scholarly journals Concurrent effects of cold and hyperkalaemia cause insect chilling injury

2015 ◽  
Vol 282 (1817) ◽  
pp. 20151483 ◽  
Author(s):  
Heath A. MacMillan ◽  
Erik Baatrup ◽  
Johannes Overgaard
Keyword(s):  
Cell Death ◽  
Low Temperature ◽  
Cold Exposure ◽  
Low Temperatures ◽  
Locusta Migratoria ◽  
Chilling Injury ◽  
Distribution Patterns ◽  
Temperature Tolerance ◽  
Migratory Locust

Chilling injury and death are the ultimate consequence of low temperature exposure for chill susceptible insects, and low temperature tolerance is considered one of the most important factors determining insect distribution patterns. The physiological mechanisms that cause chilling injury are unknown, but chronic cold exposure that causes injury is consistently associated with elevated extracellular [K + ], and cold tolerant insects possess a greater capacity to maintain ion balance at low temperatures. Here, we use the muscle tissue of the migratory locust ( Locusta migratoria ) to examine whether chill injury occurs during cold exposure or following return to benign temperature and we specifically examine if elevated extracellular [K + ], low temperature, or a combination thereof causes cell death. We find that in vivo chill injury occurs during the cold exposure (when extracellular [K + ] is high) and that there is limited capacity for repair immediately following the cold stress. Further, we demonstrate that that high extracellular [K + ] causes cell death in situ , but only when experienced at low temperatures. These findings strongly suggest that that the ability to maintain ion (particularly K + ) balance is critical to insect low temperature survival, and highlight novel routes of study in the mechanisms regulating cell death in insects in the cold.

scholarly journals Hyperkalaemia, not apoptosis, accurately predicts insect chilling injury

2020 ◽  
Vol 287 (1941) ◽  
pp. 20201663
Author(s):  
Jessica Carrington ◽  
Mads Kuhlmann Andersen ◽  
Kaylen Brzezinski ◽  
Heath A. MacMillan
Keyword(s):  
Cell Death ◽  
Low Temperature ◽  
Thermal Tolerance ◽  
Caspase 3 ◽  
Apoptotic Cell ◽  
Cell Damage ◽  
Locusta Migratoria ◽  
Chilling Injury ◽  
Thermal Adaptation ◽  
Migratory Locust

There is a growing appreciation that insect distribution and abundance are associated with the limits of thermal tolerance, but the physiology underlying thermal tolerance remains poorly understood. Many insects, like the migratory locust ( Locusta migratoria ), suffer a loss of ion and water balance leading to hyperkalaemia (high extracellular [K + ]) in the cold that indirectly causes cell death. Cells can die in several ways under stress, and how they die is of critical importance to identifying and understanding the nature of thermal adaptation. Whether apoptotic or necrotic cell death pathways are responsible for low-temperature injury is unclear. Here, we use a caspase-3 specific assay to indirectly quantify apoptotic cell death in three locust tissues (muscle, nerves and midgut) following prolonged chilling and recovery from an injury-inducing cold exposure. Furthermore, we obtain matching measurements of injury, extracellular [K + ] and muscle caspase-3 activity in individual locusts to gain further insight into the mechanistic nature of chilling injury. We found a significant increase in muscle caspase-3 activity, but no such increase was observed in either nervous or gut tissue from the same animals, suggesting that chill injury primarily relates to muscle cell death. Levels of chilling injury measured at the whole animal level, however, were strongly correlated with the degree of haemolymph hyperkalaemia, and not apoptosis. These results support the notion that cold-induced ion balance disruption triggers cell death but also that apoptosis is not the main form of cell damage driving low-temperature injury.

Heat-induced oxidative activity protects suspension-cultured plant cells from low temperature damage

2006 ◽  
Vol 33 (1) ◽  
pp. 67 ◽  
Author(s):  
Andrew C. Allan ◽  
Ratnasiri Maddumage ◽  
Joanne L. Simons ◽  
Samuel O. Neill ◽  
Ian B. Ferguson
Keyword(s):  
Heat Treatment ◽  
Cell Death ◽  
Low Temperature ◽  
Real Time ◽  
Peroxidase Activity ◽  
Low Temperatures ◽  
Temperature Tolerance ◽  
H2o2 Production ◽  
Tobacco Cells ◽  
Pre Treatment

A short heat pre-treatment (1 h at 38°C) was found to protect both suspension-cultured apple fruit cells and tobacco cells from cold-induced cell death. Tobacco cells were more sensitive to low temperatures than apple cells, with significant cell death after 48 h at 0 or –2°C. Real-time measurements of H2O2 levels during the heat pre-treatment revealed a substantial burst of this reactive oxygen species in both cell types. Real-time and longer-term measurements also showed a large burst of H2O2 production from tobacco cells, but not apple cells, when exposed to low temperatures. Lower temperatures reduced levels of peroxidase activity (both total and intracellular), with the heat pre-treatment preventing some of the cold-induced reduction of this activity in both apple and tobacco cells. The greater sensitivity to low temperature of the tobacco cells may be related to higher H2O2 production, with the heat treatment maintaining higher peroxidase activity. The lesser sensitivity of the apple cells may be due to the lack of a H2O2 burst and maintenance of peroxidase activity by the heat treatment. These results support a role for oxidative metabolism in the beneficial effects of heat in inducing low temperature tolerance.

scholarly journals Hyperkalemia, not apoptosis, accurately predicts chilling injury in individual locusts

2020 ◽  
Author(s):  
Jessica Carrington ◽  
Mads Kuhlmann Andersen ◽  
Kaylen Brzezinski ◽  
Heath MacMillan
Keyword(s):  
Cell Death ◽  
Water Balance ◽  
Cold Exposure ◽  
Caspase 3 ◽  
Apoptotic Cell ◽  
Chilling Injury ◽  
Nerve Tissue ◽  
Ion Balance ◽  
Migratory Locust ◽  
Cell Death Pathway

AbstractDuring prolonged or severe chilling, the majority of insects accrue chilling injuries that are typically quantified by scoring neuromuscular function after rewarming. In the cold, these chill susceptible insects, like the migratory locust (Locusta migratoria) suffer a loss of ion and water balance that is hypothesized to initiate cell death. Whether apoptotic or necrotic cell death pathways are responsible for this chilling injury is unclear. Here, we use a caspase-3 specific assay to indirectly quantify apoptosis in three locust tissues (muscle, nerves, and midgut) following prolonged chilling and recovery from an injury-inducing cold exposure. Furthermore, we obtain matching measurements of injury, hemolymph [K+], and muscle caspase-3 activity in individual locusts to gain further insight into mechanistic nature of chilling injury. We hypothesized that apoptotic cell death in both muscle and nerve tissue drives motor defects following cold exposure in insects, and that there would be a strong association between cold- induced injury, hyperkalemia, and muscle caspase-3 activity. We found a significant increase in muscle caspase-3 activity, but no such increase was observed in either nervous or gut tissue from the same animals, suggesting that chill injury primarily relates to apoptotic muscle cell death. However, the levels of chilling injury measured at the whole animal level prior to tissue sampling were strongly correlated with the degree of hemolymph hyperkalemia, but not apoptosis. These results support the notion that cold-induced ion balance disruption triggers cell death but also that apoptosis is not the main cell death pathway driving injury in the cold.Significance StatementTemperature has profound effects on animal fitness and sets limits to animal distribution. To understand and model insect responses to climate, we need to know how temperature sets limits to their survival. There is strong evidence that a collapse of ion and water balance occurs in insects in the cold, and it is generally held that the resulting cold injury is caused by activation of programmed cell death (apoptosis). Here, we directly test this idea and show for the first time that although the loss of ion balance is a strong predictor of individual survival outcomes, apoptosis is not the primary cause of cold-induced injury.

Changes in ACC and conjugated ACC levels following controlled atmosphere storage of nectarine

2005 ◽  
Vol 45 (12) ◽  
pp. 1635 ◽  
Author(s):  
A. Uthairatanakij ◽  
P. Penchaiya ◽  
B. McGlasson ◽  
P. Holford
Keyword(s):  
Low Temperature ◽  
Cold Storage ◽  
Low Temperatures ◽  
Prunus Persica ◽  
Chilling Injury ◽  
Controlled Atmosphere ◽  
Controlled Atmosphere Storage ◽  
Gaseous Composition ◽  
Storage Atmosphere ◽  
Atmosphere Storage

Low temperature disorders of nectarines are thought to be expressions of chilling injury. Chilling injury is a form of stress usually associated with increased synthesis of ethylene and its immediate precursor, aminocyclopropane-1-carboxylic acid (ACC). However, other mechanisms for the development of chilling injury have been proposed. To help determine the nature of the processes leading to chilling injury in nectarines (Prunus persica) and how the gaseous composition of the storage atmosphere effects the development of low temperature disorders, levels of ACC and conjugated ACC were measured in fruit of the cv. Arctic Snow. These compounds were measured in fruit ripened at 20°C immediately after harvest, in fruit on removal from cold storage and in fruit ripened at 20°C following cold storage. During storage, fruit were kept at 0°C in the 4 following atmospheres: air; air + 15% CO2; air + 15 µL/L ethylene; and air + 15% CO2 + 15 µL/L ethylene. Concentrations of ACC remained low in all treatments and no significant changes in ACC levels due to added ethylene or CO2 were observed. Concentrations of conjugated ACC were about 10-times that of ACC and again were not influenced by the composition of the storage atmosphere. No significant changes in either ACC or conjugated ACC were observed until after flesh bleeding, the major symptoms of low temperature disorder expressed in these fruit, had begun to appear. It was concluded that disorders in nectarines stored at low temperatures are not a stress response involving a disruption of ethylene metabolism but may be associated with differential changes in the metabolism of enzymes associated with normal ripening.

Effects of temperature and salinity on survival of young-of-the-year Hudson River striped bass (Morone saxatilis): implications for optimal overwintering habitats

2002 ◽  
Vol 59 (5) ◽  
pp. 787-795 ◽  
Author(s):  
Thomas P Hurst ◽  
David O Conover
Keyword(s):  
Body Size ◽  
Low Temperature ◽  
Striped Bass ◽  
Low Temperatures ◽  
Morone Saxatilis ◽  
Hudson River ◽  
Temperature Tolerance ◽  
Low Temperature Tolerance ◽  
Energetic State ◽  
Young Of The Year

We examined the role of salinity, body size, and energetic state in determining low temperature tolerance of young-of-the-year (YOY) striped bass (Morone saxatilis) and used this information to map optimal overwintering habitat in the Hudson River estuary. A long-term experiment compared survival at 15 ppt and 30 ppt. In additional experiments, winter-acclimated fish were exposed to temperature declines (2.3°C·day–1 to 1°C·week–1) at salinities from 0 ppt to 35 ppt. Highest survival at low temperatures was consistently observed at intermediate salinities. These results suggest that the observed distribution of overwintering striped bass is related to physiological constraints on osmo regulatory ability at low temperatures. Low temperature tolerance appeared unrelated to body size and energetic state. Salinity profiles were used to describe the location and extent of optimal wintering habitats under various hydrographic regimes. The location of optimal habitats was displaced by over 27 km along the river axis because of variation in salinity regime. Changes in the availability of optimal habitat may be responsible for variation in recruitment to the Hudson River population. These results demonstrate the need to consider a holistic approach encompassing all seasons of the year in assessing habitat requirements of fishes.

scholarly journals Joint Transcriptomic and Metabolomic Analysis Reveals the Mechanism of Low Temperature Tolerance in Hosta Ventricosa

2021 ◽  
Author(s):  
QianQian Zhuang ◽  
Shaopeng Chen ◽  
ZhiXin Jua ◽  
Yao Yue
Keyword(s):  
Signal Transduction ◽  
Low Temperature ◽  
Low Temperatures ◽  
Temperature Tolerance ◽  
Differentially Expressed ◽  
Metabolomic Analysis ◽  
Temperature Changes ◽  
Low Temperature Tolerance ◽  
Temperature Damage ◽  
Hosta Ventricosa

Abstract Background: Hosta ventricosa is a robust ornamental perennial plant that can tolerate low temperatures, and which is widely used in urban landscaping design in Northeast China. However, the mechanism of cold stress tolerance in this species is unclear. Methods:This study used a combination of transcriptomic and metabolomic analysis to explore the mechanism of low temperature tolerance in H. ventricosa.Results: A total of 12 059 differentially expressed genes (DEGs) and 131 differentially expressed metabolites were obtained, which were mainly concentrated in the signal transduction and phenylpropanoid metabolic pathways. In the process of low temperature signal transduction, H. ventricosa is mainly through the ion channels on the three cell membranes of COLD, CNGCs and CRLK to transmit Ca2+ inside and outside the cell to sense temperature changes, and stimulate SCRM to combine with DREB through the MAPK signal pathway and Ca2+ signal sensors such as CBL. Strengthen the low temperature resistance of H. ventricosa. The pathways of phenylpropanoid and flavonoid metabolism represent the main mechanism of low temperature tolerance in this species. The plant protects itself from low temperature damage by increasing its content of genistein, scopolentin and scopolin. It is speculated that H. ventricosa can also adjust the content ratio of sinapyl alcohol and coniferyl alcohol and thereby alter the morphological structure of its cell walls and so increase its resistance to low temperatures.Conclusions: In H. ventricosa that is subjected to low temperature stress, temperature changes are perceived through COLD, CNGCs and CRLK, and protection from low temperature damage is achieved by an increase in the levels of genistein, scopolentin and scopolin through the pathways of phenylpropanoid biosynthesis and flavonoid biosynthesis.

scholarly journals Antifreeze Protein Improves the Cryopreservation Efficiency of Hosta capitata by Regulating the Genes Involved in the Low-Temperature Tolerance Mechanism

Horticulturae ◽  
2021 ◽  
Vol 7 (4) ◽  
pp. 82
Author(s):  
Phyo Phyo Win Pe ◽  
Aung Htay Naing ◽  
Chang Kil Kim ◽  
Kyeung Il Park
Keyword(s):  
Gene Expression ◽  
Low Temperature ◽  
Cold Exposure ◽  
Expression Patterns ◽  
Antifreeze Protein ◽  
Temperature Tolerance ◽  
Gene Expressions ◽  
Low Temperature Tolerance ◽  
Binding Factor ◽  
Freezing Injuries

In this study, whether the addition of antifreeze protein (AFP) to a cryopreservative solution (plant vitrification solution 2 (PVS2)) is more effective in reducing freezing injuries in Hosta capitata than PVS2 alone at different cold exposure times (6, 24, and 48 h) is investigated. The upregulation of C-repeat binding factor 1 (CBF1) and dehydrin 1 (DHN1) in response to low temperature was observed in shoots. Shoots treated with distilled water (dH2O) strongly triggered gene expression 6 h after cold exposure, which was higher than those expressed in PVS2 and PVS2+AFP. However, 24 h after cold exposure, gene expressions detected in dH2O and PVS2 treatments were similar and higher than PVS2 + AFP. The expression was highest in PVS2+AFP when the exposure time was extended to 48 h. Similarly, nitric reductase activities 1 and 2 (Nia1 and Nia2) genes, which are responsible for nitric oxide production, were also upregulated in low-temperature-treated shoots, as observed for CBF1 and DHN1 expression patterns during cold exposure periods. Based on the gene expression patterns, shoots treated with PVS2+AFP were more likely to resist cold stress, which was also associated with the higher cryopreservation efficiency of PVS2+AFP compared to PVS2 alone. This finding suggests that the improvement of cryopreservation efficiency by AFP could be due to the transcriptional regulation of CBF1, DHN1, Nia1, and Nia2, which might reduce freezing injuries during cryopreservation. Thus, AFP could be potentially used as a cryoprotectant in the cryopreservation of rare and commercially important plant germplasm.

scholarly journals Survival of Clinical and Poultry-Derived Isolates of Campylobacter jejuni at a Low Temperature (4°C)

2001 ◽  
Vol 67 (9) ◽  
pp. 4186-4191 ◽  
Author(s):  
Kam Fai Chan ◽  
Huyen Le Tran ◽  
R. Y. Kanenaka ◽  
S. Kathariou
Keyword(s):  
Low Temperature ◽  
Campylobacter Jejuni ◽  
Cold Exposure ◽  
Low Temperatures ◽  
Prolonged Exposure ◽  
Dependent Manner ◽  
Temperature Requirements ◽  
Bacterial Gastroenteritis ◽  
Different Strains ◽  
Strain Dependent

ABSTRACT Campylobacter jejuni is a leading cause of bacterial gastroenteritis in humans, and contamination of poultry has been implicated in illness. The bacteria are fastidious in terms of their temperature requirements, being unable to grow below ca. 31°C, but have been found to be physiologically active at lower temperatures and to tolerate exposure to low temperatures in a strain-dependent manner. In this study, 19 field isolates of C. jejuni (10 of clinical and 9 of poultry origin) were studied for their ability to tolerate prolonged exposure to low temperature (4°C). Although substantial variability was found among different strains, clinical isolates tended to be significantly more likely to remain viable following cold exposure than poultry-derived strains. In contrast, the relative degree of tolerance of the bacteria to freezing at −20°C and freeze-thawing was strain specific but independent of strain source (poultry versus clinical) and degree of cold (4°C) tolerance.

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