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Stress Resistance (stress + resistance)
Kinds of Stress Resistance Selected AbstractsStress Resistance and Environmental Dependency of Inbreeding Depression in Drosophila melanogasterCONSERVATION BIOLOGY, Issue 4 2000Jesper Dahlgaard Two important issues are whether stress and inbreeding effects are independent as opposed to synergistic, and whether inbreeding effects are general across stresses as opposed to stress-specific. We found that inbreeding reduced resistance to acetone and desiccation in adult Drosophila melanogaster, whereas resistance to knockdown heat stress was not affected. Inbred flies, however, experienced a greater proportional decrease in productivity than outbreds following heat stress. Correlations using line means indicated that all resistance traits were uncorrelated in the inbred as well as in the outbred flies. Recessive, deleterious alleles therefore did not appear to have any general deleterious effects on stress resistance. Inbreeding within a specific environment and selection for resistant genotypes may therefore purge a population of deleterious genes specific to only one environmental stress. Resumen: Tanto la endogamia como el estrés ambiental pueden tener efectos adversos sobre la adaptabilidad afectando la conservación de especies en peligro de extinción. Dos temas importantes son determinar si los efectos del estrés y la endogamia son independientes en lugar de ser sinérgicos, y determinar si los efectos de la endogamia son generales para distintos tipos de estrés o si son específicos para un tipo determinado de estrés. Encontramos que la endogamia reduce la resistencia a la acetona y la desecación en adultos de Drosophila melanogaster, mientras que la resistencia al efecto demoledor del estrés por calor no fue afectada. Sin embargo, las moscas endogámicas experimentaron una disminución proporcionalmente mayor en la productividad que aquellas moscas sin endogamia después de experimentar un estrés por calor. Las correlaciones obtenidas usando líneas medias indicaron que las características de resistencia no estuvieron correlacionadas ni en moscas con endogamia, ni en moscas sin ella. Aparentemente los alelos nocivos recesivos no tuvieron ningún efecto nocivo general en la resistencia al estrés. La endogamia dentro de un ambiente específico y la selección por genotipos resistentes podrían, por lo tanto, eliminar una población de genes nocivos específicos a un solo estrés ambiental. [source] Interactive effects of dietary vitamin C and phospholipid in micro-bound diet for growth, survival, and stress resistance of larval red sea bream, Pagrus majorAQUACULTURE NUTRITION, Issue 5 2010T. REN Abstract This study was conducted to examine the effects of dietary ascorbic acid (AsA) and phospholipid (PL) and their interaction on growth, survival, and stress resistance in red sea bream larvae. Twenty-six days old red sea bream were fed nine micro-bound diets supplemented three levels of AsA (0, 800 and 1600 mg kg,1 diet) and PL (0, 20 and 40 g kg,1 diet) for 15 days. Dietary AsA and PL were both significant factors on survival rates. There was also an interaction between dietary AsA and PL on survival rate (P < 0.05). The larvae fed 800 or 1600 mg kg,1 AsA with 40 g kg,1 PL diets showed the highest survival rate, with values similar to those of the live-food supplemented group. Stress resistance against low salinity exposure significantly increased with increased dietary level of AsA and PL. However, significant interaction of AsA and PL was not detected. The larvae fed 1600 mg kg,1 AsA with 40 g kg,1 PL diet showed the highest stress resistance among all diets, but it was not significantly different than that of larvae fed 800 mg kg,1 AsA with 40 g kg,1 PL diet. This study clearly demonstrated that combined use of AsA and PL can improve survival of 26,40 days posthatching red sea bream larvae. Moreover, the present study suggested that 800 mg kg,1 AsA with 40 g kg,1 PL in diet was needed for producing high quality seedling under the stressful conditions. [source] Stress Resistance and Environmental Dependency of Inbreeding Depression in Drosophila melanogasterCONSERVATION BIOLOGY, Issue 4 2000Jesper Dahlgaard Two important issues are whether stress and inbreeding effects are independent as opposed to synergistic, and whether inbreeding effects are general across stresses as opposed to stress-specific. We found that inbreeding reduced resistance to acetone and desiccation in adult Drosophila melanogaster, whereas resistance to knockdown heat stress was not affected. Inbred flies, however, experienced a greater proportional decrease in productivity than outbreds following heat stress. Correlations using line means indicated that all resistance traits were uncorrelated in the inbred as well as in the outbred flies. Recessive, deleterious alleles therefore did not appear to have any general deleterious effects on stress resistance. Inbreeding within a specific environment and selection for resistant genotypes may therefore purge a population of deleterious genes specific to only one environmental stress. Resumen: Tanto la endogamia como el estrés ambiental pueden tener efectos adversos sobre la adaptabilidad afectando la conservación de especies en peligro de extinción. Dos temas importantes son determinar si los efectos del estrés y la endogamia son independientes en lugar de ser sinérgicos, y determinar si los efectos de la endogamia son generales para distintos tipos de estrés o si son específicos para un tipo determinado de estrés. Encontramos que la endogamia reduce la resistencia a la acetona y la desecación en adultos de Drosophila melanogaster, mientras que la resistencia al efecto demoledor del estrés por calor no fue afectada. Sin embargo, las moscas endogámicas experimentaron una disminución proporcionalmente mayor en la productividad que aquellas moscas sin endogamia después de experimentar un estrés por calor. Las correlaciones obtenidas usando líneas medias indicaron que las características de resistencia no estuvieron correlacionadas ni en moscas con endogamia, ni en moscas sin ella. Aparentemente los alelos nocivos recesivos no tuvieron ningún efecto nocivo general en la resistencia al estrés. La endogamia dentro de un ambiente específico y la selección por genotipos resistentes podrían, por lo tanto, eliminar una población de genes nocivos específicos a un solo estrés ambiental. [source] Environmental tuning of mutation ratesENVIRONMENTAL MICROBIOLOGY, Issue 2 2006Claude Saint-Ruf Summary Through their life cycles, bacteria experience many different environments in which the relationship between available energy resources and the frequency and the nature of various stresses is highly variable. In order to survive in such changeable environments, bacteria must balance the need for nutritional competence with stress resistance. In Escherichia coli natural populations, this is most frequently achieved by changing the regulation of the RpoS sigma factor-dependent general stress response. One important secondary consequence of altered regulation of the RpoS regulon is the modification of mutation rates. For example, under nutrient limitation during stationary phase, the high intracellular concentration of RpoS diminishes nutritional competence, increases stress resistance, and, by downregulating the mismatch repair system and downregulating the expression of the dinB gene (coding for PolIV translesion synthesis polymerase) increases mutation rates. The reduction of the intracellular concentration of RpoS has exactly opposite effects on nutritional competence, stress resistance and mutation rates. Therefore, the natural selection that favours variants having the highest fitness under different environmental conditions results in high variability of stress-associated mutation rates in those variants. [source] Dynamics of heat-induced thermal stress resistance and hsp70 expression in the springtail, Orchesella cinctaFUNCTIONAL ECOLOGY, Issue 2 2009Simon Bahrndorff Summary 1The relationship between thermal resistance and expression of inducible heat shock proteins, especially Hsp70, depends on the species and temperature treatments. The induction of Hsp70 has been shown to be essential for heat stress survival in a number of species, yet the maximum protein expression levels do not coincide with peak survival after heat hardening in Drosophila. 2Here we study the functional relationship between heat-induced expression of the heat shock protein Hsp70, and thermal resistance in adult Orchesella cincta by comparing thermal resistance (survival of 37·4 °C for 60 min) with Hsp70 gene and protein expression levels, all three measured at time points 2, 4, 6, 23, 27, 49 h after a heat hardening treatment (35·4 °C for 60 min). 3Thermotolerance increased over time after heat hardening until 49 h after exposure when the experiment ended. On the other hand the expression of hsp70 messenger RNA reached a peak within the first 2 h and then sharply decreased after 6 h. Within 23 h hsp70 expression was back to control levels. 4Surprisingly, protein levels of Hsp70 followed thermotolerance and reached the highest levels 49 h after heat hardening. A significant positive association was found between thermotolerance and Hsp70 protein levels, but not with hsp70 mRNA levels. 5Our results support a strong correlation between Hsp70 expression levels and thermal resistance following a heat hardening treatment. They also show that gene and protein expression follow different dynamics, a difference that may be important for our understanding of the role of candidate genes in functional studies. [source] Transcription elongation factor S-II maintains transcriptional fidelity and confers oxidative stress resistanceGENES TO CELLS, Issue 10 2003Hiroshi Koyama Background:, During transcription elongation, RNA polymerase II is arrested on the template when incorrect ribonucleotides are incorporated into the nascent transcripts. Transcription factor S-II enhances the excision of these mis-incorporated nucleotides by RNA polymerase II and stimulates transcription elongation in vitro. This mechanism is considered to be transcriptional proof-reading, but its physiological relevance remains unknown. Results:, We report that S-II contributes to the maintenance of transcriptional fidelity in vivo. We employed a genetic reporter assay utilizing a mutated lacZ gene from which active ,-galactosidase protein is expressed when mRNA proof-reading is compromised. In S-II-disrupted mutant yeasts, ,-galactosidase activity was ninefold higher than that in wild-type. The S-II mutant exhibited sensitivity to oxidants, which was suppressed by introduction of the S-II gene. The mutant S-II proteins, which are unable to stimulate transcription by RNA polymerase II in vitro, did not suppress the sensitivity of the mutants to oxidative stress or maintain transcriptional fidelity. Conclusion:, These results suggest that S-II confers oxidative stress resistance by providing an mRNA proof-reading mechanism during transcription elongation. [source] The evolution of water transport in plants: an integrated approachGEOBIOLOGY, Issue 2 2010J. PITTERMANN This review examines the evolution of the plant vascular system from its beginnings in the green algae to modern arborescent plants, highlighting the recent advances in developmental, organismal, geochemical and climatological research that have contributed to our understanding of the evolution of xylem. Hydraulic trade-offs in vascular structure,function are discussed in the context of canopy support and drought and freeze,thaw stress resistance. This qualitative and quantitative neontological approach to palaeobotany may be useful for interpreting the water-transport efficiencies and hydraulic limits in fossil plants. Large variations in atmospheric carbon dioxide levels are recorded in leaf stomatal densities, and may have had profound impacts on the water conservation strategies of ancient plants. A hypothesis that links vascular function with stomatal density is presented and examined in the context of the evolution of wood and/or vessels. A discussion of the broader impacts of plant transport on hydrology and climate concludes this review. [source] GROWTH OF CRUSTOSE LICHENS: A REVIEWGEOGRAFISKA ANNALER SERIES A: PHYSICAL GEOGRAPHY, Issue 1 2010RICHARD ARMSTRONG ABSTRACT. Crustose species are the slowest growing of all lichens. Their slow growth and longevity, especially of the yellow-green Rhizocarpon group, has made them important for surface-exposure dating (lichenometry). This review considers various aspects of the growth of crustose lichens revealed by direct measurement including: 1) early growth and development; 2) radial growth rates (RGR, mm yr,1); 3) the growth rate,size curve; and 4) the influence of environmental factors. Many crustose species comprise discrete areolae that contain the algal partner growing on the surface of a non-lichenized fungal hypothallus. Recent data suggest that ,primary' areolae may develop from free-living algal cells on the substratum while ,secondary' areolae develop from zoospores produced within the thallus. In more extreme environments, the RGR of crustose species may be exceptionally slow but considerably faster rates of growth have been recorded under more favourable conditions. The growth curves of crustose lichens with a marginal hypothallus may differ from the ,asymptotic' type of curve recorded in foliose and placodioid species; the latter are characterized by a phase of increasing RGR to a maximum and may be followed by a phase of decreasing growth. The decline in RGR in larger thalli may be attributable to a reduction in the efficiency of translocation of carbohydrate to the thallus margin or to an increased allocation of carbon to support mature ,reproductive' areolae. Crustose species have a low RGR accompanied by a low demand for nutrients and an increased allocation of carbon for stress resistance; therefore enabling colonization of more extreme environments. [source] Genome-wide linkage and QTL mapping in porcine F2 families generated from Pietrain, Meishan and Wild Boar crossesJOURNAL OF ANIMAL BREEDING AND GENETICS, Issue 6 2003H. Geldermann Summary Three informative pig F2 families based on European Wild Boar (W), Meishan (M) and Pietrain (P) crosses have been used for genome-wide linkage and quantitative trait loci (QTL) analysis. Altogether 129 microsatellites, 56 type I loci and 46 trait definitions (specific to growth, fattening, fat deposition, muscling, meat quality, stress resistance and body conformation) were included in the study. In the linkage maps of M × P, W × P and W × M families, average spacing of markers were 18.4, 19.7 and 18.8 cM, the numbers of informative meioses were 582, 534 and 625, and the total lengths of autosomes measured were 27.3, 26.0 and 26.2 Morgan units, respectively. Maternal maps were on average 1.3 times longer than paternal maps. QTLs contributing more than 3% of F2 phenotypic variance could be identified at p < 0.05 chromosome-wide level. Differences in the numbers and positions of QTLs were observed between families. Genome-wide significant QTL effects were mapped for growth and fattening traits on eight chromosomes (1, 2, 4, 13, 14, 17, 18 and X), for fat deposition traits on seven chromosomes (1, 2, 3, 4, 6, 7 and X), for muscling traits on 11 chromosomes (1, 2, 3, 4, 6, 7, 8, 12, 14, 15 and X), for meat quality and stress resistance traits on seven chromosomes (2, 3, 6, 13, 16, 18 and X), and QTLs for body-conformation traits were detected on 14 chromosomes. Closely correlated traits showed similar QTL profiles within families. Major QTL effects for meat quality and stress resistance traits were found on SSC6 in the interval RYR1-A1BG in the W × P and M × P families, and could be attributed to segregation of the RYR1 allele T derived from Pietrain, whereas no effect in the corresponding SSC6 interval was found in family W × M, where Wild Boar and Meishan both contributed the RYR1 allele C. QTL positions were mostly similar in two of the three families for body conformation traits and for growth, fattening, fat deposition and muscling traits, especially on SSC4 (interval SW1073-NGFB). QTLs with large effects were also mapped on SSC7 in the major histocompatibility complex (MHC) (interval CYP21A2-S0102) and affected body length, weight of head and many other traits. The identification of DNA variants in genes causative for the QTLs requires further fine mapping of QTL intervals and a positional cloning. However, for these subsequent steps, the genome-wide QTL mapping in F2 families represents an essential starting point and is therefore significant for animal breeding. Zusammenfassung Drei informative F2 -Familien, die aus Kreuzungen von Europäischem Wildschwein (W), Meishan (M) und Pietrain (P) erstellt worden waren, wurden für eine genomweite Kopplungs- und QTL-Analyse benutzt. Insgesamt wurden 129 Mikrosatellitenloci, 56 Type-I-Loci und 46 Merkmalsdefinitionen (für Wachstum, Mastleistung, Fettansatz, Bemuskelung, Fleischqualität, Stressresistenz und Körperform) in die Untersuchungen einbezogen. In den Kopplungskarten der Familien M × P, W × P und W × M wurden durchschnittliche Markerabstände von 18.4, 19.7 bzw. 18.8 cM erreicht und 582, 534 bzw. 625 informative Meiosen beobachtet. Für die Gesamtlängen der Autosomen wurden in den drei Familien 27.3, 26.0 bzw. 26.2 Morgan-Einheiten gemessen. Die maternalen Kopplungskarten waren durchschnittlich 1.3-fach länger als die paternalen. QTLs, die mehr als 3% der phänotypischen Varianz in der F2 -Generation erklärten, konnten mit p < 0.05 chromosomenweitem Signifikanzniveau nachgewiesen werden. Zwischen den Familien wurden Differenzen in den Anzahlen und Positionen der QTLs beobachtet. Genomweit signifikante QTL-Effekte wurden für Wachstum und Fettansatz auf acht Chromosomen (1, 2, 4, 13, 14, 17, 18 und X) kartiert, für Fettansatz auf sieben Chromosomen (1, 2, 3, 4, 6, 7 und X), für Bemuskelung auf elf Chromosomen (1, 2, 3, 4, 6, 7, 8, 12, 14, 15 und X), für Fleischqualität/Stressresistenz auf sieben Chromosomen (2, 3, 6, 13, 16, 18 und X), und QTLs für die Körperform wurden auf 14 Chromosomen kartiert. Eng korrelierte Merkmale zeigten ähnliche QTL-Profile innerhalb Familien. Die bedeutsamsten QTL-Effekte wurden für Fleischqualitäts- und Stressresistenzmerkmale auf Chromosom 6, Intervall RYR1-A1BG, in den Familien W × P und M × P gefunden, während in diesem Chromosomenintervall in der Familie W × M, in der der RYR1 -Locus keine segregierenden Exon-Allele aufwies, kein QTL zu erkennen war. Mehrere der QTL-Positionen waren für die Körperform wie auch für Wachstum, Mastleistung, Fettansatz und Bemuskelung in zwei von drei Familien ähnlich. Dies galt besonders für Chromosom 4 (Intervall SW1073-NGFB). QTLs mit großen Effekten wurden auf Chromosom 7 im MHC (Intervall CYP21A2-S0102) kartiert; sie beeinflussten Körperlänge, Kopfgewicht, aber auch viele weitere Merkmale. Zur Identifizierung der DNA-Varianten, die einem QTL zugrunde liegen, ist eine Feinkartierung von QTLs und positionale Klonierung erforderlich. Für diese nachfolgenden Untersuchungsmethoden ist jedoch die genomweite QTL-Kartierung in F2 -Familien ein entscheidender Ausgangspunkt; sie ist deshalb bedeutungsvoll für die Tierzüchtung. [source] Changes in the Lactobacillus community during Ricotta forte cheese natural fermentationJOURNAL OF APPLIED MICROBIOLOGY, Issue 5 2000F. Baruzzi The loss of microbial biodiversity due to the increase in large-scale industrial processes led to the study of the natural microflora present in a typical little known dairy product. The community of lactobacilli was studied in order to understand the natural fermentation of Ricotta forte cheese. The combined use of RAPD analysis, 16S rDNA sequencing and physiological tests allowed 33 different strains belonging to 10 species of Lactobacillus to be characterized. RAPD analysis revealed the heterogeneity of both the Lact. kefiri and Lact. paracasei species. The sequence analysis of the large 16S/23S rRNA spacer region enabled Lact. plantarum to be distinguished from Lact. paraplantarum, two closely related species belonging to the Lact. plantarum group. The recovery of strains endowed with interesting physiological characteristics, such as strong stress resistance, could improve technological and/or organoleptic characteristics of Ricotta forte cheese and other fermented foods. [source] The response of Aeromonas hydrophila to oxidative stress induced by exposure to hydrogen peroxideJOURNAL OF APPLIED MICROBIOLOGY, Issue 1 2000J.P.B. Landre Aeromonas hydrophila, an opportunist human pathogen of low virulence, was shown to display a high degree of sensitivity upon exposure to hydrogen peroxide. As with other species, Aer. hydrophila is able to develop the capacity to resist loss of viability induced by such oxidative stress. Development of stress resistance follows the archetypal profile where pre-exposure of a population to sub-lethal levels of H2O2 stimulates onset of tolerance to further exposure. Acquisition of tolerance critically requires nascent protein synthesis. Further analysis demonstrated population growth phase influences the degree of sensitivity of the organism. Late stationary phase cultures demonstrate a decreased sensitivity compared with younger populations. Significantly, it was also determined that stock culture age influenced the level of sensitivity of the derived experimental culture, where an increased stock culture age corresponded with enhanced resistance to H2O2. These data show that Aer. hydrophila population phenotype is influenced by the phenotype of the donor stock culture. [source] Age-related differences in insulin-like growth factor-1 receptor signaling regulates Akt/FOXO3a and ERK/Fos pathways in vascular smooth muscle cellsJOURNAL OF CELLULAR PHYSIOLOGY, Issue 2 2008Muyao Li Advanced age is a major risk factor for atherosclerosis, but how aging per se influences pathogenesis is not clear. Insulin-like growth factor-1 receptor (IGF-1R) promotes aortic vascular smooth muscle cell (VSMC) growth, migration, and extracellular matrix formation, but how IGF-1R signaling changes with age in VSMC is not known. We previously found age-related differences in the activation of Akt/FOXO3a and ERK1/2 pathways in VSMC, but the upstream signaling remains unclear. Using explanted VSMC from Fischer 344/Brown Norway F1 hybrid rats shown to display age-related vascular pathology similar to humans, we compared IGF-1R expression in early passages of VSMC and found a constitutive activation of IGF-1R in VSMC from old compared to young rats, including IGF-1R expression and its tyrosine kinase activity. The link between IGF-1R activation and the Akt/FOXO3a and ERK pathways was confirmed through the induction of IGF-1R with IGF-1 in young cells and attenuation of IGF-1R with an inhibitor in old cells. The effects of three kinase inhibitors: AG1024, LY294002, and TCN, were compared in VSMC from old rats to differentiate IGF-1R from other upstream signaling that could also regulate the Akt/FOXO and ERK pathways. Genes for p27kip-1, catalase and MnSOD, which play important roles in the control of cell cycle arrest and stress resistance, were found to be FOXO3a-targets based on FOXO3a-siRNA treatment. Furthermore, IGF-1R signaling modulated these genes through activation of the Akt/FOXO3a pathway. Therefore, activation of IGF-1R signaling influences VSMC function in old rats and may contribute to the increased risk for atherosclerosis. J. Cell. Physiol. 217: 377,387, 2008. © 2008 Wiley-Liss, Inc. [source] Genome-wide screen identifies Escherichia coli TCA-cycle-related mutants with extended chronological lifespan dependent on acetate metabolism and the hypoxia-inducible transcription factor ArcAAGING CELL, Issue 5 2010Stavros Gonidakis Summary Single-gene mutants with extended lifespan have been described in several model organisms. We performed a genome-wide screen for long-lived mutants in Escherichia coli, which revealed strains lacking tricarboxylic acid (TCA)-cycle-related genes that exhibit longer stationary-phase survival and increased resistance to heat stress compared to wild-type. Extended lifespan in the sdhA mutant, lacking subunit A of succinate dehydrogenase, is associated with the reduced production of superoxide and increased stress resistance. On the other hand, the longer lifespan of the lipoic acid synthase mutant (lipA) is associated with reduced oxygen consumption and requires the acetate-producing enzyme pyruvate oxidase, as well as acetyl-CoA synthetase, the enzyme that converts extracellular acetate to acetyl-CoA. The hypoxia-inducible transcription factor ArcA, acting independently of acetate metabolism, is also required for maximum lifespan extension in the lipA and lpdA mutants, indicating that these mutations promote entry into a mode normally associated with a low-oxygen environment. Because analogous changes from respiration to fermentation have been observed in long-lived Saccharomyces cerevisiae and Caenorhabditis elegans strains, such metabolic alterations may represent an evolutionarily conserved strategy to extend lifespan. [source] Altered signalling from germline to intestine pushes daf-2;pept-1 Caenorhabditis elegans into extreme longevityAGING CELL, Issue 4 2010Britta Spanier Summary The insulin-like signalling pathway is a central regulator of development, metabolism, stress resistance and lifespan in eukaryotes. Caenorhabditis elegans daf-2(e1370) animals with a loss-of-function mutation in the insulin-like receptor live twice as long as wild-type animals, and the additional knockout of the intestinal di- and tripeptide transporter pept-1 further increases lifespan by 60%. In assessing the underlying molecular mechanisms for this phenomenon, microarray-based transcriptome data sets of daf-2(e1370) and daf-2(e1370);pept-1(lg601) animals were compared with a focus on genes that showed significantly higher changes in expression levels in daf-2;pept-1 than in daf-2. We identified 187 genes with at least fourfold decreased transcript levels and 170 with more than a fourfold increase. A large fraction of the down-regulated genes encode proteins involved in germline proliferation and reproduction. The DAF-9/DAF-12 signalling cascade was identified as a prime pathway that mediates the longevity of daf-2;pept-1 with a strict dependance on DAF-16. Loss of DAF-9/DAF-12 or KRI-1 reduces the lifespan of daf-2;pept-1 to that of the daf-2 mutant. Amongst the DAF-16 target genes, numerous enzymes involved in the defence of reactive oxygen species were with increased expression level in daf-2;pept-1. On a functional level, it was demonstrated that amongst those, a high de novo synthesis rate of glutathione is most important for the longevity phenotype of this strain. Taken together, a close interdependence of endocrine hormone signalling from germline to intestine was identified as an essential element in the control of the extreme longevity of C. elegans lacking a proper function of the insulin receptor and lacking the intestinal peptide transporter. [source] FoxO1 is involved in the antineoplastic effect of calorie restrictionAGING CELL, Issue 3 2010Haruyoshi Yamaza Summary The FoxO transcription factors may be involved in the antiaging effect of calorie restriction (CR) in mammals. To test the hypothesis, we used FoxO1 knockout heterozygotic (HT) mice, in which the FoxO1 mRNA level was reduced by 50%, or less, of that in wild-type (WT) mouse tissues. The WT and HT mice were fed ad libitum (AL) or 30% CR diets from 12 weeks of age. Aging- and CR-related changes in body weight, food intake, blood glucose, and insulin concentrations were similar between the WT and HT mice in the lifespan study. The response to oxidative stress, induced by intraperitoneal injection of 3-nitropropionic acid (3-NPA), was evaluated in the liver and hippocampus at 6 months of age. Several of the selected FoxO1-target genes for cell cycle arrest, DNA repair, apoptosis, and stress resistance were up-regulated in the WT-CR tissues after 3-NPA injection, while the effect was mostly diminished in the HT-CR tissues. Of these gene products, we focused on the nuclear p21 protein level in the liver and confirmed its up-regulation only in the WT-CR mice in response to oxidative stress. The lifespan did not differ significantly between the WT and HT mice in AL or CR conditions. However, the antineoplastic effect of CR, as indicated by reduced incidence of tumors at death in the WT-CR mice, was mostly abrogated in the HT-CR mice. The present results suggest a role for FoxO1 in the antineoplastic effect of CR through the induction of genes responsible for protection against oxidative and genotoxic stress. [source] Methionine sulfoxide reductase A expression is regulated by the DAF-16/FOXO pathway in Caenorhabditis elegansAGING CELL, Issue 6 2009Alicia N. Minniti Summary The methionine sulfoxide reductase system has been implicated in aging and protection against oxidative stress. This conserved system reverses the oxidation of methionine residues within proteins. We analyzed one of the components of this system, the methionine sulfoxide reductase A gene, in Caenorhabditis elegans. We found that the msra-1 gene is expressed in most tissues, particularly in the intestine and the nervous system. Worms carrying a deletion of the msra-1 gene are more sensitive to oxidative stress, show chemotaxis and locomotory defects, and a 30% decrease in median survival. We established that msra-1 expression decreases during aging and is regulated by the DAF-16/FOXO3a transcription factor. The absence of this enzyme decreases median survival and affects oxidative stress resistance of long lived daf-2 worms. A similar effect of MSRA-1 absence in wild-type and daf-2 (where most antioxidant enzymes are activated) backgrounds, suggests that the lack of this member of the methionine repair system cannot be compensated by the general antioxidant response. Moreover, FOXO3a directly activates the human MsrA promoter in a cell culture system, implying that this could be a conserved mechanism of MsrA regulation. Our results suggest that repair of oxidative damage in proteins influences the rate at which tissues age. This repair mechanism, rather than the general decreased of radical oxygen species levels, could be one of the main determinants of organisms' lifespan. [source] Caenorhabditis elegans PI3K mutants reveal novel genes underlying exceptional stress resistance and lifespanAGING CELL, Issue 6 2009Srinivas Ayyadevara Summary Two age-1 nonsense mutants, truncating the class-I phosphatidylinositol 3-kinase catalytic subunit (PI3KCS) before its kinase domain, confer extraordinary longevity and stress-resistance to Caenorhabditis elegans. These traits, unique to second-generation homozygotes, are blunted at the first generation and are largely reversed by additional mutations to DAF-16/FOXO, a transcription factor downstream of AGE-1 in insulin-like signaling. The strong age-1 alleles (mg44, m333) were compared with the weaker hx546 allele on expression microarrays, testing four independent cohorts of each allele. Among 276 genes with significantly differential expression, 92% showed fewer transcripts in adults carrying strong age-1 alleles rather than hx546. This proportion is significantly greater than the slight bias observed when contrasting age-1 alleles to wild-type worms. Thus, transcriptional changes peculiar to nonsense alleles primarily involve either gene silencing or failure of transcriptional activation. A subset of genes responding preferentially to age-1- nonsense alleles was reassessed by real-time polymerase chain reaction, in worms bearing strong or weak age-1 alleles; nearly all of these were significantly more responsive to the age-1(mg44) allele than to age-1(hx546). Additional mutation of daf-16 reverted the majority of altered mg44 -F2 expression levels to approximately wild-type values, although a substantial number of genes remained significantly distinct from wild-type, implying that age-1(mg44) modulates transcription through both DAF-16/FOXO-dependent and independent channels. When age-1 -inhibited genes were targeted by RNA interference (RNAi) in wild-type or age-1(hx546) adults, most conferred significant oxidative-stress protection. RNAi constructs targeting two of those genes were shown previously to extend life, and RNAi's targeting five novel genes were found here to increase lifespan. PI3K - null mutants may thus implicate novel mechanisms of life extension. [source] Condition-adapted stress and longevity gene regulation by Caenorhabditis elegans SKN-1/NrfAGING CELL, Issue 5 2009Riva P. Oliveira Summary Studies in model organisms have identified regulatory processes that profoundly influence aging, many of which modulate resistance against environmental or metabolic stresses. In Caenorhabditis elegans, the transcription regulator SKN-1 is important for oxidative stress resistance and acts in multiple longevity pathways. SKN-1 is the ortholog of mammalian Nrf proteins, which induce Phase 2 detoxification genes in response to stress. Phase 2 enzymes defend against oxygen radicals and conjugate electrophiles that are produced by Phase 1 detoxification enzymes, which metabolize lipophilic compounds. Here, we have used expression profiling to identify genes and processes that are regulated by SKN-1 under normal and stress,response conditions. Under nonstressed conditions SKN-1 upregulates numerous genes involved in detoxification, cellular repair, and other functions, and downregulates a set of genes that reduce stress resistance and lifespan. Many of these genes appear to be direct SKN-1 targets, based upon presence of predicted SKN-binding sites in their promoters. The metalloid sodium arsenite induces skn-1- dependent activation of certain detoxification gene groups, including some that were not SKN-1-upregulated under normal conditions. An organic peroxide also triggers induction of a discrete Phase 2 gene set, but additionally stimulates a broad SKN-1-independent response. We conclude that under normal conditions SKN-1 has a wide range of functions in detoxification and other processes, including modulating mechanisms that reduce lifespan. In response to stress, SKN-1 and other regulators tailor transcription programs to meet the challenge at hand. Our findings reveal striking complexity in SKN-1 functions and the regulation of systemic detoxification defenses. [source] d4eBP acts downstream of both dTOR and dFoxo to modulate cardiac functional aging in DrosophilaAGING CELL, Issue 5 2009Robert Wessells Summary dTOR (target of rapamycin) and dFoxo respond to changes in the nutritional environment to induce a broad range of responses in multiple tissue types. Both dTOR and dFoxo have been demonstrated to control the rate of age-related decline in cardiac function. Here, we show that the Eif4e-binding protein (d4eBP) is sufficient to protect long-term cardiac function against age-related decline and that up-regulation of dEif4e is sufficient to recapitulate the effects of high dTOR or insulin signaling. We also provide evidence that d4eBP acts tissue-autonomously and downstream of dTOR and dFoxo in the myocardium, where it enhances cardiac stress resistance and maintains normal heart rate and myogenic rhythm. Another effector of dTOR and insulin signaling, dS6K, may influence cardiac aging nonautonomously through its activity in the insulin-producing cells, possibly by regulating dilp2 expression. Thus, elevating d4eBP activity in cardiac tissue represents an effective organ-specific means for slowing or reversing cardiac functional changes brought about by normal aging. [source] Reduced expression of alpha-1,2-mannosidase I extends lifespan in Drosophila melanogaster and Caenorhabditis elegansAGING CELL, Issue 4 2009Ya-Lin Liu Summary Exposure to sub-lethal levels of stress, or hormesis, was a means to induce longevity. By screening for mutations that enhance resistance to multiple stresses, we identified multiple alleles of alpha-1,2-mannosidase I (mas1) which, in addition to promoting stress resistance, also extended longevity. Longevity enhancement is also observed when mas1 expression is reduced via RNA interference in both Drosophila melanogaster and Caenorhabditis elegans. The screen also identified Edem1 (Edm1), a gene downstream of mas1, as a modulator of lifespan. As double mutants for both mas1 and Edm1 showed no additional longevity enhancement, it appeared that both mutations function within a common pathway to extend lifespan. Molecular analysis of these mutants revealed that the expression of BiP, a putative biomarker of dietary restriction (DR), is down-regulated in response to reductions in mas1 expression. These findings suggested that mutations in mas1 may extend longevity by modulating DR. [source] The DAF-2 insulin-like signaling pathway independently regulates aging and immunity in C. elegansAGING CELL, Issue 6 2008Eric A. Evans Summary The Caenorhabditis elegans DAF-2 insulin-like signaling pathway, which regulates lifespan and stress resistance, has also been implicated in resistance to bacterial pathogens. Loss-of-function daf-2 and age-1 mutants have increased lifespans and are resistant to a variety of bacterial pathogens. This raises the possibility that the increased longevity and the pathogen resistance of insulin-like signaling pathway mutants are reflections of the same underlying mechanism. Here we report that regulation of lifespan and resistance to the bacterial pathogen Pseudomonas aeruginosa is mediated by both shared and genetically distinguishable mechanisms. We find that loss of germline proliferation enhances pathogen resistance and this effect requires daf-16, similar to the regulation of lifespan. In contrast, the regulation of pathogen resistance and lifespan is decoupled within the DAF-2 pathway. Long-lived mutants of genes downstream of daf-2, such as pdk-1 and sgk-1, show wildtype resistance to pathogens. However, mutants of akt-1 and akt-2, which we find to individually have modest effects on lifespan, show enhanced resistance to pathogens. We also demonstrate that pathogen resistance of daf-2, akt-1, and akt-2 mutants is associated with restricted bacterial colonization, and that daf-2 mutants are better able to clear an infection after challenge with P. aeruginosa. Moreover, we find that pathogen resistance among insulin-like signaling mutants is associated with increased expression of immunity genes during infection. Other processes that affect organismal longevity, including Jun kinase signaling and caloric restriction, do not affect resistance to bacterial pathogens, further establishing that aging and innate immunity are regulated by genetically distinct mechanisms. [source] Functional genomic approach to identify novel genes involved in the regulation of oxidative stress resistance and animal lifespanAGING CELL, Issue 4 2007Yongsoon Kim Summary Genetic studies in many organisms suggest that an increased animal lifespan phenotype is often accompanied by enhanced resistance toward reactive oxygen species (ROS). In Caenorhabditis elegans, mutations in daf-2, which encode an insulin/insulin-like growth factor 1 receptor-like molecule, lead to an extended animal lifespan and increased resistance to ROS. We have optimized an assay to monitor ROS resistance in worms using the ROS-generating chemical paraquat. We have employed this assay to screen the RNAi library along chromosomes III and IV for genes that, when silenced, confer paraquat resistance. The positive RNAi clones were subsequently screened for a lifespan extension phenotype. Using this approach, we have identified 84 genes that, when inactivated by RNAi, lead to significant increases in animal lifespan. Among the 84 genes, 29 were found to act in a manner dependent on daf-16. DAF-16, a forkhead transcription factor, is known to integrate signals from multiple pathways, including the daf-2 pathway, to regulate animal lifespan. Most of the 84 genes have not been previously linked to aging, and potentially participate in important cellular processes such as signal transduction, cell,cell interaction, gene expression, protein degradation, and energy metabolism. Our screen has also identified a group of genes that potentially function in a nutrient-sensing pathway to regulate lifespan in C. elegans. Our study provides a novel approach to identify genes involved in the regulation of aging. [source] Skin-derived fibroblasts from long-lived species are resistant to some, but not all, lethal stresses and to the mitochondrial inhibitor rotenoneAGING CELL, Issue 1 2007James M. Harper Summary Fibroblast cell lines were developed from skin biopsies of eight species of wild-trapped rodents, one species of bat, and a group of genetically heterogeneous laboratory mice. Each cell line was tested in vitro for their resistance to six varieties of lethal stress, as well as for resistance to the nonlethal metabolic effects of the mitochondrial inhibitor rotenone and of culture at very low glucose levels. Standard linear regression of species-specific lifespan against each species mean stress resistance showed that longevity was associated with resistance to death induced by cadmium and hydrogen peroxide, as well as with resistance to rotenone inhibition. A multilevel regression method supported these associations, and suggested a similar association for resistance to heat stress. Regressions for resistance to cadmium, peroxide, heat, and rotenone remained significant after various statistical adjustments for body weight. In contrast, cells from longer-lived species did not show significantly greater resistance to ultraviolet light, paraquat, or the DNA alkylating agent methylmethanesulfonate. There was a strong correlation between species longevity and resistance to the metabolic effects of low-glucose medium among the rodent cell lines, but this test did not distinguish mice and rats from the much longer-lived little brown bat. These results are consistent with the idea that evolution of long-lived species may require development of cellular resistance to several forms of lethal injury, and provide justification for evaluation of similar properties in a much wider range of mammals and bird species. [source] Correlated responses to selection for stress resistance and longevity in a laboratory population of Drosophila melanogasterJOURNAL OF EVOLUTIONARY BIOLOGY, Issue 4 2005O. A. BUBLIY Abstract Laboratory studies on Drosophila have revealed that resistance to one environmental stress often correlates with resistance to other stresses. There is also evidence on genetic correlations between stress resistance, longevity and other fitness-related traits. The present work investigates these associations using artificial selection in Drosophila melanogaster. Adult flies were selected for increased survival after severe cold, heat, desiccation and starvation stresses as well as increased heat-knockdown time and lifespan (CS, HS, DS, SS, KS and LS line sets, respectively). The number of selection generations was 11 for LS, 27 for SS and 21 for other lines, with selection intensity being around 0.80. For each set of lines, the five stress-resistance parameters mentioned above as well as longevity (in a nonstressful environment) were estimated. In addition, preadult developmental time, early age productivity and thorax length were examined in all lines reared under nonstressful conditions. Comparing the selection lines with unselected control revealed clear-cut direct selection responses for the stress-resistance traits. Starvation resistance increased as correlated response in all sets of selection lines, with the exception of HS. Positive correlated responses were also found for survival after cold shock (HS and DS) and heat shock (KS and DS). With regard to values of resistance across different stress assays, the HS and KS lines were most similar. The resistance values of the SS lines were close to those of the LS lines and tended to be the lowest among all selection lines. Developmental time was extended in the SS and KS lines, whereas the LS lines showed a reduction in thorax length. The results indicate a possibility of different multiple-stress-resistance mechanisms for the examined traits and fitness costs associated with stress resistance and longevity. [source] Lifespan extension by conditions that inhibit translation in Caenorhabditis elegansAGING CELL, Issue 1 2007Malene Hansen Summary Many conditions that shift cells from states of nutrient utilization and growth to states of cell maintenance extend lifespan. We have carried out a systematic lifespan analysis of conditions that inhibit protein synthesis. We find that reducing the levels of ribosomal proteins, ribosomal-protein S6 kinase or translation-initiation factors increases the lifespan of Caenorhabditis elegans. These perturbations, as well as inhibition of the nutrient sensor target of rapamycin (TOR), which is known to increase lifespan, all increase thermal-stress resistance. Thus inhibiting translation may extend lifespan by shifting cells to physiological states that favor maintenance and repair. Interestingly, different types of translation inhibition lead to one of two mutually exclusive outputs, one that increases lifespan and stress resistance through the transcription factor DAF-16/FOXO, and one that increases lifespan and stress resistance independently of DAF-16. Our findings link TOR, but not sir-2.1, to the longevity response induced by dietary restriction (DR) in C. elegans, and they suggest that neither TOR inhibition nor DR extends lifespan simply by reducing protein synthesis. [source] Calorie restriction mimetics: an emerging research fieldAGING CELL, Issue 2 2006Donald K. Ingram Summary When considering all possible aging interventions evaluated to date, it is clear that calorie restriction (CR) remains the most robust. Studies in numerous species have demonstrated that reduction of calories 30,50% below ad libitum levels of a nutritious diet can increase lifespan, reduce the incidence and delay the onset of age-related diseases, improve stress resistance, and decelerate functional decline. A current major focus of this research area is whether this nutritional intervention is relevant to human aging. Evidence emerging from studies in rhesus monkeys suggests that their response to CR parallels that observed in rodents. To assess CR effects in humans, clinical trials have been initiated. However, even if results from these studies could eventually substantiate CR as an effective pro-longevity strategy for humans, the utility of this intervention would be hampered because of the degree and length of restriction required. As an alternative strategy, new research has focused on the development of ,CR mimetics'. The objective of this strategy is to identify compounds that mimic CR effects by targeting metabolic and stress response pathways affected by CR, but without actually restricting caloric intake. For example, drugs that inhibit glycolysis (2-deoxyglucose), enhance insulin action (metformin), or affect stress signaling pathways (resveratrol), are being assessed as CR mimetics (CRM). Promising results have emerged from initial studies regarding physiological responses which resemble those observed in CR (e.g. reduced body temperature and plasma insulin) as well as protection against neurotoxicity (e.g. enhanced dopamine action and up-regulated neurotrophic factors). Ultimately, lifespan analyses in addition to expanded toxicity studies must be accomplished to fully assess the potential of any CRM. Nonetheless, this strategy clearly offers a very promising and expanding research endeavor. [source] The chronological life span of Saccharomyces cerevisiaeAGING CELL, Issue 2 2003Paola Fabrizio Summary Simple model systems have played an important role in the discovery of fundamental mechanisms of aging. Studies in yeast, worms and fruit flies have resulted in the identification of proteins and signalling pathways that regulate stress resistance and longevity. New findings indicate that these pathways may have evolved to prevent damage and postpone aging during periods of starvation and may be conserved from yeast to mammals. We will review the yeast S. cerevisiae model system with emphasis on the chronological life span as a model system to study aging and the regulation of stress resistance in eukaryotes. [source] Molecular interactions of the neuronal GPI-anchored lipocalin LazarilloJOURNAL OF MOLECULAR RECOGNITION, Issue 5 2008Diego Sanchez Abstract Lazarillo, a glycoprotein involved in axon growth and guidance in the grasshopper embryo, is the only member of the lipocalin family that is attached to the cell surface by a GPI anchor. Recently, the study of Lazarillo homologous genes in Drosophila and mouse has revealed new functions in the regulation of lifespan, stress resistance and neurodegeneration. Here we report an analysis of biochemical properties of Lazarillo to gain insight into the molecular basis of its physiological function. Recombinant forms of the grasshopper protein were expressed in two different systems to test: (1) potential binding of several hydrophobic ligands; (2) protein,protein homophilic interactions; and (3) whether interaction with the function-blocking mAb 10E6 interferes with ligand binding. We tested 10 candidate ligands (retinoic acid, heme, bilirubin, biliverdin, ecdysterone, juvenile hormone, farnesol, arachidonic acid, linoleic acid and palmitic acid), and monitored binding using electrophoretic mobility shift, absorbance spectrum, and fluorimetry assays. Our work indicates binding to heme and retinoic acid, resulting in increased electrophoretic mobility, as well as to fatty acids, resulting in multimerization. Retinoic acid and fatty acids binding were confirmed by fluorescence titration, and heme binding was confirmed with absorbance spectrum assays. We demonstrate that Lazarillo oligomerizes in solution and can form clusters in the plasma membrane when expressed and GPI-anchored to the cell surface, however it is unable to mediate cell,cell adhesion. Finally, by ligand-mAb competition experiments we show that ligand-binding alone cannot be the key factor for Lazarillo to perform its function during axonal growth in the grasshopper embryo. Copyright © 2008 John Wiley & Sons, Ltd. [source] Insulin-like signalling in neurons controls lifespan in C. elegansJOURNAL OF NEUROCHEMISTRY, Issue 2002C. A. Wolkow Insulin-like signalling controls C. elegans lifespan, development and metabolism. Mutations that weaken this insulin-like signalling pathway extend lifespan. Severe mutations abolishing insulin-like signalling cause animals to arrest development as dauer larvae, a larval form specialized for stress resistance and long-term survival. A number of the genes acting in this pathway have been cloned, including daf-2, which encodes a homolog of vertebrate insulin/IGF-I receptors, and age-1, encoding the C. elegans homolog of the PI(3)K p110 catalytic subunit. In order to identify cells from which insulin-like signalling controls lifespan and development, transgenic animals were constructed which possessed insulin-like signalling only in specific cell types. To achieve this, cell-type specific promoters were used to drive expression of daf-2 or age-1 cDNAs in daf-2(,/,) or age-1(,/,) backgrounds, respectively. By utilizing this strategy, we could restore wild-type daf-2 or age-1 activity only in cells that are capable of expressing each transgene. Restoring insulin-like signalling to the nervous system of daf-2 or age-1 mutants could rescue long lifespan. This result was specific for transgenes restoring insulin-like signalling to the nervous system. Expressing daf-2 or age-1 cDNAs from muscle- or intestinally-restricted promoters was insufficient to rescue lifespan. In contrast, age-1 and daf-2 expression in either neuronal or non-neuronal cell types rescued dauer larval arrest in the mutants. These findings demonstrate that insulin-like signalling pathways in the nervous system control C. elegans lifespan. [source] Plant responses to drought and phosphorus deficiency: contribution of phytohormones in root-related processesJOURNAL OF PLANT NUTRITION AND SOIL SCIENCE, Issue 4 2005Lutz Wittenmayer Abstract Environmental stresses are one of the most limiting factors in agricultural productivity. A large portion of the annual crop yield is lost to pathogens (biotic stress) or the detrimental effects of abiotic-stress conditions. There are numerous reports about chemical characterization of quantitatively significant substrate fluxes in plant responses to stress factors in the root-rhizosphere system, e.g., nutrient mobilization, heavy-metal and aluminum immobilization, or establishment of plant-growth-promoting rhizobacteria (PGPR) by exudation of organic anions, phytosiderophores, or carbohydrates into the soil, respectively. The hormonal regulation of these responses is not well understood. This paper highlights this complex process, stressing the involvement of phytohormones in plant responses to drought and phosphorus deficiency as examples. Beside ethylene, abscisic acid (ABA) plays an important role in drought-stress adaptation of plants. This hormone causes morphological and chemical changes in plants, ensuring plant survival under water-limited conditions. For example, ABA induces stomata closure, reduction in leaf surface, and increase in root : shoot ratio and, thus, reduction in transpiration and increase in soil volume for water uptake. Furthermore, it supports water uptake in soil with decreasing water potential by osmotic adjustment. Suitability of hormonal parameters in the selection for improving stress resistance is discussed. Auxins, ethylene, and cytokinins are involved in morphological adaption processes to phosphorus (P) deficiency (increase in root surface, e.g., by the formation of more dense root hairs or cluster roots). Furthermore, indole-3-acetic acid increases root exudation for direct and indirect phosphorus mobilization in soil. Nevertheless, the direct use of the trait "hormone content" of a particular plant organ or tissue, for example the use of the drought-stress-induced ABA content of detached leaves in plant breeding for drought-stress-resistant crops, seems to be questionable, because this procedure does not consider the systemic principle of hormonal regulation in plants. Reaktionen von Pflanzen auf Trockenstress und Phosphormangel: Die Rolle von Phytohormonen in wurzelbezogenen Prozessen Umweltstress stellt den wesentlichsten Limitierungsfaktor für die landwirtschaftliche Produktion dar. Ein erheblicher Teil der jährlichen Ernten geht durch pathogene Organismen (biotischer Stress) oder durch die verheerende Wirkung abiotischer Stressoren verloren (v. a. Trockenstress und Nährstoffmangel). Es gibt zahlreiche Untersuchungen zur stofflichen Charakterisierung der pflanzlichen Stressreaktion an der Wurzel, z.,B. Nährstoffmobilisierung, Schadstoffimmobilisierung oder Etablierung von wachstumsfördernden Rhizobakterien durch Wurzelabscheidungen. Die hormonelle Steuerung dieser Prozesse ist bisher weniger erforscht. Der Artikel geht dieser Problematik am Beispiel von Trockenstress und Phosphormangel unter besonderer Berücksichtigung von Phytohormonen nach. Bei der Anpassung von Pflanzen an Wassermangelbedingungen spielt neben Ethylen das Phytohormon Abscisinsäure (ABA) eine wichtige Rolle. Es induziert morphologische und chemische Veränderungen in der Pflanze, die ein Überleben unter Wassermangelbedingungen ermöglichen. Beispielsweise induziert die ABA den Stomataschluss, eine Verringerung der Blattoberfläche sowie eine Erhöhung des Wurzel:Spross-Verhältnisses und bewirkt dadurch eine verringerte Transpiration und Vergrößerung des Bodenvolumens zur Erschließung von Wasservorräten. Darüber hinaus kann eine ABA-induzierte Anreicherung von osmotisch wirksamen Verbindungen zur Wasseraufnahme bei sinkendem Wasserpotential im Boden beitragen. Bei Phosphat (P)-Mangel sind vor allem Auxine, Cytokine und Ethylen an der morphologischen Anpassung der Wurzeln (Vergrößerung der Wurzeloberfläche durch verstärkte Bildung von Wurzelhaaren oder Proteoidwurzeln) beteiligt. Darüber hinaus bewirkt Indolyl-3-Essigäure eine Intensivierung der Abgabe von Wurzelabscheidungen zur direkten oder indirekten P-Mobilisierung in der Rhizosphäre. Trotzdem wird die unmittelbare Verwendung des Indikators "Hormongehalt" eines bestimmten Pflanzenorganes, beispielsweise der trockenstressinduzierte ABA-Gehalt von abgeschnittenen Blättern, für die Züchtung auf Stressresistenz als problematisch angesehen, da sie das systemische Prinzip der Hormonregulation nicht berücksichtigt. [source] |