scholarly journals A mitochondria-targeted antioxidant affects the carotenoid-based plumage of red crossbills

2019 ◽  
Author(s):  
Alejandro Cantarero ◽  
Rafael Mateo ◽  
Pablo Camarero ◽  
Daniel Alonso ◽  
Blanca Fernandez-Eslava ◽  
...  

ABSTRACTThe mechanisms involved in the production of red carotenoid-based ornaments in vertebrates are still poorly understood. Those colours generated by red carotenoids often depend on the enzymatic production (ketolation) of these pigments from dietary yellow carotenoids. Recently, it has been proposed that this conversion takes place at the inner mitochondrial membrane (IMM). This implies that carotenoid ketolation and cell respiration could share the same biochemical pathways. Such a link would favour the evolution of red ketocarotenoid-based ornaments as reliable indices of individual quality under a sexual selection scenario. We exposed captive male red crossbills (Loxia curvirostra Linnaeus) to two different synthetic antioxidants designed to penetrate into the IMM: a synthetic ubiquinone (mitoQ) and a superoxide dismutase mimetic (mitoTEMPO). MitoQ decreased the blood levels of substrate yellow carotenoids and tocopherol. This could be attributed to the characteristics of the mitoQ molecule, which can distort the IMM structure, increasing free radical (superoxide) production and, potentially, antioxidant consumption. Contrarily, mitoTEMPO-treated birds increased the plasma levels of the second most abundant red ketocarotenoid of red crossbills (i.e. canthaxanthin). MitoTEMPO also increased plumage redness and total ketocarotenoid concentration in feathers among those birds exhibiting a redder plumage at the beginning of the study, rising the plasma values of the main red pigment (3-hydroxyechinenone) in paler birds. The results as a whole support the involvement of the mitochondrial antioxidant machinery in carotenoid biotransformation. The fact that the initial plumage redness determined the effect of mitoTEMPO suggests that the mitochondrial-based mechanism is intimately linked to individual quality.Summary statementAntioxidants designed to penetrate the mitochondrial membrane increased avian plumage redness but depending on pre-existing colouration. This supports mitochondrial involvement in the evolution of carotenoid-based ornaments as reliable quality signals.

2020 ◽  
Vol 287 (1938) ◽  
pp. 20201067
Author(s):  
Alejandro Cantarero ◽  
Pedro Andrade ◽  
Miguel Carneiro ◽  
Adrián Moreno-Borrallo ◽  
Carlos Alonso-Alvarez

Ornaments can evolve to reveal individual quality when their production/maintenance costs make them reliable as ‘signals’ or if their expression level is intrinsically linked to condition by some unfalsifiable mechanism (indices). The latter has been mostly associated with traits constrained by body size. In red ketocarotenoid-based colorations, that link could, instead, be established with cell respiration at the inner mitochondrial membrane (IMM). The production mechanism could be independent of resource (yellow carotenoids) availability, thus discarding costs linked to allocation trade-offs. A gene coding for a ketolase enzyme (CYP2J19) responsible for converting dietary yellow carotenoids to red ketocarotenoids has recently been described. We treated male zebra finches with an antioxidant designed to penetrate the IMM (mitoTEMPO) and a thyroid hormone (triiodothyronine) with known hypermetabolic effects. Among hormone controls, MitoTEMPO downregulated CYP2J19 in the bill (a red ketocarotenoid-based ornament), supporting the mitochondrial involvement in ketolase function. Both treatments interacted when increasing hormone dosage, indicating that mitochondria and thyroid metabolisms could simultaneously regulate coloration. Moreover, CYP2J19 expression was positively correlated to redness but also to yellow carotenoid levels in the blood. However, treatment effects were not annulated when controlling for blood carotenoid variability, which suggests that costs linked to resource availability could be minor.


2021 ◽  
Author(s):  
Carlos Alonso-Alvarez ◽  
Pedro Andrade ◽  
Alejandro Cantarero ◽  
Miguel Carneiro

Sexual and social selections promote the evolution of many conspicuous colorations in animals. These traits would act as individual quality signals when they transmit reliable information. Reliability should be assured by production costs unaffordable for low-quality trait bearers or guaranteed if trait expression is tightly linked to individual quality and cannot be falsified (“index signals”). It has been suggested that colored ornaments produced by red ketocarotenoid pigments could meet the latter. These ketocarotenoids are often obtained by enzymatic transformation of dietary yellow carotenoids. Recently, the first enzyme performing this transformation has been described: CYP2J19. This enzyme, belonging to the cytochrome p450 superfamily, is presumably located in the inner mitochondrial membrane, thus linking color expression with cell respiration efficacy. However, it remains to be clarified if the tissue where this intracellular mechanism acts could influence signal reliability and trait evolution. CYP2J19 expression data are now available for different species and tissues. Here, we review current data in birds and hypothesize that CYP2J19 activity could have evolved in some species by being relocated from the liver tissue to the ornaments (epidermis), a pattern more strongly observed in those birds where the red is expressed in non-feathered bare parts (e.g. bill, legs). One potential explanation is that bare parts, unlike feathers, require a constant carotenoid mobilization to maintain color throughout the year. We propose that tissue relocation allows for avoiding production costs derived from potential CYP2J19 interference on vital liver functions. Implications for signal reliability in ornamental evolution are discussed.


Biochemistry ◽  
2009 ◽  
Vol 48 (35) ◽  
pp. 8335-8342 ◽  
Author(s):  
Cintia Kawai ◽  
Felipe S. Pessoto ◽  
Tiago Rodrigues ◽  
Katia C. U. Mugnol ◽  
Veronica Tórtora ◽  
...  

2019 ◽  
Author(s):  
Tak Shun Fung ◽  
Wei-Ke Ji ◽  
Henry N. Higgs ◽  
Rajarshi Chakrabarti

AbstractRecent studies show that mitochondria and actin filaments work together in two contexts: 1) increased cytoplasmic calcium induces cytoplasmic actin polymerization that stimulates mitochondrial fission, and 2) mitochondrial depolarization causes actin assembly around mitochondria, with roles in mitophagy. It is unclear whether these two processes utilize similar actin assembly mechanisms. Here, we show that these are distinct actin assembly mechanisms in the acute phase after treatment (<10 min). Calcium-induced actin assembly is INF2-dependent and Arp2/3 complex-independent, whereas depolarization-induced actin assembly is Arp2/3 complex-dependent and INF2-independent. The two types of actin polymerization are morphologically distinct, with calcium-induced filaments throughout the cytosol and depolarization-induced filaments as “clouds” around depolarized mitochondria. We have previously shown that calcium-induced actin stimulates increases in both mitochondrial calcium and recruitment of the dynamin GTPase Drp1. In contrast, depolarization-induced actin is temporally-associated with extensive mitochondrial dynamics that do not result in mitochondrial fission, but in circularization of the inner mitochondrial membrane (IMM). These dynamics are dependent upon the protease Oma1 and independent of Drp1. Actin cloud inhibition causes increased IMM circularization, suggesting that actin clouds limit these dynamics.Summary statementMitochondrial depolarization induces Arp2/3 complex-dependent actin clouds that restrain mitochondrial shape changes induced by Oma1 on the inner mitochondrial membrane. A distinct actin network stimulates mitochondrial fission in response to calcium.


2007 ◽  
Vol 34 (S 2) ◽  
Author(s):  
D Siemen ◽  
Y Cheng ◽  
X Gu ◽  
P Bednarczyk ◽  
GG Haddad ◽  
...  

1999 ◽  
Vol 5 (S2) ◽  
pp. 1118-1119
Author(s):  
Heide Schatten ◽  
Marian Lewis

Spaceflight induced mitochondrial alterations have been reported for muscle and may be associated with altered physiological functions in space. Mitochondrial alterations are also indicative of preapoptotic events which are seen in greater amounts in cells exposed to spaceflight when compared with cells cultured at 1 g. Preapoptotic mitochondrial changes include alterations of processes at the inner mitochondrial membrane and can result in changes in mitochondrial volume. Higher amounts of oxidative stress during space flight may be one of the causes for changes which lead to apoptosis. Jurkat cells flown on the STS-76 space shuttle mission showed an increase in the number of cells with apoptotic bodies early in the mission and a time-dependent, microgravity-related increase in the Fas/APO-1 cell death factor. Here we investigated the morphology of mitochondria in Jurkat cells exposed to spaceflight during the STS-76 mission.


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