Anestis Andreas, Lazou Antigone, Pörtner Hans O, Michaelidis Basile
Laboratory of Animal Physiology, Department of Zoology, School of Biology, Faculty of Science, Aristotle Univaersity of Thessaloniki, Thessaloniki 54124, Greece.
Am J Physiol Regul Integr Comp Physiol. 2007 Aug;293(2):R911-21. doi: 10.1152/ajpregu.00124.2007. Epub 2007 May 23.
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.
本研究旨在通过整合来自生物组织各个层次的信息,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。行为反应通过检查升温对瓣膜关闭和打开的影响来确定。代谢影响通过检查关键糖酵解酶丙酮酸激酶(PK)的活性来评估。分子反应通过Hsp70和Hsp90的表达以及应激激活蛋白激酶、p38丝裂原活化蛋白激酶(p38 MAPK)和cJun氨基末端激酶(JNKs)的磷酸化来研究。当适应24摄氏度而非17摄氏度时,贻贝将瓣膜关闭的持续时间增加了约六倍。如PK的活性所示,这种行为导致代谢抑制,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磷酸化的增加表明MAPK信号级联被激活。讨论了结丝裂原活化蛋白激酶在贻贝组织中热休克蛋白基因诱导中的潜在作用。总之,似乎贻贝的生存接近其适应极限和初始致死温度,并且小程度的升温将在整个生物体和分子水平引发应激反应。