Insect mitochondria as targets of freezing-induced injury

Kód výsledku v IS VaVaI

<a href="https://www.isvavai.cz/riv?ss=detail&h=RIV%2F60076658%3A12310%2F20%3A43901144" target="_blank" >RIV/60076658:12310/20:43901144 - isvavai.cz</a>

Výsledek na webu

<a href="https://royalsocietypublishing.org/doi/10.1098/rspb.2020.1273" target="_blank" >https://royalsocietypublishing.org/doi/10.1098/rspb.2020.1273</a>

DOI - Digital Object Identifier

<a href="http://dx.doi.org/10.1098/rspb.2020.1273" target="_blank" >10.1098/rspb.2020.1273</a>

Jazyk výsledku

angličtina

Název v původním jazyce

Insect mitochondria as targets of freezing-induced injury

Popis výsledku v původním jazyce

Many insects survive internal freezing, but the great complexity of freezing stress hinders progress in understanding the ultimate nature of freezing-induced injury. Here, we use larvae of the drosophilid fly,Chymomyza costatato assess the role of mitochondrial responses to freezing stress. Respiration analysis revealed that fat body mitochondria of the freeze-sensitive (non-diapause) phenotype significantly decrease oxygen consumption upon lethal freezing stress, while mitochondria of the freeze-tolerant (diapausing, cold-acclimated) phenotype do not lose respiratory capacity upon the same stress. Using transmission electron microscopy, we show that fat body and hindgut mitochondria swell, and occasionally burst, upon exposure of the freeze-sensitive phenotype to lethal freezing stress. By contrast, mitochondrial swelling is not observed in the freeze-tolerant phenotype exposed to the same stress. We hypothesize that mitochondrial swelling results from permeability transition of the inner mitochondrial membrane and loss of its barrier function, which causes osmotic influx of cytosolic water into the matrix. We therefore suggest that the phenotypic transition to diapause and cold acclimation could be associated with adaptive changes that include the protection of the inner mitochondrial membrane against permeability transition and subsequent mitochondrial swelling. Accumulation of high concentrations of proline and other cryoprotective substances might be a part of such adaptive changes as we have shown that freezing-induced mitochondrial swelling was abolished by feeding the freeze-sensitive phenotype larvae on a proline-augmented diet.

Název v anglickém jazyce

Insect mitochondria as targets of freezing-induced injury

Popis výsledku anglicky

Many insects survive internal freezing, but the great complexity of freezing stress hinders progress in understanding the ultimate nature of freezing-induced injury. Here, we use larvae of the drosophilid fly,Chymomyza costatato assess the role of mitochondrial responses to freezing stress. Respiration analysis revealed that fat body mitochondria of the freeze-sensitive (non-diapause) phenotype significantly decrease oxygen consumption upon lethal freezing stress, while mitochondria of the freeze-tolerant (diapausing, cold-acclimated) phenotype do not lose respiratory capacity upon the same stress. Using transmission electron microscopy, we show that fat body and hindgut mitochondria swell, and occasionally burst, upon exposure of the freeze-sensitive phenotype to lethal freezing stress. By contrast, mitochondrial swelling is not observed in the freeze-tolerant phenotype exposed to the same stress. We hypothesize that mitochondrial swelling results from permeability transition of the inner mitochondrial membrane and loss of its barrier function, which causes osmotic influx of cytosolic water into the matrix. We therefore suggest that the phenotypic transition to diapause and cold acclimation could be associated with adaptive changes that include the protection of the inner mitochondrial membrane against permeability transition and subsequent mitochondrial swelling. Accumulation of high concentrations of proline and other cryoprotective substances might be a part of such adaptive changes as we have shown that freezing-induced mitochondrial swelling was abolished by feeding the freeze-sensitive phenotype larvae on a proline-augmented diet.

Druh

J_imp - Článek v periodiku v databázi Web of Science

CEP obor

—

OECD FORD obor

10602 - Biology (theoretical, mathematical, thermal, cryobiology, biological rhythm), Evolutionary biology

Projekt

—

Návaznosti

I - Institucionalni podpora na dlouhodoby koncepcni rozvoj vyzkumne organizace

Rok uplatnění

2020

Kód důvěrnosti údajů

S - Úplné a pravdivé údaje o projektu nepodléhají ochraně podle zvláštních právních předpisů

Název periodika

Proceedings of the Royal Society of London Series B - Biological Sciences

ISSN

0962-8452

e-ISSN

—

Svazek periodika

287

Číslo periodika v rámci svazku

1931

Stát vydavatele periodika

GB - Spojené království Velké Británie a Severního Irska

Počet stran výsledku

9

Strana od-do

—

Kód UT WoS článku

000554927100008

EID výsledku v databázi Scopus

2-s2.0-85088522985