Project Title

Does Thermo-tolerance in Daphnia depend on the mitochondrial function?

Authors' Affiliations

Rajib Hasan, MS Candidate, Department of Biological Sciences, East Tennessee State University, Johnson City, TN. Lev Yampolsky, Professor, Department of Biological Sciences, East Tennessee State University, Johnson City, TN.

Location

RIPSHIN MTN. ROOM 130

Start Date

4-12-2019 2:00 PM

End Date

4-12-2019 2:15 PM

Faculty Sponsor’s Department

Biological Sciences

Name of Project's Faculty Sponsor

Dr. Lev Yampolsky

Type

Oral Presentation

Classification of First Author

Graduate Student-Master’s

Project's Category

Biological Sciences, Ecosystems, Environmental Toxicology

Abstract Text

The thermotolerance, an adaptive phenomenon that is accompanied by the phenotypic plasticity which is the adjustment of physiology, biochemistry and metabolism of every cellular function by the hidden mechanism. Mitochondrion, the powerhouse of the cell that determines the functional integrity of every cellular homeostasis and functional phycological processes should provide its association in regulating the thermotolerance as well. This study assessed the mitochondrial function in regulating and determining the limit of thermo tolerance in the Daphnia magna of different geographical regions of the world, mainly sub grouped as temperature tolerant clones (IL) and temperature sensitive clones (GB). The acclimation effects or the adjustment of the preexisting biological properties help the organism adjust its biological processes to the changing habitat to maintain the cellular functional integrity. The clonal divergence as well as the acclimation show a clear pattern in limiting the thermotolerance and the prediction is the temperature tolerant clones should show higher adjustment of the mitochondrial function than temperature sensitive ones. We hypothesize that the damage in the mitochondrial membrane integrity by different mito-toxins should decrease the heat tolerance by decreasing the membrane potential and fluidity. The integrated mitochondrial function was assessed in acclimated clones by using the molecular studies as well as observation of behavioral and phenotypic plasticity. Due to the specific effects of each mito-toxins (CCCP, NaN3 and DNP) on different complexes (I-IV and ATP synthase) in ETC, we determined the mitochondrial membrane integrity by the Rhodamine 123 alongside with the lactate assay for measuring the mitochondrial integrity. Among all these three mito-toxins, CCCP show significant effect on limiting the heat tolerance. The lower lactate accumulation was observed in the temperature-tolerant clones acclimated in cold temperatures (18°C) which indicates the higher mitochondrial adjustment than the temperature sensitive clones. The concluding remark is that thermal tolerance is determined by the adjustment of mitochondrial function which accompanied with the adjustment to the mitochondrial respiration as well as the adjustment to membrane potential and fluidity.

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Apr 12th, 2:00 PM Apr 12th, 2:15 PM

Does Thermo-tolerance in Daphnia depend on the mitochondrial function?

RIPSHIN MTN. ROOM 130

The thermotolerance, an adaptive phenomenon that is accompanied by the phenotypic plasticity which is the adjustment of physiology, biochemistry and metabolism of every cellular function by the hidden mechanism. Mitochondrion, the powerhouse of the cell that determines the functional integrity of every cellular homeostasis and functional phycological processes should provide its association in regulating the thermotolerance as well. This study assessed the mitochondrial function in regulating and determining the limit of thermo tolerance in the Daphnia magna of different geographical regions of the world, mainly sub grouped as temperature tolerant clones (IL) and temperature sensitive clones (GB). The acclimation effects or the adjustment of the preexisting biological properties help the organism adjust its biological processes to the changing habitat to maintain the cellular functional integrity. The clonal divergence as well as the acclimation show a clear pattern in limiting the thermotolerance and the prediction is the temperature tolerant clones should show higher adjustment of the mitochondrial function than temperature sensitive ones. We hypothesize that the damage in the mitochondrial membrane integrity by different mito-toxins should decrease the heat tolerance by decreasing the membrane potential and fluidity. The integrated mitochondrial function was assessed in acclimated clones by using the molecular studies as well as observation of behavioral and phenotypic plasticity. Due to the specific effects of each mito-toxins (CCCP, NaN3 and DNP) on different complexes (I-IV and ATP synthase) in ETC, we determined the mitochondrial membrane integrity by the Rhodamine 123 alongside with the lactate assay for measuring the mitochondrial integrity. Among all these three mito-toxins, CCCP show significant effect on limiting the heat tolerance. The lower lactate accumulation was observed in the temperature-tolerant clones acclimated in cold temperatures (18°C) which indicates the higher mitochondrial adjustment than the temperature sensitive clones. The concluding remark is that thermal tolerance is determined by the adjustment of mitochondrial function which accompanied with the adjustment to the mitochondrial respiration as well as the adjustment to membrane potential and fluidity.