Characterization of the bicarbonate transporter ABTS-1 in Caenorhabditis elegans
碩士 === 國立臺灣大學 === 生物環境系統工程學研究所 === 99 === Arsenic poisoning affects millions of people worldwide. Although there is evidence to suggest that the nervous system is a target of arsenic, relatively little information is known regarding its effects on nervous system. The effects of arsenite on the ner...
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ndltd-TW-099NTU054040752015-10-16T04:03:27Z http://ndltd.ncl.edu.tw/handle/30415487216279642310 Characterization of the bicarbonate transporter ABTS-1 in Caenorhabditis elegans Caenorhabditis elegans碳酸氫鹽傳輸蛋白ABTS-1之功能探討 Yi-Chen Hsieh 謝翼振 碩士 國立臺灣大學 生物環境系統工程學研究所 99 Arsenic poisoning affects millions of people worldwide. Although there is evidence to suggest that the nervous system is a target of arsenic, relatively little information is known regarding its effects on nervous system. The effects of arsenite on the nervous system in Caenorhabditis elegans were investigated in the present study. Arsenic is also a chemical which can induce the generation of reactive oxygen species. We found that abts-1, which encodes a Na+-dependent Cl-/HCO3- transporter, is required to protect C. elegans from arsenite toxicity. The transgenic strain abts-1::GFP showed the expression of abts-1 is primarily on the neurons and the hypodernis, but stronger expression was also found in the pharynx and body wall muscle cells after exposure to arsenite. On the contrary, the level of GFP decreased after exposing to juglone. The mRNA expression of abts-1 in transgenic strain increased after arsenite exposure comparing to those unexposed animals. We showed that worms lacking of abts-1 is hypersensitive to the paralytic effects of the cholinesterase inhibitor, aldicarb, and the nicotinic acetylcholine receptor agonist, levamisole. Arsenic exposure can enhance the effect to aldicarb and levamisole in abts-1 mutant worms. Moreover, we showed that abts-1 mutants and RNAi-mediated abts-1 knockdown worms have an increase in life span comparing to wild-type worms, and the regulation between abts-1 and insulin signaling. We also showed that lacking of abts-1 can resist to juglone-induced oxidative stress, which might be regulated by insulin signaling pathway. It means that the function of abts-1 to protect C. elegans from arsenite toxicity is not by decreasing the arsenite-induced oxidative stress. Our results indicate the effects of arsenite, insulin/IGF-1 signaling, and the ABTS-1 bicarbonate transporter. Vivian Hsiu-Chuan Liao 廖秀娟 2011 學位論文 ; thesis 61 en_US |
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碩士 === 國立臺灣大學 === 生物環境系統工程學研究所 === 99 === Arsenic poisoning affects millions of people worldwide. Although there is evidence to suggest that the nervous system is a target of arsenic, relatively little information is known regarding its effects on nervous system. The effects of arsenite on the nervous system in Caenorhabditis elegans were investigated in the present study. Arsenic is also a chemical which can induce the generation of reactive oxygen species. We found that abts-1, which encodes a Na+-dependent Cl-/HCO3- transporter, is required to protect C. elegans from arsenite toxicity. The transgenic strain abts-1::GFP showed the expression of abts-1 is primarily on the neurons and the hypodernis, but stronger expression was also found in the pharynx and body wall muscle cells after exposure to arsenite. On the contrary, the level of GFP decreased after exposing to juglone. The mRNA expression of abts-1 in transgenic strain increased after arsenite exposure comparing to those unexposed animals. We showed that worms lacking of abts-1 is hypersensitive to the paralytic effects of the cholinesterase inhibitor, aldicarb, and the nicotinic acetylcholine receptor agonist, levamisole. Arsenic exposure can enhance the effect to aldicarb and levamisole in abts-1 mutant worms. Moreover, we showed that abts-1 mutants and RNAi-mediated abts-1 knockdown worms have an increase in life span comparing to wild-type worms, and the regulation between abts-1 and insulin signaling. We also showed that lacking of abts-1 can resist to juglone-induced oxidative stress, which might be regulated by insulin signaling pathway. It means that the function of abts-1 to protect C. elegans from arsenite toxicity is not by decreasing the arsenite-induced oxidative stress. Our results indicate the effects of arsenite, insulin/IGF-1 signaling, and the ABTS-1 bicarbonate transporter.
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author2 |
Vivian Hsiu-Chuan Liao |
author_facet |
Vivian Hsiu-Chuan Liao Yi-Chen Hsieh 謝翼振 |
author |
Yi-Chen Hsieh 謝翼振 |
spellingShingle |
Yi-Chen Hsieh 謝翼振 Characterization of the bicarbonate transporter ABTS-1 in Caenorhabditis elegans |
author_sort |
Yi-Chen Hsieh |
title |
Characterization of the bicarbonate transporter ABTS-1 in Caenorhabditis elegans |
title_short |
Characterization of the bicarbonate transporter ABTS-1 in Caenorhabditis elegans |
title_full |
Characterization of the bicarbonate transporter ABTS-1 in Caenorhabditis elegans |
title_fullStr |
Characterization of the bicarbonate transporter ABTS-1 in Caenorhabditis elegans |
title_full_unstemmed |
Characterization of the bicarbonate transporter ABTS-1 in Caenorhabditis elegans |
title_sort |
characterization of the bicarbonate transporter abts-1 in caenorhabditis elegans |
publishDate |
2011 |
url |
http://ndltd.ncl.edu.tw/handle/30415487216279642310 |
work_keys_str_mv |
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