Thermal Range and Physiological Tolerance Mechanisms in Two Shark Species from the Northwest Atlantic.

Spiny dogfish () and smoothhound () sharks in the northwest Atlantic undergo seasonal migrations driven by changes in water temperature. However, the recognized thermal habitats of these regional populations are poorly described. Here, we report the thermal range, catch frequency with bottom temperature, and catch frequency with time of year for both shark species in Narragansett Bay, Rhode Island.

Synthetic capacity does not predict elasmobranchs' ability to maintain trimethylamine oxide without a dietary contribution.

Trimethylamine oxide (TMAO) is an organic osmolyte and universal protein stabilizer. Its role as a cytoprotectant is particularly important in ureosmotic elasmobranchs that accumulate high levels of urea, a macromolecular perturbant. Feeding is a key component in the turnover and maintenance of these nitrogenous compounds.

Effects of short-term hyper- and hypo-osmotic exposure on the osmoregulatory strategy of unfed North Pacific spiny dogfish (Squalus suckleyi).

The North Pacific spiny dogfish (Squalus suckleyi) is a partially euryhaline species of elasmobranch that often enter estuaries where they experience relatively large fluctuations in environmental salinity that can affect plasma osmolality. Previous studies have investigated the effects of altered salinity on elasmobranchs over the long term, but fewer studies have conducted time courses to investigate how rapidly they can adapt to such changes. In this study, we exposed unfed (no exogenous source of nitrogen or TMAO) spiny dogfish to hyper- and hypo-osmotic conditions and measured plasma and tissue osmolytes, nitrogen excretion, and changes in enzyme activity and mRNA levels in the rectal gland over 24h.

Parkin and mitofusins reciprocally regulate mitophagy and mitochondrial spheroid formation.

Mitochondrial homeostasis via mitochondrial dynamics and quality control is crucial to normal cellular functions. Mitophagy (mitochondria removed by autophagy) stimulated by a mitochondrial uncoupler, carbonyl cyanide m-chlorophenylhydrazone (CCCP), requires Parkin, but it is not clear why Parkin is crucial to this process. We found that in the absence of Parkin, carbonyl cyanide m-chlorophenylhydrazone induced the formation of mitochondrial spheroids.

Activation of autophagy protects against acetaminophen-induced hepatotoxicity.

Unlabelled: Autophagy can selectively remove damaged organelles, including mitochondria, and, in turn, protect against mitochondria-damage-induced cell death. Acetaminophen (APAP) overdose can cause liver injury in animals and humans by inducing mitochondria damage and subsequent necrosis in hepatocytes. Although many detrimental mechanisms have been reported to be responsible for APAP-induced hepatotoxicity, it is not known whether APAP can modulate autophagy to regulate hepatotoxicity in hepatocytes.

Differential roles of unsaturated and saturated fatty acids on autophagy and apoptosis in hepatocytes.

Fatty acid-induced lipotoxicity plays a critical role in the pathogenesis of nonalcoholic liver disease. Saturated fatty acids and unsaturated fatty acids have differential effects on cell death and steatosis, but the mechanisms responsible for these differences are not known. Using cultured HepG2 cells and primary mouse hepatocytes, we found that unsaturated and saturated fatty acids differentially regulate autophagy and apoptosis.

Dissecting the dynamic turnover of GFP-LC3 in the autolysosome.

Determination of autophagic flux is essential to assess and differentiate between the induction or suppression of autophagy. Western blot analysis for free GFP fragments resulting from the degradation of GFP-LC3 within the autolysosome has been proposed as one of the autophagic flux assays. However, the exact dynamics of GFP-LC3 during the autophagy process are not clear.