Pokorna, E. | bioRxiv Science

bioRxiv2024

Physiological and Molecular Responses of Projected Future Temperatures on Potato Tuberization

Potato (Solanum tuberosum L.) is one of the most important food crops globally and is especially vulnerable to heat stress. Significant knowledge gaps remain however, in our understanding of the developmental mechanisms associated with tuber responses to heat stress. This study uses whole-plant physiology, transcriptomics, and hormone profiling to gain insights into the mechanisms associated with heat stress impacts on potato tuber development. When plants were grown in projected future temperature conditions, levels of abscisic acid (ABA) were significantly decreased in leaf and tuber tissues while rates of leaf carbon assimilation and stomatal conductance were not significantly affected. While plants grown in elevated temperature conditions initiated more tubers on average per plant, there was a significant decrease (66%) in mature tubers at final harvest. We hypothesize that reduced tuber yields at elevated temperatures are not due to reductions in tuber initiation, but due to impaired tuber filling. Transcriptomic analysis found significant changes in transcript expression for genes related to response to ABA, heat and auxin biosynthetic process. The known tuberization repressor genes SELF PRUNING 5G (StSP5G) and CONSTANS-LIKE1 (StCOL1) were found to be differentially expressed in tubers grown in elevated temperatures. IDENTITY OF TUBER 1 (StIT1) and TIMING OF CAB EXPRESSION 1 (StTOC1) are other known tuberization genes that displayed distinct expression patterns in elevated versus ambient temperatures but were not differentially expressed. This work highlights potential gene targets and key developmental stages associated with tuberization to development more heat tolerant potatoes.

plant biology↗

bioRxiv2019

Kinetic characteristics of propofol-induced inhibition of electron-transfer chain and fatty acid oxidation in human and rodent skeletal and cardiac muscles

IntroductionPropofol causes a profound inhibition of fatty acid oxidation (FAO) and reduces spare electron transfer chain (ETC) capacity in a range of human and rodent cells and tissues - a feature that might be related to the pathogenesis of Propofol Infusion Syndrome. We aimed to explore the mechanism of propofol-induced alteration of bioenergetic pathways by describing its kinetic characteristics.\n\nMethodsWe obtained samples of skeletal and cardiac muscle from Wistar rat (n=3) and human subjects: vastus lateralis from hip surgery patients (n=11) and myocardium from brain-dead organ donors (n=10). We assessed mitochondrial functional indices using standard SUIT protocol and high resolution respirometry in fresh tissue homogenates with or without short-term exposure to a range of propofol concentration (2.5-100 g/ml). After finding concentrations of propofol causing partial inhibition of a particular pathways, we used that concentration to construct kinetic curves by plotting oxygen flux against substrate concentration during its stepwise titration in the presence or absence of propofol. By spectrophotometry we also measured the influence of the same propofol concentrations on the activity of isolated respiratory complexes.\n\nResultsWe found that human muscle and cardiac tissues are more sensitive to propofol-mediated inhibition of bioenergetic pathways than rats tissue. In human homogenates, palmitoyl carnitine-driven respiration was inhibited at much lower concentrations of propofol than that required for a reduction of ETC capacity, suggesting FAO inhibition mechanism different from downstream limitation or carnitine-palmitoyl transferase-1 inhibition. Inhibition of Complex I was characterised by more marked reduction of Vmax, in keeping with non-competitive nature of the inhibition and the pattern was similar to the inhibition of Complex II or ETC capacity. There was no inhibition of Complex IV nor increased leak through inner mitochondrial membrane with up to 100 g/ml of propofol. If measured in isolation by spectrophotometry, propofol 10 g/ml did not affect the activity of any respiratory complexes.\n\nConclusionIn human skeletal and heart muscle homogenates, propofol in concentrations that are achieved in propofol-anaesthetized patients, causes a direct inhibition of fatty acid oxidation, in addition to inhibiting flux of electrons through inner mitochondrial membrane. The inhibition is more marked in human as compared to rodent tissues.

pharmacology and toxicology↗