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Light and pheromone-sensing neurons regulates cold habituation through insulin signalling in Caenorhabditis elegans.

Ohta A, Ujisawa T, Sonoda S, Kuhara A - Nat Commun (2014)

Bottom Line: However, how animals habituate to temperature is poorly understood.Calcium imaging reveals that ASJ neurons respond to temperature.Thus, temperature sensation in a light and pheromone-sensing neuron produces a robust effect on insulin signalling that controls experience-dependent temperature habituation.

View Article: PubMed Central - PubMed

Affiliation: 1] Laboratory of Molecular and Cellular Regulation, Faculty of Science and Engineering, Institute for Integrative Neurobiology, Konan University, 8-9-1 Okamoto, Higashinada-ku, Kobe 658-8501, Japan [2].

ABSTRACT
Temperature is a critical environmental stimulus that has a strong impact on an organism's biochemistry. Animals can respond to changes in ambient temperature through behaviour or altered physiology. However, how animals habituate to temperature is poorly understood. The nematode C. elegans stores temperature experiences and can induce temperature habituation-linked cold tolerance. Here we show that light and pheromone-sensing neurons (ASJ) regulate cold habituation through insulin signalling. Calcium imaging reveals that ASJ neurons respond to temperature. Cold habituation is abnormal in a mutant with impaired cGMP signalling in ASJ neurons. Insulin released from ASJ neurons is received by the intestine and neurons regulating gene expression for cold habituation. Thus, temperature sensation in a light and pheromone-sensing neuron produces a robust effect on insulin signalling that controls experience-dependent temperature habituation.

No MeSH data available.


Related in: MedlinePlus

Downstream molecules of insulin signalling in cold tolerance.(a) Cold tolerance of mutant animals with impaired genes identified from previous DNA microarray analysis were used to measure temperature change-dependent gene expression34. The gene and encoding protein of the mutants that showed abnormal cold tolerance (with asterisks) are listed in the table in Supplementary Fig. 5a. For each assay, n≥6. Asterisks indicate statistical significance between the wild type and mutant. (b) Results of quantitative PCR of each gene in the daf-2(e1370) mutant. Each bar represents the relative value of wild type cultivated at each temperature (n=3). Error bars indicate standard error of the mean. Analysis of variance followed by Dunnet post-hoc test was used for multiple comparisons. *P<0.05; **P<0.01. (c) A molecular and cellular model for temperature experience-inducing cold tolerance. Temperature is detected by the ASJ neuron, in which the trimeric G protein-coupled temperature signal controls insulin secretion. Insulin is received by the intestine and neuron, where insulin signalling regulates gene expression for cold tolerance. We describe here a simple plausible model.
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f7: Downstream molecules of insulin signalling in cold tolerance.(a) Cold tolerance of mutant animals with impaired genes identified from previous DNA microarray analysis were used to measure temperature change-dependent gene expression34. The gene and encoding protein of the mutants that showed abnormal cold tolerance (with asterisks) are listed in the table in Supplementary Fig. 5a. For each assay, n≥6. Asterisks indicate statistical significance between the wild type and mutant. (b) Results of quantitative PCR of each gene in the daf-2(e1370) mutant. Each bar represents the relative value of wild type cultivated at each temperature (n=3). Error bars indicate standard error of the mean. Analysis of variance followed by Dunnet post-hoc test was used for multiple comparisons. *P<0.05; **P<0.01. (c) A molecular and cellular model for temperature experience-inducing cold tolerance. Temperature is detected by the ASJ neuron, in which the trimeric G protein-coupled temperature signal controls insulin secretion. Insulin is received by the intestine and neuron, where insulin signalling regulates gene expression for cold tolerance. We describe here a simple plausible model.

Mentions: To determine a downstream insulin-signalling pathway for temperature-dependent cold tolerance, we used previous DNA microarray analysis results measuring temperature change-dependent gene expression34. We found that mutants of some genes, such as endonuclease (M60.2) and cysteine protease (cpr-1), showed abnormal cultivation-dependent cold tolerance (Fig. 7a; Supplementary Fig. 5a). Expression levels of these genes were significantly changed in daf-2/insulin receptor mutants (Fig. 7b; Supplementary Fig. 5b), indicating that expression of these genes is directly or indirectly regulated downstream of insulin signalling for temperature experience-dependent cold tolerance.


Light and pheromone-sensing neurons regulates cold habituation through insulin signalling in Caenorhabditis elegans.

Ohta A, Ujisawa T, Sonoda S, Kuhara A - Nat Commun (2014)

Downstream molecules of insulin signalling in cold tolerance.(a) Cold tolerance of mutant animals with impaired genes identified from previous DNA microarray analysis were used to measure temperature change-dependent gene expression34. The gene and encoding protein of the mutants that showed abnormal cold tolerance (with asterisks) are listed in the table in Supplementary Fig. 5a. For each assay, n≥6. Asterisks indicate statistical significance between the wild type and mutant. (b) Results of quantitative PCR of each gene in the daf-2(e1370) mutant. Each bar represents the relative value of wild type cultivated at each temperature (n=3). Error bars indicate standard error of the mean. Analysis of variance followed by Dunnet post-hoc test was used for multiple comparisons. *P<0.05; **P<0.01. (c) A molecular and cellular model for temperature experience-inducing cold tolerance. Temperature is detected by the ASJ neuron, in which the trimeric G protein-coupled temperature signal controls insulin secretion. Insulin is received by the intestine and neuron, where insulin signalling regulates gene expression for cold tolerance. We describe here a simple plausible model.
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4109018&req=5

f7: Downstream molecules of insulin signalling in cold tolerance.(a) Cold tolerance of mutant animals with impaired genes identified from previous DNA microarray analysis were used to measure temperature change-dependent gene expression34. The gene and encoding protein of the mutants that showed abnormal cold tolerance (with asterisks) are listed in the table in Supplementary Fig. 5a. For each assay, n≥6. Asterisks indicate statistical significance between the wild type and mutant. (b) Results of quantitative PCR of each gene in the daf-2(e1370) mutant. Each bar represents the relative value of wild type cultivated at each temperature (n=3). Error bars indicate standard error of the mean. Analysis of variance followed by Dunnet post-hoc test was used for multiple comparisons. *P<0.05; **P<0.01. (c) A molecular and cellular model for temperature experience-inducing cold tolerance. Temperature is detected by the ASJ neuron, in which the trimeric G protein-coupled temperature signal controls insulin secretion. Insulin is received by the intestine and neuron, where insulin signalling regulates gene expression for cold tolerance. We describe here a simple plausible model.
Mentions: To determine a downstream insulin-signalling pathway for temperature-dependent cold tolerance, we used previous DNA microarray analysis results measuring temperature change-dependent gene expression34. We found that mutants of some genes, such as endonuclease (M60.2) and cysteine protease (cpr-1), showed abnormal cultivation-dependent cold tolerance (Fig. 7a; Supplementary Fig. 5a). Expression levels of these genes were significantly changed in daf-2/insulin receptor mutants (Fig. 7b; Supplementary Fig. 5b), indicating that expression of these genes is directly or indirectly regulated downstream of insulin signalling for temperature experience-dependent cold tolerance.

Bottom Line: However, how animals habituate to temperature is poorly understood.Calcium imaging reveals that ASJ neurons respond to temperature.Thus, temperature sensation in a light and pheromone-sensing neuron produces a robust effect on insulin signalling that controls experience-dependent temperature habituation.

View Article: PubMed Central - PubMed

Affiliation: 1] Laboratory of Molecular and Cellular Regulation, Faculty of Science and Engineering, Institute for Integrative Neurobiology, Konan University, 8-9-1 Okamoto, Higashinada-ku, Kobe 658-8501, Japan [2].

ABSTRACT
Temperature is a critical environmental stimulus that has a strong impact on an organism's biochemistry. Animals can respond to changes in ambient temperature through behaviour or altered physiology. However, how animals habituate to temperature is poorly understood. The nematode C. elegans stores temperature experiences and can induce temperature habituation-linked cold tolerance. Here we show that light and pheromone-sensing neurons (ASJ) regulate cold habituation through insulin signalling. Calcium imaging reveals that ASJ neurons respond to temperature. Cold habituation is abnormal in a mutant with impaired cGMP signalling in ASJ neurons. Insulin released from ASJ neurons is received by the intestine and neurons regulating gene expression for cold habituation. Thus, temperature sensation in a light and pheromone-sensing neuron produces a robust effect on insulin signalling that controls experience-dependent temperature habituation.

No MeSH data available.


Related in: MedlinePlus