The parental care behaviour of Paratilapia polleni (Perciformes, Labroidei), a phylogenetically primitive cichlid from Madagascar, with a discussion of the evolution of maternal care in the family Cichlidae

The parental behaviour of the Madagascan cichlid, Paratilapia polleni , was studied in the laboratory. According to current hypotheses of phylogenetic intrarelationship for the family Cichlidae, Paratilapia is a representative of a phylogenetically primitive cichlid lineage, and as such is of particular interest in comparative evolutionary studies. Given the basal phylogenetic placement of Paratilapia it seems reasonable to expect that, if maternal participation in brood care arose within the extant Cichlidae, then the proposed plesiomorphic system of extensive male care of eggs and embryos may be retained in this taxon. This is not the case, and already by the fertilized-egg interval male and female roles in Paratilapia are strongly differentiated with the female as the primary care giver. In addition to specialized behavioural roles, a unique egg morphology and mobile egg mass is described for Paratilapia . The results of the study are discussed in the context of theories of the evolution of maternal brood care within the Cichlidae.Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/42636/1/10641_2004_Article_BF00004768.pd

Macrophage miR-210 induction and metabolic reprogramming in response to pathogen interaction boost life-threatening inflammation

Unbalanced immune responses to pathogens can be life-threatening although the underlying regulatory mechanisms remain unknown. Here, we show a hypoxia-inducible factor 1α-dependent microRNA (miR)-210 up-regulation in monocytes and macrophages upon pathogen interaction. MiR-210 knockout in the hematopoietic lineage or in monocytes/macrophages mitigated the symptoms of endotoxemia, bacteremia, sepsis, and parasitosis, limiting the cytokine storm, organ damage/dysfunction, pathogen spreading, and lethality. Similarly, pharmacologic miR-210 inhibition improved the survival of septic mice. Mechanistically, miR-210 induction in activated macrophages supported a switch toward a proinflammatory state by lessening mitochondria respiration in favor of glycolysis, partly achieved by downmodulating the iron-sulfur cluster assembly enzyme ISCU. In humans, augmented miR-210 levels in circulating monocytes correlated with the incidence of sepsis, while serum levels of monocyte/macrophage-derived miR-210 were associated with sepsis mortality. Together, our data identify miR-210 as a fine-tuning regulator of macrophage metabolism and inflammatory responses, suggesting miR-210-based therapeutic and diagnostic strategies