Mammals have two insulin-like growth factors (IGF) that are key mediators of somatic growth, of tissue differentiation and cellular responses to stress. Thus, the mechanisms that regulate the bioavailability of IGFs are important in both normal and aberrant development. IGF-I levels are primarily controlled via the growth hormone-IGF axis, in response to nutritional status, and also reflect metabolic diseases and cancer. One mechanism that controls IGF bioavailablity is the binding of circulating IGF to a number of binding proteins that keep IGF in a stable, but receptor non-binding state. But even before IGF is released from the cells that produce it, it undergoes an obligatory association with a ubiquitous chaperone protein, GRP94. This binding is required for secretion of a properly folded, mature IGF. This chapter reviews the known aspects of the interaction and highlights the specificity issues yet to be determined. The IGF-GRP94 interaction provides a potential novel mechanism of idiopathic short stature, involving the obligatory chaperone and not just IGF gene expression. It also provides a novel target for cancer treatment, as GRP94 activity can be either inhibited or enhanced.

Corals are an important habitat for a diverse fauna which is especially rich in branching species. Each colony harbors several species and dozens of individuals forming an integrated symbiotic community. Factors affecting the diversity and abundance of coral symbionts are poorly understood. The present study tested experimentally the relationship between the population density of coral Pocillopora verrucosa and the diversity and abundance of symbionts in planted coral fragments exposed during three months. Colony size and bleaching were also considered as two additional factors. We demonstrated that even at the early stage of the colonies’ formation, the diversity of obligate symbiontson on these corals was higher than in any other studied local faunas of the World Ocean.Species richness and abundance of symbionts were positively related to colony size and density, while no impact of bleaching was found. Species richness and abundance of obligate symbionts increased along with the host population density, while in facultative symbionts, these indexes decreased. We hypothesized that the negative effect of the host density on species richness and abundance of facultative symbionts is caused by the competitive pressure of obligates, which increases with their abundance. Reasons for the different responses of obligate and facultative symbionts to host density were considered.

The extension of virology beyond its traditional medical, veterinary or agricultural applications, now called environmental virology, has shown that viruses are both the most numerous and diverse biological entities on earth. In particular, virus isolation studies involving unicellular eukaryotic hosts (heterotrophic and photosynthetic protozoans) revealed numerous viral types previously unexpected in terms of virion structure and morphology, genome size and gene content, or mode of replication. Complemented by large-scale metagenomic analyzes, these discoveries have rekindled interest in the enigma of the evolutionary origin of viruses, for which no simple definition encompassing all of their diversity is still unanimous. Several laboratories have repeatedly tackled the deep reconstruction of the evolutionary history of viruses, using various methods of molecular phylogeny applied to the few shared genes detected in certain virus groups (e.g. the Nucleocytoviricota). Beyond the practical difficulties of establishing reliable homology relationships from extremely divergent sequences, I present here purely conceptual arguments highlighting several fundamental limitations plaguing the reconstruction of the deep evolutionary history of viruses, and even more the identification of their unique of multiple origin (s). Those limitations are direct consequences of the particularly random mechanisms which govern the reductive evolution of obligate intracellular parasites.