Fat body disintegration after freezing stress is a consequence rather than a cause of freezing injury in larvae of Drosophila melanogaster

0503763 - BC 2020 RIV GB eng J - Článek v odborném periodiku
Rozsypal, Jan - Toxopeus, J. - Berková, Petra - Moos, Martin - Šimek, Petr - Košťál, Vladimír
Fat body disintegration after freezing stress is a consequence rather than a cause of freezing injury in larvae of Drosophila melanogaster.
Journal of Insect Physiology. Roč. 115, MAY-JUN 2019 (2019), s. 12-19. ISSN 0022-1910. E-ISSN 1879-1611
Grant CEP: GA ČR(CZ) GA16-06374S
Institucionální podpora: RVO:60077344
Klíčová slova: cold hardiness * freeze tolerance * supercooling
Obor OECD: Biology (theoretical, mathematical, thermal, cryobiology, biological rhythm), Evolutionary biology
Impakt faktor: 2.246, rok: 2019
Způsob publikování: Omezený přístup
https://www.sciencedirect.com/science/article/pii/S0022191018304244?via%3Dihub

We present results showing that the macroscopic damage (cell ruptures, tissue disintegration) to fat body of /Drosophila melanogaster/ is not directly caused by mechanical forces linked to growth of ice crystals but rather represents a secondary consequence of other primary freeze injuries occurring at subcellular or microscopic levels. The larval survival and macroscopic damage to fat body tissue was scored in 1,632 larvae exposed to cold stress. In most cases, fat body damage was not evident immediately following cold stress but developed later. Analysis of fat body membrane phospholipids revealed that increased freeze tolerance was associated with increased relative proportion of phosphatidylethanolamines (PEs) at the expense of phosphatidylcholines (PCs). The PE/PC ratio increased from 1.08 in freeze-susceptible larvae to 2.10 in freeze-tolerant larvae.


Trvalý link: http://hdl.handle.net/11104/0296832