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Please use this identifier to cite or link to this item: http://ntour.ntou.edu.tw:8080/ir/handle/987654321/48800

Title: 熱休克可能會藉由轉錄因子SP1活化基因表現提升斑馬魚胚胎中DNA傷害辨識活性
Heat hock up-regulates UV-damaged-DNA and base mispair binding activities in zebrafish (Danio rerio) embryos possibly via SP1-activated gene expression
Authors: Yen-Hung Chen
陳彥宏
Contributors: 國立臺灣海洋大學:生命科學暨生物科技學系
Keywords: 熱休克;;SP1;錯誤配對修補
Heat shock;cadmium;SP1;Mismatch Repair
Date: 2017
Issue Date: 2018-08-22T06:31:26Z
Abstract: 高溫導致標準代謝率上升,並結合壓力因素的出現會抑制有氧代謝能力造成抗逆性的能力降低。DNA主要修復能力有nucleotide excision repair (NER),base excision repair (BER)以及mismatch repair (MMR),本論文探討鎘和熱休克對斑馬魚胚胎DNA的修補中是否有共同影響或者有不同的作用。在24 h post fertilization (hpf)的胚胎經由熱休克處理0.5小時會促使heat shock protein 70 (HSP 70)之mRNA大量的表現出來。NER會修復UV照射的DNA病變,例如(6-4) photoproducts (6-4PPs) 和cyclobutane pyrimidine dimers (CPDs)。本論文研究發現熱休克會刺激NER(nucleotide excision repair)基因XPC之mRNA表現量上升,熱休克會使CPD之辨識能力上升約214%,但不會刺激6-4PP之辨識能力。熱休克會刺激MMR蛋白MutS homolog 2 (MSH2) and MSH6之基因表現,熱休克也會刺激GT和2-Loop DNA錯誤配對的結合能力,與control組相比分別上升約130%和160%。在BER機制中,熱休克並不會刺激8-oxoguanine DNA glycosylase (OGG1)的基因表現。由於已知人類msh6啟動子被SP1所轉錄調控,鎘和熱休克會影響MSH的基因表現是否經由SP1的活化進行探討,熱休克會使SP1 結合活性與control組相比上升約160%,而經由鎘(3μM)處理23h微弱抑制至控制組約77%。熱休克無法提高預先暴露於鎘中胚胎的SP1結合活性。至於熱休克如何活化SP1轉錄因子需要近一步的研究與探討。
Increasing temperature exposure led to a rise in standard metabolic rates, and combined stressors appeared to override the capability for aerobic energy production resulting in impaired stress tolerance. Because of the importance of DNA damage repair, including nucleotide excision repair (NER), base excision repair (BER) and mismatch repair (MMR) in maintaining the integrity of genetic materials, this study explored the effects of Cd and heat shock on the gene expression of DNA repair factors in zebrafish embryos. Exposure of embryos at 24 h post fertilization (hpf) to a high water temperature at 37℃for 30 min induced a drastic production of heat shock protein 70 (HSP 70) mRNA, indicating the induction of heat stress under this condition. NER removes UV-induced DNA lesions such as (6-4) photoproducts (6-4PPs) and cyclobutane pyrimidine dimers (CPDs). Heat shock weakly stimulated the gene expression of xeroderma pigmentosum group C (XPC), a NER-associated damage recognition factor. Consistent with QPCR analysis, CPD-specific binding activity was stimulated to 214 % of control. Conversely, heat shock failed to stimulate 6-4PP-specific binding activity based on band shift assay. Heat stress activated the gene activities of MutS homolog 2 (MSH2) and MSH6 involved in MMR-associated mispair detection. Heat shock increased G-T and 2-loop mismatch binding activities to 130 % and 160% of control in zebrafish embryos. Heat stress did not activate the gene expression of 8-oxoguanine DNA glycosylase (OGG1) that is known to remove oxidized guanine. As the human MSH6 gene promotor is regulated by SP1-mediated transcription, whether heat stress affected MSH gene expression via SP1 activation was also explored. SP1 binding activity in zebrafish embryos was stimulated to 160% of control by heat shock, while SP1 binding activity was weakly suppressed to 77% of control after exposing embryos to cadmium (Cd)at 3μM for 23 h. Heat stress failed to boost SP1 binding activity in embryos preexposed to Cd, suggesting that heat stress activated SP1 activity via a mechanism from Cd inactivation. Whether HSP 70 induced in heat stress participates in the up-regulation of SP1 binding intensity awaits further investigation.
URI: http://ethesys.lib.ntou.edu.tw/cgi-bin/gs32/gsweb.cgi?o=dstdcdr&s=G0010236025.id
http://ntour.ntou.edu.tw:8080/ir/handle/987654321/48800
Appears in Collections:[生命科學暨生物科技學系] 博碩士論文

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