scholarly journals SELECTION FOR HEAT-SHOCK RESISTANCE IN LARVAL AND IN ADULT DROSOPHILA BUZZATII : COMPARING DIRECT AND INDIRECT RESPONSES

Evolution ◽  
1996 ◽  
Vol 50 (6) ◽  
pp. 2354-2359
Author(s):  
Volker Loeschcke ◽  
Robert A. Krebs
Genetics ◽  
1996 ◽  
Vol 142 (2) ◽  
pp. 471-479 ◽  
Author(s):  
Robert A Krebs ◽  
Volker Loeschcke

Abstract Direct selection for increased resistance to a heat shock (41.9° for 90 min) was carried out using two replicate lines of Drosophila buzzatii that were derived from a large base population. Selected individuals were first acclimated to high temperature before selection, while control individuals were acclimated but not selected, and selection was performed every second generation. Resistance to heat shock with acclimation increased in selected lines. Without acclimation, a correlated smaller increase in heat-shock resistance was suggested. Survival of males was higher than that of females in all lines when tested with acclimation, but with direct exposure to high temperatures, survival of females was greater than that of males both in selection and control lines but not in the base population. From analysis of reciprocal cross progeny between lines, one selection line was found to possess a dominant autosomal factor that significantly increased resistance of males much more than resistance of females. Also suggestive was recessive traits on the X chromosome in both selection lines that increased thermotolerance. No cytoplasmic effects were found. After accounting for other effects, survival of F1 flies was intermediate, suggesting that additive variation is present for one or more of the autosomes.


Author(s):  
Joost Schymkowitz ◽  
Frederic Rousseau ◽  
Abram Aertsen ◽  
Bert Houben ◽  
Sebastien Carpentier ◽  
...  

2010 ◽  
Vol 391 (10) ◽  
Author(s):  
Stavros Gonidakis ◽  
Steven E. Finkel ◽  
Valter D. Longo

Abstract We have previously shown that both the hypoxia-inducible transcription factor ArcA and the PoxB/Acs bypass of the pyruvate dehydrogenase complex contribute to extended lifespan in Escherichia coli. In agreement with studies in higher eukaryotes, we also demonstrated that long-lived E. coli mutants, including LipA-deficient cells, are stress resistant. Here, we show that ArcA contributes to the enhanced lifespan and heat shock resistance of the lipA mutant by suppressing expression of the acetyl-CoA synthetase (acs) gene. The deletion of acs reversed the reduced lifespan of the lipA arcA mutant and promoted the accumulation of extracellular acetate, indicating that inhibition of carbon source uptake contributes to survival extension. However, Acs also sensitized cells lacking ArcA to heat shock, in the absence of extracellular acetate. These results provide evidence for the role of Acs in regulating lifespan and/or stress resistance by both carbon source uptake-dependent and -independent mechanisms.


Hereditas ◽  
2004 ◽  
Vol 124 (1) ◽  
pp. 47-55 ◽  
Author(s):  
Robert A. Krebs ◽  
Vittoria Torre ◽  
Volker Loeschcke ◽  
Sandro Cavicchi

1988 ◽  
Vol 155-157 ◽  
pp. 261-266 ◽  
Author(s):  
H. Brinkschulte ◽  
E. Deksins ◽  
A.S. Bransden

1988 ◽  
Vol 8 (8) ◽  
pp. 3423-3431
Author(s):  
R C Findly ◽  
H Alavi ◽  
T Platt

Transcription of SSA1 (formerly YG100), a member of the hsp70 gene family in Saccharomyces cerevisiae, increases dramatically upon heat shock. An expression vector in which the promoter of SSA1 is fused to the Escherichia coli galactokinase gene (galK) was constructed and transformed into a galactokinase-deficient yeast strain. The transformants grew on galactose at 23 degrees C, but increased expression of the SSA1-galK fusion gene inhibited growth of cells on galactose at 37 degrees C. Selection for survivors under nonpermissive conditions yielded a class of mutants, termed HSR (for heat shock regulation), which showed reduced levels of expression of the hsp70-galK gene fusion as determined by measurement of galactokinase activity. Similar effects on beta-galactosidase activity were obtained when an SSA1-lacZ fusion vector was introduced into the mutants, suggesting action in trans through the SSA1 promoter. Analysis of Northern (RNA) blots demonstrated that the reduction in expression was a result of decreased mRNA levels for the fusion gene. In addition, mRNA levels of the endogenous SSA1 gene are reduced in an HSR mutant. Genetic analysis has shown that these mutations act in trans and affect both transcription from the SSA1 promoter and turnover of the fusion transcript. These are the first trans-acting mutations known to affect directly the transcriptional regulation and transcript stability of heat shock genes in eucaryotes.


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