell respiration due to strong inhibition of the cytochrome pathway. The residual respiration depends on the alternative pathway and novel synthesis of alternative oxidase occurs. These modifications are associated with depolarisation of the mitochondrial membrane potential and release of cytochrome c from mitochondria, suggesting a conserved signalling pathway in plants and animals. This signal cascade is triggered at the mitochondrial level and induces about 20% of cell death. In order to achieve a higher level of cell death, the addition of H(2)O(2) is necessary
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