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热休克介导的黑腹果蝇幼虫运动热保护作用因Hsp70在全身过表达而受损。

Heat shock-mediated thermoprotection of larval locomotion compromised by ubiquitous overexpression of Hsp70 in Drosophila melanogaster.

作者信息

Klose Markus K, Chu David, Xiao Chengfeng, Seroude Laurent, Robertson R Meldrum

机构信息

Department of Biology, Queen's University, 3118 Biosciences Complex, Kingston, ON, K7L 3N6, Canada.

出版信息

J Neurophysiol. 2005 Nov;94(5):3563-72. doi: 10.1152/jn.00723.2005. Epub 2005 Aug 10.

Abstract

Maintaining the competence of locomotor circuitry under stressful conditions can benefit organisms by enabling locomotion to more tolerable microhabitats. We show that prior heat shock protects locomotion and the locomotor central pattern generator of larval Drosophila against subsequent hyperthermic stress. We combined molecular genetic, electrophysiological, and behavioral techniques to investigate heat shock-mediated thermoprotection. Prior heat shock increased the distance traveled by larvae during hyperthermia before failure. The frequency of the rhythm of peristaltic locomotor contractions and the velocity of locomotion were both less thermosensitive after heat shock and were less susceptible to failure at high temperatures. Rhythmic coordinated motor patterns, recorded intracellularly as excitatory junction potentials in body wall muscles of dissected preparations, were centrally generated because patterns could still be generated in the absence of sensory feedback (sensory function disrupted with shibire). Prior heat shock protected central circuit operation during hyperthermic stress by increasing the temperature at which it failed. Overexpression of Hsp70 after a heat shock using transgenic flies (traII) did not enhance thermoprotection, as expected, but had deleterious effects on parameters of behavior.

摘要

在压力条件下维持运动神经回路的功能能力,可使生物体通过移动到更适宜的微生境而受益。我们发现,预先的热休克可保护果蝇幼虫的运动能力以及运动中枢模式发生器免受随后的高温应激影响。我们结合分子遗传学、电生理学和行为学技术来研究热休克介导的热保护作用。预先的热休克增加了幼虫在热应激下直至运动衰竭前的移动距离。热休克后,蠕动运动收缩节律的频率和运动速度对温度的敏感性均降低,且在高温下更不易出现运动衰竭。在解剖标本的体壁肌肉中,作为兴奋性连接电位细胞内记录的节律性协调运动模式是由中枢产生的,因为在没有感觉反馈(利用失活蛋白破坏感觉功能)的情况下仍能产生该模式。预先的热休克通过提高运动神经回路在高温应激下出现功能障碍的温度来保护其正常运作。如预期的那样,使用转基因果蝇(traII)在热休克后过表达Hsp70并没有增强热保护作用,反而对行为参数产生了有害影响。

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