Metabolomics,Unknown,Transcriptomics,Genomics,Proteomics

Dataset Information

Transcription profiling of brains from honey bees treated with compounds that accelerate the onset of foraging

ABSTRACT: Expression profiling of honey bee brains as a function of treatments that accelerate the onset of foraging. Treatment groups included three treatments that accelerate the onset of foraging (methoprene [juvenile hormone analog], manganese, and cGMP) and two treatments that do not accelerate the onset of foraging (cAMP and vehicle control).

ORGANISM(S): Apis mellifera

SUBMITTER: Charles Whitfield

PROVIDER: E-TABM-150 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Publications

Genomic dissection of behavioral maturation in the honey bee.

Whitfield Charles W CW Ben-Shahar Yehuda Y Brillet Charles C Leoncini Isabelle I Crauser Didier D Leconte Yves Y Rodriguez-Zas Sandra S Robinson Gene E GE

Proceedings of the National Academy of Sciences of the United States of America 20061025 44

Honey bees undergo an age-related, socially regulated transition from working in the hive to foraging that has been previously associated with changes in the expression of thousands of genes in the brain. To understand the meaning of these changes, we conducted microarray analyses to examine the following: (i) the ontogeny of gene expression preceding the onset of foraging, (ii) the effects of physiological and genetic factors that influence this behavioral transition, and (iii) the effects of f ...[more]

PMID: 17065327

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Project description:Tienilic acid (TA) was withdrawn from the US market due to numerous cases of liver necrosis. Two major hypotheses currently used to understand the mechanisms of idiosyncratic reactions such as TA-induced hepatotoxicity are the hapten and danger hypotheses. Both human cytochrome (CYP) P450 2C9 and the rat ortholog CYP 2C11 metabolize TA, and it was reported that a reactive metabolite of TA binds almost exclusively to these enzymes, thus acting as a mechanism-based inhibitor. TA-induced liver toxicity is associated with antibodies against CYP 2C9, thus TA appears to act as a hapten. However, if the binding were limited to CYP 2C, it is unlikely that this would lead to significant cell stress. Thus, if TA does not cause cell stress it would suggest that a drug does not have to generate a âdanger signalâ in order to cause an idiosyncratic drug reaction and acting as a hapten is sufficient. In order to test whether TA can cause cell stress, male Sprague Dawley rats were orally dosed with TA, and hepatic gene expression was profiled at 6 and 24 h after drug administration. Results showed that TA induced robust changes in genes involved in oxidative stress (e.g. aldo-keto reductase, glutathione-S-transferase, thioredoxin reductase, epoxide hydrolase), inflammation and cytotoxicity (e.g. IL-1b, interferon regulatory factor 1, macrophage stimulating protein 1, caspase-12), as well as those promoting liver regeneration (e.g. p27Kip1, DUSP6, serine dehydratase, spectrin bII, inhibin bA). These data support the hypothesis that danger signals in the form of cell-stress proteins and the generation of oxidative stress may be involved in initiating the immune response observed in TA-induced toxicity. Other recent data also indicate that the reactive metabolite of TA binds to other proteins in addition to CYP 2C Experiment Overall Design: Rats were orally dosed with TA or control sodium bicarbonate. Eight animals were divided into two groups: Group 1 consisted of two animals that received a single dose of TA, and the two control animals received only sodium bicarbonate. Group 1 was sacrificed 6 h after drug/vehicle administration. Group 2 also comprised of two animals, and they were given two doses of TA (given at t=0 and t=16 h) and sacrificed at 24 h. Control rats in group 2 received two oral doses of sodium bicarbonate. For microarray analysis, six Affymetrix chips were used: Group 1 samples (3 chips) was comprised of pooled RNA from control rats C1 and C2, and an individual chip for each treated animal T1 and T2; Group 2 (3 chips) pooled RNA from control rats C3 and C4, and an individual chip for each treated animal T3 and T4.

Dataset Information

Transcription profiling of brains from honey bees treated with compounds that accelerate the onset of foraging

Publications

Genomic dissection of behavioral maturation in the honey bee.

Similar Datasets

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