Faunal mortality associated with massive beaching and decomposition of pelagic Sargassum.

In 2018, the Mexican Caribbean coast received a massive influx of pelagic Sargassum spp. that accumulated and decayed on beaches producing organic decomposition products that made the water turbid and brown. Between May and September of the same year there were several reports of mass mortality of marine biota in this area. From these reports we estimate that organisms belonging to 78 faunal species died as result of this event, with demersal neritic fish and Crustacea being the most affected groups. The cause of mortality appears to be the combined effect of high ammonium and hydrogen sulfide concentrations, together with hypoxic conditions. If massive arrival of pelagic Sargassum spp. continues and algae is left to decay on the beach in large volumes then deterioration in water quality could affect coral reefs close to shore. Furthermore, barriers placed in lagoons to intercept the Sargassum spp. before it reaches the beach could impact reef fauna if the algae is left to die and sink on site.

Opposite regulation of PPAR-alpha and -gamma gene expression by both their ligands and retinoic acid in brown adipocytes.

The peroxisome proliferator-activated receptors (PPARs) are lipid-activated transcription factors involved in the regulation of lipid metabolism and adipocyte differentiation. Little is known, however, about the control of the expression of the genes encoding each of all three receptor subtypes: alpha, delta, and gamma. We have addressed this question in the brown adipocyte, the only cell type that co-expresses high levels of the three PPAR subtypes. Differentiation of brown adipocytes is associated with enhanced expression of PPAR genes. However, whereas PPARgamma and PPARdelta genes are already expressed in preadipocytes, the mRNA for PPARalpha appears suddenly in association with the acquisition of the terminally differentiated phenotype. Both retinoic acid isomers and PPAR agonists, specific for either PPARalpha or PPARgamma, regulate expression of each PPAR subtype gene in the opposite way: they up-regulate PPARalpha and down-regulate PPARgamma. The effects on PPARalpha mRNA are independent of protein synthesis, whereas inhibition of PPARgamma mRNA expression depends on protein synthesis, except when its specific ligand prostaglandin J2 is used. Our results indicate a strictly opposite autoregulation of PPAR subtypes, which supports specific physiological roles for them in controlling brown fat differentiation and thermogenic activity.

Differential regulation of uncoupling protein-2 and uncoupling protein-3 gene expression in brown adipose tissue during development and cold exposure.

The expression of the two novel uncoupling proteins genes, UCP2 and UCP3, is differentially regulated during prenatal maturation of brown adipose tissue in the mouse. UCP2 gene is expressed early in prenatal development, when neither UCP1 nor UCP3 gene expression yet occurs. UCP3 mRNA is absent at any stage of fetal life; it appears suddenly at birth and reaches adult levels in a few hours. UCP2 mRNA increased after birth but more slowly than UCP3 and UCP1 mRNA. Short-time exposure of adult mice to cold caused a rise in UCP2 or UCP1 mRNA levels but not in that of UCP3. The postnatal rise in UCP2 gene expression appears to be a response to the thermic stress associated with birth, similarly to UCP1, whereas different biological signals may be responsible for the surge in UCP3 gene expression at birth.

9-cis retinoic acid induces the expression of the uncoupling protein-2 gene in brown adipocytes.

The expression of uncoupling protein-2 (UCP2) mRNA is up-regulated during the differentiation of brown adipocytes in primary culture. When differentiation of brown adipocytes is impaired, UCP2 mRNA expression is down-regulated. 9-cis Retinoic acid causes a dose-dependent induction of UCP2 mRNA levels in brown adipocytes, whereas all-trans retinoic acid has no effect. Specific agonists of retinoid X receptors (RXR) induce UCP2 mRNA expression, whereas specific activators of retinoic acid receptors do not. 9-cis Retinoic acid, acting through RXR receptors, is identified as a major regulator of the expression of the UCP2 gene in the brown fat cell.