Cold-Shock Injury and Rapid Cold Hardening in the Flesh Fly Sarcophaga crassipalpis

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Oleic acid is elevated in cell membranes during rapid cold-hardening and pupal diapause in the flesh fly, Sarcophaga crassipalpis.

The integrity of cellular membranes is critical to the survival of insects at low temperatures, thus an advantage is conferred to insects that can adjust their composition of membrane fatty acids (FAs). Such changes contribute to homeoviscous adaption, a process that allows cellular membranes to maintain a liquid-crystalline state at temperatures that are potentially low enough to cause the mem...

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p38 MAPK is a likely component of the signal transduction pathway triggering rapid cold hardening in the flesh fly Sarcophaga crassipalpis.

Rapid cold hardening (RCH) is an adaptation enabling insects to quickly respond to low temperature, but little is known about the molecular events that trigger this response. In this study of the flesh fly Sarcophaga crassipalpis, we explore a possible role for mitogen-activated protein kinases (MAPKs) in the low temperature signaling that elicits RCH. We report that p38 MAPK from S. crassipalp...

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Cold hardiness of the fly pupal parasitoid Nasonia vitripennis is enhanced by its host Sarcophaga crassipalpis.

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A rapid cold-hardening response protecting against cold shock injury in Drosophila melanogaster.

In studies of insect cold-hardiness, the supercooling point (SCP) is defined as the temperature at which spontaneous nucleation of body fluids occurs. Despite having an SCP of -20 degrees C, adults of Drosophila melanogaster did not survive exposure to -5 degrees C, which suggests that cold shock causes lethal injury that is not associated with freezing. If, however, flies were chilled at 5 deg...

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ژورنال

عنوان ژورنال: Physiological Zoology

سال: 1987

ISSN: 0031-935X

DOI: 10.1086/physzool.60.3.30162282