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E' ormai tempo per una nuova sintesi? Riflessioni sullo stato delle teorie evoluzioniste
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AtFer1 ferritin gene regulates senescence in Arabidopsis
No full textThe ferritins are multimeric, iron-storage proteins involved in the regulation of free iron levels in the cells. Four different ferritin genes have been identified in Arabidopsis.
AtFer1 transcript strongly accumulates upon treatment with excess iron, via a nitric oxide-mediated pathway: an Iron Dependent Regulatory Sequence (IDRS), responsible for repression of AtFer1 gene transcription under low iron supply, is the end-target of such signal transduction pathway. However other cis-elements, different from the IDRS, regulate the developmental expression of the AtFer1 isoform as the AtFer1 promoter is also activated in leaves during age-dependent senescence in a IDRS-independent manner.
In order to investigate physiological relevance of Arabidopsis AtFer1 ferritin during senescence we isolated a mutant line KO in the AtFer1 gene. This AtFer1 KO line shows symptoms of accelerated senescence: the decrease of maximal photochemical efficiency and the degradation of chlorophyll and proteins are indeed accelerated with respect to the wild-type. Interestingly, the KO line shows no accelerated dark-induced senescence. These results, together with the evidence that AtFer1 promoter activation precedes any visible senescing symptoms, suggest that AtFer1 is one key gene in the regulation of the onset of age-dependent senescence program in Arabidopsis
Mitochondrial iron metabolism in plants: frataxin comes into play
No full textFriedreich ataxia (FRDA), an autosomal
recessive neurological dysfunction that severely impairs motor coordination and reduction of life expectancy in humans, is caused by a deficiency in frataxin, a nuclear-encoded mitochondrial protein.
Recently, a frataxin ortholog has been identified in Arabidopsis thaliana, named AtFH, with a transit peptide for localization in mitochondria and 65%
sequence identity with human frataxin (Busi et al. FEBS Lett 576:141–144, 2004). Complementation of S. cerevisiae mutant strain Δyfh1 deficient in frataxin
with AtFH, proved that the plant isoform is a
functional protein, able to restore normal respiration and growth rates in the mutant yeast (Busi et al. FEBS Lett 576:141–144, 2004). AtFH is localized in mitochondria as its animal counterparts (Busi et al.
Plant J 48:873–882, 2006); it is expressed mainly in flowers and developing embryos and it is an essential protein, since the knocking out of AtFH gene causes arrest of embryo development at the globular stage
(Vazzola et al. FEBS Lett 581:667–672, 2007). A TDNA insertional A.thaliana mutant showing a greater than 50% reduction of AtFH protein content, named atfh-1, has impaired activity of two mitochondrial enzymes possessing [Fe-S] clusters: aconitase and
succinate dehydrogenase (Busi et al. Plant J 48:873-882, 2006). The results obtained in the last ten years on animal systems can contribute, without any doubt, to the elucidation of the role of frataxin in plant
mitochondria; however, mitochondria of photosynthetically active cells, differently from animal ones, are not the major source of Reactive Oxygen Species (ROS) which could suggest possible differences in function between plant and animal frataxin
NITRIC OXIDE MEDIATES IRON INDUCTION OF FERRITIN ACCUMULATION IN ARABIDOPSIS THALIANA
No full textNitric oxide (NO) is a signaling molecule involved in many different functions in mammal cells, among which the regulation of iron homeostasis. The recent discovery of NO-mediated regulation of aconitase activity also in plant cells prompted us to investigate the possible role of NO as regulator of iron homeostasis in plant cells, in particular its involvement in the regulation of A.thaliana ferritin, an iron-storage protein which accumulates in response to iron increase. The infiltration of the NO-donor SNP in Arabidopsis leaves caused a sustained accumulation of the transcript encoding ferritin; protein accumulation was also observed, although at much lower extent. The NO-dependent accumulation of ferritin transcript was observed also in iron-depleted Arabidopsis cells, whereas CPTIO, a NO scavenger, was able to completely abolish ferritin transcript accumulation caused by iron loading. To establish a possible involvement of cGMP as signal in in NO-mediated ferritin accumulation, we treated cells with 8 Br-cGMP, a cGMP analogous able to permeate cells. 8Br-cGMP was not sufficient to either induce ferritin accumulation nor to act synergistically with iron or SNP cGMP was not even found to participate to this signalling pathway since ODQ, an inhibitor of NO-dependent guanilate cyclase was not able to repress iron- nor SNP-induced ferritin accumulation. Furthermore calyculin, a Ser/Thr phosphatase inhibitor, completely abolished iron- or SNP-induced transcript accumulation. We propose that NO locates downstream of iron in the signalling pathway leading to ferritin accumulation which proceeds, beyond NO, through cGMP independent, Ser/Thr phosphatase dependent steps
ISOLATION OF AN ARABIDOPSIS THALIANA MUTANT KNOCKED-OUT IN THE FERRITIN (ATFER1) GENE
No full textIron is a critical element in photosynthetic tissues: it is an essential constituent of the photosynthetic complexes involved in electron transport but it is toxic when it is in a free, not complexed form, because it acts as a catalyst in the production of hydroxyl radicals during the Haber-Weiss reaction. The ability of the leaves to store iron in the chloroplasts in a soluble, readily available and non toxic form is provided by ferritins, a class of proteins present in plants as well as in bacteria, fungi and animals. Goal of our research is to better understand ferritin involvement in the plant protection against various oxidative stresses, like photoinhibition or iron excess. For that purpose we isolated, from the KO Wisconsin mutants collection, an Arabidopsis mutant bearing a T-DNA insertion in the ferritin Atfer1 promoter, 40 bp upstream the starting ATG. A description of the molecular steps through which the isolation of the mutant was performed and a preliminary physiological characterization will be given
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