Cell apoptosis is an essential mechanism for multicellular organisms, which occurs in the life processes such as a normal development, deletion the rogue cells during cell differentiation. It is tightly related to cell damage caused by adversity stresses. Under the extreme stresses, an amount of free radicals were produced and caused DNA damaged, induced cell apoptosis via the mitochondrial apoptosis pathway. The molecular mechanisms are relatively clear in vertebrates, but very little is known in the mollusk. Following the completion of the oyster genome project, all of the molecular mechanisms have a change to be revealed in the oyster. Recently, we have discovered the oyster cells apoptosis depend on the mitochondrial apoptotic pathway under the air exposure, which may be actived by the DNA injury which caused by the superoxide free radical stress during hypoxia. In order to reveal the molecular mechanisms of the pathological progress, our grant is about to discover the proteins which involved in the biological process, illuminate the relations among of them and explain the activation mechanisms about the DNA damage response system and the mitochondria apoptotic pathway when the oysters were challenged with air exposure at tissular, cellular and molecular levels. In a word, this grant will clarify the oyster molecular biology mechanism of the DNA damage response and mitochondrial apoptosis under the extreme stresses, and provides the theory basis for shellfish disease, environmental resistances, molecular breeding and so on.
细胞凋亡是多细胞生物正常发育、分化过程中进行细胞删除的一种基本机制,与逆境胁迫下的细胞损伤密切相关。在极端环境胁迫下,细胞产生大量的自由基并导致DNA损伤,并通过活化线粒体凋亡途径,诱导细胞凋亡,相关分子机制在脊椎动物中研究的比较清楚,但是局限于科学技术的发展,相关研究在软体动物中开展的非常少。随着牡蛎基因组计划的完成,上述相关课题得到了系统阐述的机会。最近,申请者发现在干露胁迫下,牡蛎细胞发生了线粒体依赖性的凋亡,可能与缺氧产生的超氧自由基引起的DNA损伤有关。为了揭示牡蛎在上述病理损伤过程中的分子生物学应答机制,项目申请者拟在组织、细胞和分子水平,对牡蛎在干露胁迫下的DNA损伤应答系统、线粒体凋亡途径的分子组成与活化机制展开深入的研究,为贝类抗病、抗逆以及分子育种等提供理论依据。
细胞凋亡是多细胞生物正常发育、分化过程中进行细胞删除的一种基本机制,与逆境胁迫下的细胞损伤密切相关。在极端环境胁迫下,细胞产生大量的自由基并导致DNA损伤,并通过活化线粒体凋亡途径,诱导细胞凋亡,相关分子机制在脊椎动物中研究的比较清楚,但是局限于科学技术的发展,相关研究在软体动物中开展的非常少。随着牡蛎基因组计划的完成,上述相关课题得到了系统阐述的机会。本申请者发现在干露胁迫下,牡蛎细胞发生了线粒体依赖性的凋亡,与缺氧产生的超氧自由基引起的DNA损伤有关。项目申请者在组织、细胞和分子水平,对牡蛎在干露胁迫下的DNA损伤应答系统、线粒体凋亡途径的分子组成与活化机制展开深入的研究,为贝类抗病、抗逆以及分子育种等提供理论依据。
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数据更新时间:2023-05-31
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