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Increased Aggressiveness (increased + aggressiveness)
Selected AbstractsInactivation of the gene for the nuclear receptor tailless in the brain preserving its function in the eyeEUROPEAN JOURNAL OF NEUROSCIENCE, Issue 8 2007Thorsten Belz Abstract During embryogenesis, tailless, an orphan member of the nuclear receptor family, is expressed in the germinal zones of the brain and the developing retina, and is involved in regulating the cell cycle of progenitor cells. Consequently, a deletion of the tailless gene leads to decreased cell number with associated anatomical defects in the limbic system, the cortex and the eye. These structural abnormalities are associated with blindness, increased aggressiveness, poor performance in learning paradigms and reduced anxiousness. In order to assess the contribution of blindness to the behavioural changes, we established tailless mutant mice with intact visual abilities. We generated a mouse line in which the second exon of the tailless gene is flanked by loxP sites and crossed these animals with a transgenic line expressing the Cre recombinase in the neurogenic area of the developing brain, but not in the eye. The resulting animals have anatomically indistinguishable brains compared with tailless germline mutants, but are not blind. They are less anxious and much more aggressive than controls, like tailless germline mutants. In contrast to germline mutants, the conditional mutants are not impaired in fear conditioning. Furthermore, they show good performance in the Morris water-maze despite severely reduced hippocampal structures. Thus, the pathological aggressiveness and reduced anxiety found in tailless germline mutants are due to malformations caused by inactivation of the tailless gene in the brain, but the poor performance of tailless null mice in learning and memory paradigms is dependent on the associated blindness. [source] Role of TPH-2 in brain function: News from behavioral and pharmacologic studiesJOURNAL OF NEUROSCIENCE RESEARCH, Issue 14 2007Roberto W. Invernizzi Abstract The recent discovery of TPH-2, a new isoform of tryptophan hydroxylase, the enzyme that catalyses the transformation of tryptophan into 5-hydroxytryptophan and the rate-limiting step in brain serotonin (5-HT) biosynthesis, has boosted new interest in the many functions of 5-HT in the brain and non-nervous tissues. Recent studies on TPH-2 are reviewed with particular attention to the role of this enzyme in behavior and in response to drugs as assessed by comparing strains of mice carrying a functional polymorphism of TPH-2. Most studies concur to indicate that 5-HT synthesis through TPH-2 influence nervous tissues whereas TPH-1 is responsible for the synthesis and action of 5-HT in peripheral organs. Partial impairment of brain 5-HT synthesis caused by polymorphism of the gene encoding TPH-2 causes reduced release of the neurotransmitter, increased aggressiveness, and alters the response to drugs inhibiting the reuptake of 5-HT. Strain comparison might be a useful strategy to investigate the genotype-dependent alterations of TPH-2. © 2007 Wiley-Liss, Inc. [source] How will plant pathogens adapt to host plant resistance at elevated CO2 under a changing climate?NEW PHYTOLOGIST, Issue 3 2003Sukumar Chakraborty Summary , , To better understand evolution we have studied aggressiveness of the anthracnose pathogen, Colletotrichum gloeosporioides, collected from Stylosanthes scabra pastures between 1978 and 2000 and by inoculating two isolates onto two cultivars over 25 sequential infection cycles at ambient (350 ppm) and twice-ambient atmospheric CO2 in controlled environments. , , Regression analysis of the field population showed that aggressiveness increased towards a resistant cultivar, but not towards a susceptible cultivar, that is no longer grown commercially. , , Here we report for the first time that aggressiveness increased on both cultivars after a few initial infection cycles at twice-ambient CO2 as isolates adapted to combat enhanced host resistance, while at ambient CO2 this increased steadily for most cycles as both cultivars selected for increased aggressiveness. Genetic fingerprint and karyotype of isolates changed for some CO2 -cultivar combinations, but these were not related to changed aggressiveness. , , At 700 ppm fecundity increased for both isolates, and this increased population size, in combination with a conducive microclimate for anthracnose from an enlarged plant canopy under elevated CO2, could accelerate pathogen evolution. [source] Genetic structure and pathogenicity of populations of Phytophthora infestans from organic potato crops in France, Norway, Switzerland and the United KingdomPLANT PATHOLOGY, Issue 4 2007W. G. Flier Genetic variation and pathogenicity of Phytophthora infestans isolates collected from organic potato crops of the susceptible cv. Bintje and the moderately resistant cv. Santé were assessed in France, Norway, and the United Kingdom in 2001 and in Switzerland in 2001 and 2002. Population structures differed considerably between the four P. infestans populations. Those from France, Switzerland and the UK were mainly clonal populations showing restricted levels of genetic diversity, whilst those from Norway were mixed A1 and A2 mating type populations with high levels of genetic diversity, suggesting periodical sexual reproduction. Isolates collected from cv. Bintje were on average more aggressive than or comparable to isolates from cv. Santé. Race complexity varied considerably between the regional P. infestans populations, with isolates from France and Switzerland showing the highest number of virulence factors. In all pathogen samples but the French, isolates collected from cv. Santé were more complex than isolates collected from cv. Bintje. No directional selection towards increased aggressiveness towards the more resistant cultivar Santé was observed. This suggests that there is no shift towards increased levels of pathogenicity in P. infestans populations following the large-scale introduction of more resistant potato varieties in organic production systems in Europe. [source] Proteomic analysis identified N-cadherin, clusterin, and HSP27 as mediators of SPARC (secreted protein, acidic and rich in cysteines) activity in melanoma cellsPROTEINS: STRUCTURE, FUNCTION AND BIOINFORMATICS, Issue 22 2007María Soledad Sosa Abstract Secreted protein, acidic and rich in cysteines (SPARC) is a secreted protein associated with increased aggressiveness of different human cancer types. In order to identify downstream mediators of SPARC activity, we performed a 2-DE proteomic analysis of human melanoma cells following antisense-mediated downregulation of SPARC expression. We found 23/504 differential spots, 15 of which were identified by peptide fingerprinting analysis. Three of the differential proteins (N-cadherin (N-CAD), clusterin (CLU), and HSP27) were validated by immunoblotting, confirming decreased levels of N-CAD and CLU and increased amounts of HSP27 in conditioned media of cells with diminished SPARC expression. Furthermore, transient knock down of SPARC expression in melanoma cells following adenoviral-mediated transfer of antisense RNA confirmed these changes. We next developed two different RNAs against SPARC that were able to inhibit in vivo melanoma cell growth. Immunoblotting of the secreted fraction of RNAi-transfected melanoma cells confirmed that downregulation of SPARC expression promoted decreased levels of N-CAD and CLU and increased secretion of HSP27. Transient re-expression of SPARC in SPARC-downregulated cells reverted extracellular N-CAD, CLU, and HSP27 to levels similar to those in the control. These results constitute the first evidence that SPARC, N-CAD, CLU, and HSP27 converge in a unique molecular network in melanoma cells. [source] | |||||||||||||||||||