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Comparison of the evolutionary dynamics of symbiotic and housekeeping loci: a case for the genetic coherence of rhizobial lineages 总被引:6,自引:1,他引:5
In prokaryotes, lateral gene transfer across chromosomal lineages may be
mediated by plasmids, phages, transposable elements, and other accessory
DNA elements. However, the importance of such transfer and the evolutionary
forces that may restrict gene exchange remain largely unexplored in native
settings. In this study, tests of phylogenetic congruence are employed to
explore the range of horizontal transfer of symbiotic (sym) loci among
distinct chromosomal lineages of native rhizobia, the nitrogen-fixing
symbiont of legumes. Rhizobial strains isolated from nodules of several
host plant genera were sequenced at three loci: symbiotic nodulation genes
(nodB and nodC), the chromosomal housekeeping locus glutamine synthetase II
(GSII), and a portion of the 16S rRNA gene. Molecular phylogenetic analysis
shows that each locus generally subdivides strains into the same major
groups, which correspond to the genera Rhizobium, Sinorhizobium, and
Mesorhizobium. This broad phylogenetic congruence indicates a lack of
lateral transfer across major chromosomal subdivisions, and it contrasts
with previous studies of agricultural populations showing broad transfer of
sym loci across divergent chromosomal lineages. A general correspondence of
the three rhizobial genera with major legume groups suggests that host
plant associations may be important in the differentiation of rhizobial nod
and chromosomal loci and may restrict lateral transfer among strains. The
second major result is a significant incongruence of nod and GSII
phylogenies within rhizobial subdivisions, which strongly suggests
horizontal transfer of nod genes among congenerics. This combined evidence
for lateral gene transfer within, but not between, genetic subdivisions
supports the view that rhizobial genera are "reproductively isolated" and
diverge independently. Differences across rhizobial genera in the
specificity of host associations imply that the evolutionary dynamics of
the symbiosis vary considerably across lineages in native settings.
相似文献
109.
Finocchietto P Barreyro F Holod S Peralta J Franco MC Méndez C Converso DP Estévez A Carreras MC Poderoso JJ 《PloS one》2008,3(3):e1749
Background
In the metabolic syndrome with hyperinsulinemia, mitochondrial inhibition facilitates muscle fat and glycogen accumulation and accelerates its progression. In the last decade, nitric oxide (NO) emerged as a typical mitochondrial modulator by reversibly inhibiting citochrome oxidase and oxygen utilization. We wondered whether insulin-operated signaling pathways modulate mitochondrial respiration via NO, to alternatively release complete glucose oxidation to CO2 and H2O or to drive glucose storage to glycogen.Methodology/Principal Findings
We illustrate here that NO produced by translocated nNOS (mtNOS) is the insulin-signaling molecule that controls mitochondrial oxygen utilization. We evoke a hyperinsulinemic-normoglycemic non-invasive clamp by subcutaneously injecting adult male rats with long-lasting human insulin glargine that remains stable in plasma by several hours. At a precise concentration, insulin increased phospho-Akt2 that translocates to mitochondria and determines in situ phosphorylation and substantial cooperative mtNOS activation (+4–8 fold, P<.05), high NO, and a lowering of mitochondrial oxygen uptake and resting metabolic rate (−25 to −60%, P<.05). Comparing in vivo insulin metabolic effects on gastrocnemius muscles by direct electroporation of siRNA nNOS or empty vector in the two legs of the same animal, confirmed that in the silenced muscles disrupted mtNOS allows higher oxygen uptake and complete (U-14C)-glucose utilization respect to normal mtNOS in the vector-treated ones (respectively 37±3 vs 10±1 µmolO2/h.g tissue and 13±1 vs 7.2±1 µmol 3H2O/h.g tissue, P<.05), which reciprocally restricted glycogen-synthesis by a half.Conclusions/Significance
These evidences show that after energy replenishment, insulin depresses mitochondrial respiration in skeletal muscle via NO which permits substrates to be deposited as macromolecules; at discrete hyperinsulinemia, persistent mtNOS activation could contribute to mitochondrial dysfunction with insulin resistance and obesity and therefore, to the progression of the metabolic syndrome. 相似文献110.