University of Alcalá

About: University of Alcalá is a education organization based out in Alcalá de Henares, Spain. It is known for research contribution in the topics: Population & Context (language use). The organization has 10795 authors who have published 20718 publications receiving 410089 citations. The organization is also known as: University of Alcala & University of Alcala de Henares.

Polymorphism at the ribosomal DNA ITS and its relation to postglacial re-colonization routes of the Perigord truffle Tuber melanosporum.

Abstract: Summary • Glaciations and postglacial migrations are major factors responsible for the present patterns of genetic variation we see in natural populations in Europe. For ectomycorrhizal fungi, escape from refugia can only follow range expansion by their specific hosts. • To infer phylogeographic relationships within Tuber melanosporum, sequences of internal transcribed spacers (ITS) and the 5.8S coding region of the ribosomal DNA repeat were obtained for 188 individuals sampled over the entire distribution of this species in France, and in north-western Italy and north-eastern Spain. • Ten distinct ITS haplotypes were distinguished, mapped and treated using F- and NST-statistics and nested clade (NCA) analyses. They showed a significant genetic differentiation between regional populations. NCA revealed a geographical association of ITS haplotypes, an old fragmentation into two major groups of populations, which likely colonized regions on different sides of the French Central Massif. • This re-colonization pattern is reminiscent of the one observed for host trees of the Perigord truffle, such as oaks and hazelnut trees. This suggests that host postglacial expansion was one of the major factors that shaped the mycobiont population structure.

Ligand stabilization of CXCR4/δ‐opioid receptor heterodimers reveals a mechanism for immune response regulation

Abstract: The CXCR4 chemokine receptor and the delta opioid receptor (DOR) are pertussis toxin-sensitive G protein-coupled receptors (GPCR). Both are widely distributed in brain tissues and immune cells, and have key roles in inflammation processes and in pain sensation on proximal nerve endings. We show that in immune cells expressing CXCR4 and DOR, simultaneous addition of their ligands CXCL12 and [D-Pen2, D-Pen5]enkephalin does not trigger receptor function. This treatment does not affect ligand binding or receptor expression, nor does it promote heterologous desensitization. Our data indicate that CXCR4 and DOR form heterodimeric complexes that are dynamically regulated by the ligands. This is compatible with a model in which GPCR oligomerization leads to suppression of signaling, promoting a dominant negative effect. Knockdown of CXCR4 and DOR signaling by heterodimerization might have repercussions on physiological and pathological processes such as inflammation, pain sensation and HIV-1 infection.