Trophic specialization influences the rate of environmental niche evolution in damselfishes (Pomacentridae).

The rate of environmental niche evolution describes the capability of species to explore the available environmental space and is known to vary among species owing to lineage-specific factors. Trophic specialization is a main force driving species evolution and is responsible for classical examples of adaptive radiations in fishes. We investigate the effect of trophic specialization on the rate of environmental niche evolution in the damselfish, Pomacentridae, which is an important family of tropical reef fishes. First, phylogenetic niche conservatism is not detected in the family using a standard test of phylogenetic signal, and we demonstrate that the environmental niches of damselfishes that differ in trophic specialization are not equivalent while they still overlap at their mean values. Second, we estimate the relative rates of niche evolution on the phylogenetic tree and show the heterogeneity among rates of environmental niche evolution of the three trophic groups. We suggest that behavioural characteristics related to trophic specialization can constrain the evolution of the environmental niche and lead to conserved niches in specialist lineages. Our results show the extent of influence of several traits on the evolution of the environmental niche and shed new light on the evolution of damselfishes, which is a key lineage in current efforts to conserve biodiversity in coral reefs.

Catalogue des vases, colonnes, tables de marbres rares, figures de bronze, porcelaines de choix, laques, meubles précieux, pendules, lustres... et autres effets importants qui composent le cabinet de feu M. le duc d'Aumont . Par P. F. Julliot fils, & A. J. Paillet. La vente se fera le 12 Décembre 1782...

[Vente. Art. 1782-12-12. Paris]

Recueil de quelques pieces de littérature, en prose et en vers

Comprend : Portrait historique du charlatanisme, fait par lui-même dans un moment de franchise ; Dissertation epistolaire sur les monumens antiques et les monumens funèbres... ; Les Échecs, poëme

Les guerres du règne de Louis XIII et de la minorité de Louis XIV : mémoires de Jacques de Chastenet, seigneur de Puységur. Tome 1 / publiés et annotés par Ph. Tamizey de Larroque

Collection : Petits mémoires sur l'histoire de France ; 7

Les guerres du règne de Louis XIII et de la minorité de Louis XIV : mémoires de Jacques de Chastenet, seigneur de Puységur. Tome 2 / publiés et annotés par Ph. Tamizey de Larroque

Collection : Petits mémoires sur l'histoire de France ; 7

Pharmacological inhibition of fibroblast growth factor (FGF) receptor signaling ameliorates FGF23-mediated hypophosphatemic rickets.

Fibroblast growth factor 23 (FGF23) is a circulating factor secreted by osteocytes that is essential for phosphate homeostasis. In kidney proximal tubular cells FGF23 inhibits phosphate reabsorption and leads to decreased synthesis and enhanced catabolism of 1,25-dihydroxyvitamin D3 (1,25[OH]2 D3 ). Excess levels of FGF23 cause renal phosphate wasting and suppression of circulating 1,25(OH)2 D3 levels and are associated with several hereditary hypophosphatemic disorders with skeletal abnormalities, including X-linked hypophosphatemic rickets (XLH) and autosomal recessive hypophosphatemic rickets (ARHR). Currently, therapeutic approaches to these diseases are limited to treatment with activated vitamin D analogues and phosphate supplementation, often merely resulting in partial correction of the skeletal aberrations. In this study, we evaluate the use of FGFR inhibitors for the treatment of FGF23-mediated hypophosphatemic disorders using NVP-BGJ398, a novel selective, pan-specific FGFR inhibitor currently in Phase I clinical trials for cancer therapy. In two different hypophosphatemic mouse models, Hyp and Dmp1-null mice, resembling the human diseases XLH and ARHR, we find that pharmacological inhibition of FGFRs efficiently abrogates aberrant FGF23 signaling and normalizes the hypophosphatemic and hypocalcemic conditions of these mice. Correspondingly, long-term FGFR inhibition in Hyp mice leads to enhanced bone growth, increased mineralization, and reorganization of the disturbed growth plate structure. We therefore propose NVP-BGJ398 treatment as a novel approach for the therapy of FGF23-mediated hypophosphatemic diseases.