Seasonality of the red blood cell stress response in rainbow trout (Oncorhynchus mykiss)

The β-adrenergic stress response in red blood cells (RBCs) of rainbow trout shows seasonal changes in expression. We have explored the mechanisms underpinning this response by following over a period of 27 months changes in β-adrenergic receptor (β-AR) binding characteristics, β-adrenergically stimulated RBC Na+/H+ exchanger (βNHE) activity, together with β-AR and βNHE mRNA levels and plasma steroid hormone and lactate levels. These parameters were measured at approximately monthly intervals in a single population of fish held under semi-natural conditions. Membrane-bound, high-affinity β-ARs were present in RBCs at all sampling times, varying from 668 ± 112 to 2654 ± 882 receptors cell-1 (mean ± SEM; n=8). βNHE activity, however, was reduced by 57 and 34% in December 1999 and February 2001, respectively, compared to an otherwise sustained influx that averaged 110.4 ± 2.3 mmol l-1 RBCs h-1 (n = 119). Only one reduction coincided with a spawning period but both were preceded by transient increases in circulating testosterone. βNHE activity measured under standard conditions was not correlated with the number or affinity of β-ARs nor with water temperature, but both β-AR numbers and βNHE activity were positively related to their respective mRNA levels (P = 0.005 and 0.038, respectively). Pharmaceutical intervention in the transduction cascade linking the β-AR and βNHE failed to indicate any failure of the transduction elements in RBCs displaying low βNHE activity. Similarly, we failed to demonstrate any link between seasonal cortisol fluctuations and seasonally reduced βNHE activity. However, the βNHE activity of age-separated RBC fractions showed that younger RBCs had a significantly higher βNHE response than older RBCs, consistent with the seasonal reductions in βNHE being linked to turnover of red cells and erythropoiesis. Testosterone is known to induce erythropoiesis and we conclude that seasonal reductions in βNHE are not caused by changes in β-AR numbers, but may be linked to testosterone-induced erythropoiesis

Analysis of gene expression from the Wolbachia genome of a filarial nematode supports both metabolic and defensive roles within the symbiosis

The α-proteobacterium Wolbachia is probably the most prevalent, vertically transmitted symbiont on Earth. In contrast with its wide distribution in arthropods, Wolbachia is restricted to one family of animal-parasitic nematodes, the Onchocercidae. This includes filarial pathogens such as Onchocerca volvulus, the cause of human onchocerciasis, or river blindness. The symbiosis between filariae and Wolbachia is obligate, although the basis of this dependency is not fully understood. Previous studies suggested that Wolbachia may provision metabolites (e.g., haem, riboflavin, and nucleotides) and/or contribute to immune defense. Importantly, Wolbachia is restricted to somatic tissues in adult male worms, whereas females also harbor bacteria in the germline. We sought to characterize the nature of the symbiosis between Wolbachia and O. ochengi, a bovine parasite representing the closest relative of O. volvulus. First, we sequenced the complete genome of Wolbachia strain wOo, which revealed an inability to synthesize riboflavin de novo. Using RNA-seq, we also generated endobacterial transcriptomes from male soma and female germline. In the soma, transcripts for membrane transport and respiration were up-regulated, while the gonad exhibited enrichment for DNA replication and translation. The most abundant Wolbachia proteins, as determined by geLC-MS, included ligands for mammalian Toll-like receptors. Enzymes involved in nucleotide synthesis were dominant among metabolism-related proteins, whereas the haem biosynthetic pathway was poorly represented. We conclude that Wolbachia may have a mitochondrion-like function in the soma, generating ATP for its host. Moreover, the abundance of immunogenic proteins in wOo suggests a role in diverting the immune system toward an ineffective antibacterial response

The genetic basis and evolution of red blood cell sickling in deer

Crescent-shaped red blood cells, the hallmark of sickle-cell disease, present a striking departure from the biconcave disc shape normally found in mammals. Characterized by increased mechanical fragility, sickled cells promote haemolytic anaemia and vaso-occlusions and contribute directly to disease in humans. Remarkably, a similar sickle-shaped morphology has been observed in erythrocytes from several deer species, without obvious pathological consequences. The genetic basis of erythrocyte sickling in deer, however, remains unknown. Here, we determine the sequences of human β-globin orthologues in 15 deer species and use protein structural modelling to identify a sickling mechanism distinct from the human disease, coordinated by a derived valine (E22V) that is unique to sickling deer. Evidence for long-term maintenance of a trans-species sickling/non-sickling polymorphism suggests that sickling in deer is adaptive. Our results have implications for understanding the ecological regimes and molecular architectures that have promoted convergent evolution of sickling erythrocytes across vertebrates