Experimental Evidence for Nutrition Regulated Stress Resistance in Drosophila ananassae

Background

The amount and quality of nutrients consumed by organisms have a strong impact on stress resistance, life-history traits and reproduction. The balance between energy acquisition and expenditure is crucial to the survival and reproductive success of animals. The ability of organisms to adjust their development, physiology or behavior in response to environmental conditions, called phenotypic plasticity, is a defining property of life. One of the most familiar and important examples of phenotypic plasticity is the response of stress tolerance and reproduction to changes in developmental nutrition. Larval nutrition may affect a range of different life-history traits as well as responses to environmental stress in adult.

Principal Findings

Here we investigate the effect of larval nutrition on desiccation, starvation, chill-coma recovery, heat resistance as well as egg to adult viability, egg production and ovariole number in Drosophila ananassae. We raised larvae on either protein rich diet or carbohydrate rich diet. We found that flies consuming protein rich diet have higher desiccation and heat shock resistance whereas flies developed on carbohydrate rich diet have higher starvation and cold resistance. Egg production was higher in females developed on protein rich diet and we also found trade-off between egg production and Egg to adult viability of the flies. Viability was higher in carbohydrate rich diet. However, sex specific viability was found in different nutritional regimes. Higher Egg production might be due to higher ovariole number in females of protein rich diet.

Conclusion

Thus, Drosophila ananassae adapts different stress tolerance and life-history strategies according to the quality of the available diet, which are correlated with phenotypic adjustment at anatomical and physiological levels.     

Regarding paper: "robustness of shrunken predictors in stratified population"

Article http://dx.doi.org/10.1002/bimj.4710360113 Authors reply http://dx.doi.org/10.1002/bimj.200810432     

Deficient neurogenesis in forebrain-specific presenilin-1 knockout mice is associated with reduced clearance of hippocampal memory traces.

To examine the in vivo function of presenilin-1 (PS1), we selectively deleted the PS1 gene in excitatory neurons of the adult mouse forebrain. These conditional knockout mice were viable and grew normally, but they exhibited a pronounced deficiency in enrichment-induced neurogenesis in the dentate gyrus. This reduction in neurogenesis did not result in appreciable learning deficits, indicating that addition of new neurons is not required for memory formation. However, our postlearning enrichment experiments lead us to postulate that adult dentate neurogenesis may play a role in the periodic clearance of outdated hippocampal memory traces after cortical memory consolidation, thereby ensuring that the hippocampus is continuously available to process new memories. A chronic, abnormal clearance process in the hippocampus may conceivably lead to memory disorders in the mammalian brain.     

Immunophenotyping of human HT29 colon cancer cell primary tumours and their metastases in severe combined immunodeficient mice

The immunophenotype of HT29 human colon cancer cells implanted into severe combined immunodeficient mice was assessed in primary tumours and their metastases in the lungs using an indirect immunohistochemical method. After primary tumours were surgically removed, the metastases were given time to develop, thus paralleling the clinical situation. While vimentin was negative in both primary and secondary tumours, E-cadherin was present as membrane-bound labelling in the primary tumours only. Whereas the markers p53, MIB1, PCNA and CEA were consistently positive in both primary and metastatic tumours, CD44 variant 6 and CA125 were negative in metastases but positive in the primary tumours. There was a significant increase in the percentage of cells labelled for p53 in the primary tumours compared with the metastases. For the proliferation markers, there was no significant difference in labelling between primary tumours and metastases for MIB1. Of the cytokeratins examined, CK 20 gave the strongest and most consistent reaction in both primary and secondary tumours. The results indicate that, for certain immunohistochemical markers, results are the same in both primary tumours and metastases. Hence, in these cases, antigens that are expressed on the primary tumour as well as on the metastases can serve as target molecules for immunologically based forms of treatment of metastases. This revised version was published online in November 2006 with corrections to the Cover Date.     

Defective neurite extension is caused by a mutation in amyloid β/A4 (Aβ) protein precursor found in Familial Alzheimer's Disease

Clonal central nervous system neuronal cells, B103, do not synthesize detectable endogenous APP or APLP. B103 cells transfected with both wild-type (B103/APP) and mutant APP construct (B103/APPΔNL) secreted comparable amounts of soluble forms of APP (sAPP). B103/APP cells produced sAPP and cleaved at amyloid β/A4 (Aβ) 16, the α-secretase site, and B103/APPΔNL cells produced sAPPβ cleaved at Aβ 1, the β-secretase site. B103/APPΔNL cells developed fewer neurites than B103/APP cells in a serum-free defined medium. Neurite numbers of parent B103 cells were increased by the 50% conditioned medium (CM) from B103/APP cells but reduced by the CM from B103/APPΔNL cells. Chemically synthesized Aβ at concentration levels higher than 1 nM reduced numbers of neurites from B103 or B103/APPΔNL cells. However, Aβ at 1–100 nM could not reduce the neurite number of B103/APP cells. The protective activity against Aβ's deleterious effect to reduce neurite numbers was attributed to sAPPα in the CM. Although sAPPα could block the effect of Aβ, sAPPβ could not do so under the identical condition, suggesting the importance of the C-terminal 15-amino acid sequence in sAPPα. Nevertheless, sAPPα's protective activity required the N-terminal sequence around RERMS, previously identified to be the active domain of sAPPβ. The overall effect of APP mutation which overproduced Aβ and sAPPβ and underproduced sAPPα was a marked decline in the neurotrophic effect of APP. We suggest that the disruption of balance between the detrimental effect of Aβ and the trophic effect of sAPP may be important in the pathogenesis of AD caused by this pathogenic APP mutation © 1997 John Wiley & Sons, Inc. J Neurobiol 32: 469–480, 1997     

Amyloidogenesis in Alzheimer's disease: basic biology and animal models.

A principal neuropathological hallmark of Alzheimer's disease is deposition of beta-amyloid, composed primarily of a 4 kD peptide, A beta. This peptide is derived from larger amyloid precursor proteins. The mechanisms that are responsible for A beta formation in vivo are unknown. Recently, transgenic strategies have been employed to test several hypothetical mechanisms in order to reproduce Alzheimer's disease-specific pathology in rodents.     

Comparisons of the molecular evolutionary process at rbcL and ndhF in the grass family (Poaceae)

We examine rate heterogeneity among evolutionary lineages of the grass family at two plasmid loci, ndhF and rbcL, and we introduce a method to determine whether patterns of rate heterogeneity are correlated between loci. We show both that rates of synonymous evolution are heterogeneous among grass lineages and that are heterogeneity is correlated between loci at synonymous sites. At nonsynonymous sites, the pattern of rate heterogeneity is not correlated between loci, primarily due to an aberrant pattern of rate heterogeneity at nonsynonymous sites of rbcL. We compare patterns of synonymous rate heterogeneity to predictors based on the generation time effect and the speciation rate hypotheses. Although there is some evidence for generation time effects, neither generation time effects nor speciation rates appear to be sufficient to explain patterns of rate heterogeneity in the grass plastid sequences.      

An interchange heterozygote inThelepogon elegans roth ex roem et schult.

In a population of 231 plants of the diploidThelepogon elegans (n=5), seven were found to be interchange heterozygotes. A multiple of four, six or eight chromosomes was observed in 62.32% of the pollen mother cells at MI, the remainder having five bivalents. Chiasmata were mostly localised terminally. The orientation of the multiples was predominantly alternate. The subsequent course of meiosis was normal, and pollen fertility was high.