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首页> 外文期刊>American Journal of Physiology >Behavioral, metabolic, and molecular stress responses of marine bivalve Mytilus galloprovincialis during long-term acclimation at increasing ambient temperature.
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Behavioral, metabolic, and molecular stress responses of marine bivalve Mytilus galloprovincialis during long-term acclimation at increasing ambient temperature.

机译:在升高的环境温度下长期适应环境中,海生双壳类Mytilus galloprovincialis的行为,代谢和分子应激反应。

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The present study aimed to determine the thermal response of the Mediterranean mussel Mytilus galloprovincialis by integrating information from various levels of biological organization including behavior, metabolic adjustments, heat shock protein expression, and protein kinase activity. Behavioral responses were determined by examining the effect of warming on valve closure and opening. Metabolic impacts were assessed by examining the activity of the key glycolytic enzyme pyruvate kinase (PK). Molecular responses were addressed through the expression of Hsp70 and Hsp90 and the phosphorylation of stress-activated protein kinases, p38 mitogen-activated protein kinase (p38 MAPK) and cJun-N-terminal kinases (JNKs). Mussels increased the duration of valve closure by about sixfold when acclimated to 24 degrees C rather than to 17 degrees C. As indicated by the activity of PK, such behavior caused metabolic depression and probably a shift from aerobic to anaerobic metabolism. Acclimation to temperatures higher than 24 degrees C caused an increase in mortality and induced the expression of Hsp72. Increased phosphorylation of p38 MAPK and JNKs indicated activation of MAPK signaling cascades. The potential involvement of MAPKs in the induction of Hsp genes in the tissues of M. galloprovincialis is discussed. In conclusion, it seems that M. galloprovincialis lives close to its acclimation limits and incipient lethal temperature and that a small degree of warming will elicit stress responses at whole organism and molecular levels.
机译:本研究旨在通过整合来自生物组织各个层面的信息,包括行为,代谢调节,热休克蛋白表达和蛋白激酶活性,来确定地中海贻贝Mytilus galloprovincialis的热响应。通过检查变暖对阀门关闭和打开的影响来确定行为响应。通过检查关键糖酵解酶丙酮酸激酶(PK)的活性来评估代谢影响。通过Hsp70和Hsp90的表达以及应激激活的蛋白激酶,p38丝裂原激活的蛋白激酶(p38 MAPK)和cJun-N-末端激酶(JNKs)的磷酸化来解决分子反应。当适应于24摄氏度而不是17摄氏度时,贻贝将瓣膜关闭的持续时间增加了大约六倍。正如PK的活性所表明的那样,这种行为导致了代谢抑制,并可能从有氧代谢转变为无氧代谢。适应高于24摄氏度的温度会导致死亡率增加,并诱导Hsp72的表达。 p38 MAPK和JNKs的磷酸化增加表明MAPK信号级联反应的激活。讨论了MAPKs可能参与了墨西哥支原体组织中Hsp基因的诱导。总而言之,看起来加洛斯莫氏疟原虫的生活接近其适应极限和初期致死温度,小范围的变暖会引起整个生物体和分子水平的应激反应。

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