Proteome of the phytopathogen <Emphasis Type="Italic">Xanthomonas citri</Emphasis> subsp. <Emphasis Type="Italic">citri</Emphasis>: a global expression profile

Background  

Citrus canker is a disease caused by Xantomonas citri subsp.citri (Xac), and has emerged as one of the major threats to the worldwide citrus crop because it affects all commercial citrus varieties, decreases the production and quality of the fruits and can spread rapidly in citrus growing areas. In this work, the first proteome of Xac was analyzed using two methodologies, two-dimensional liquid chromatography (2D LC) and tandem mass spectrometry (MS/MS).     

Effects of deer,mice and dwarf bamboo on the emergence,survival and growth of <Emphasis Type="Italic">Abies homolepis</Emphasis> (Piceaceae) seedlings

In the subalpine mixed forest of Mt. Ôdaigahara, mid-western Japan, the understory is dominated by dwarf bamboo (Sasa nipponica), which is the major forage of overly populous sika deer (Cervus nippon). In the present study, we monitored the survival and growth of Abies homolepis seedlings over 5years to determine how they responded to the experimental removal of dwarf bamboo and to the exclusion of sika deer and mice (Apodemus argenteus and A.speciosus). Deer and dwarf bamboo reduced the survival of seedlings but had different effects on growth. The stems of seedlings were shorter in the presence of deer, indicating that taller seedlings were apt to be browsed by deer, whereas the diameters of seedlings were smaller in the presence of dwarf bamboo, mainly owing to its shading effect. The presence of mice decreased the number of seedlings germinating in a particular site, but had no effect on seedling survival after germination. There was no significant indirect effect whereby the survival of seedlings was predicted to be facilitated by the decreased biomass of bamboo because of grazing by deer. We supposed that this might be because the direct negative effect of deer was so large as to conceal the positive indirect effect.     

Pten deletion causes mTorc1-dependent ectopic neuroblast differentiation without causing uniform migration defects

Neuronal precursors, generated throughout life in the subventricular zone, migrate through the rostral migratory stream to the olfactory bulb where they differentiate into interneurons. We found that the PI3K-Akt-mTorc1 pathway is selectively inactivated in migrating neuroblasts in the subventricular zone and rostral migratory stream, and activated when these cells reach the olfactory bulb. Postnatal deletion of Pten caused aberrant activation of the PI3K-Akt-mTorc1 pathway and an enlarged subventricular zone and rostral migratory stream. This expansion was caused by premature termination of migration and differentiation of neuroblasts and was rescued by inhibition of mTorc1. This phenotype is reminiscent of lamination defects caused by Pten deletion in developing brain that were previously described as defective migration. However, live imaging in acute slices showed that Pten deletion did not cause a uniform defect in the mechanics of directional neuroblast migration. Instead, a subpopulation of Pten-null neuroblasts showed minimal movement and altered morphology associated with differentiation, whereas the remainder showed unimpeded directional migration towards the olfactory bulb. Therefore, migration defects of Pten-null neurons might be secondary to ectopic differentiation.     

New genes of Xanthomonas citri subsp. citri involved in pathogenesis and adaptation revealed by a transposon-based mutant library

Background  

Citrus canker is a disease caused by the phytopathogens Xanthomonas citri subsp. citri, Xanthomonas fuscans subsp. aurantifolli and Xanthomonas alfalfae subsp. citrumelonis. The first of the three species, which causes citrus bacterial canker type A, is the most widely spread and severe, attacking all citrus species. In Brazil, this species is the most important, being found in practically all areas where citrus canker has been detected. Like most phytobacterioses, there is no efficient way to control citrus canker. Considering the importance of the disease worldwide, investigation is needed to accurately detect which genes are related to the pathogen-host adaptation process and which are associated with pathogenesis.     

Escape flights of yellowhammers and greenfinches: more than just physics

Wintering birds increase their fat reserves throughout the day, and impaired escape performance is often considered to be an important cost of fat reserves. Since lifting a larger mass requires more energy, if birds escape at maximum power output, an increase in mass will impair the escape flight. In this study we did not find support for mass-dependent escape performance for yellowhammers, Emberiza citrinella, and greenfinches, Carduelis chloris, with natural daily mass increases of 7-8%. This suggests either that the birds were not performing at maximum output at dawn, when light, or that maximum power output was higher at dusk, when heavy. Either way, the birds seemed to be able to put more effort into their escape flight when heavier. In both species, when alarmed, birds took off significantly faster and at a steeper angle than when not alarmed. Yellowhammers escaped at a higher speed and angle than greenfinches, and reacted faster to the predator model. This suggests that predator escape is more than just Newtonian physics, and may be influenced by behavioural, as well as morphological, adjustments. Different species may have evolved different responses to predation risk. Our results seem to be in disagreement with recent ideas about mass-dependent predation risk. However, to build up reserves, birds have to increase exposure time, which increases predation risk. This cost may be more important than impaired escape performance when relatively small, daily, changes in body mass are considered. Copyright 2000 The Association for the Study of Animal Behaviour.     

Orphan glutamate receptor delta1 subunit required for high-frequency hearing

The function of the orphan glutamate receptor delta subunits (GluRdelta1 and GluRdelta2) remains unclear. GluRdelta2 is expressed exclusively in the Purkinje cells of the cerebellum, and GluRdelta1 is prominently expressed in inner ear hair cells and neurons of the hippocampus. We found that mice lacking the GluRdelta1 protein displayed significant cochlear threshold shifts for frequencies of >16 kHz. These deficits correlated with a substantial loss of type IV spiral ligament fibrocytes and a significant reduction of endolymphatic potential in high-frequency cochlear regions. Vulnerability to acoustic injury was significantly enhanced; however, the efferent innervation of hair cells and the classic efferent inhibition of outer hair cells were unaffected. Hippocampal and vestibular morphology and function were normal. Our findings show that the orphan GluRdelta1 plays an essential role in high-frequency hearing and ionic homeostasis in the basal cochlea, and the locus encoding GluRdelta1 represents a candidate gene for congenital or acquired high-frequency hearing loss in humans.     

Differentiated horizontal interneurons clonally expand to form metastatic retinoblastoma in mice

During neurogenesis, the progression from a progenitor cell to a differentiated neuron is believed to be unidirectional and irreversible. The Rb family of proteins (Rb, p107, and p130) regulates cell-cycle exit and differentiation during retinogenesis. Rb and p130 are redundantly expressed in the neurons of the inner nuclear layer (INL) of the retina. We have found that in the adult Rb;p130-deficient retinae p107 compensation prevents ectopic proliferation of INL neurons. However, p107 is haploinsufficient in this process. Differentiated Rb(-/-);p107(+/-);p130(-/-) horizontal interneurons re-entered the cell cycle, clonally expanded, and formed metastatic retinoblastoma. Horizontal cells were not affected in Rb(+/-);p107(-/-);p130(-/-) or Rb(-/-);p107(-/-);p130(+/-), retinae suggesting that one copy of Rb or p130 was sufficient to prevent horizontal proliferation. We hereby report that differentiated neurons can proliferate and form cancer while maintaining their differentiated state including neurites and synaptic connections.