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Glaucoma is considered a progressive optic neuropathy because of the damage and death of the retinal ganglion cells. It is also a neurodegenerative disease because it affects neural structures in the visual system and beyond, including the corpus callosum-the largest white matter structure involved in inter-hemispheric transfer of information. In this study we probed the dysfunction of the inter-hemispheric processing in patients with mild glaucoma using the phenomenon of binocular rivalry. Patients with mild glaucoma and no measurable visual field defects and age-matched controls underwent a thorough visual assessment. Then they participated in a series of psychophysical tests designed to examine the binocular rivalry derived from intra- and inter-hemispheric processing. Static horizontal and vertical sinewave gratings were presented dichoptically using a double-mirror stereoscope in 3 locations: centrally, to probe inter-hemispheric processing, and peripherally to the left or to the right, to probe intra-hemispheric processing. Although the two groups were matched in functional measures, rivalry rate of the glaucoma group was significantly lower than that of the control group for the central location, but not for the peripheral location. These results were driven mainly by the patients with normal tension glaucoma whose average rivalry rate for the central location (from which information reaches the two hemispheres) was almost half (46% lower) that of the controls. These results indicate a dysfunction in inter-hemispheric transfer in mild glaucoma that can be detected behaviourally before any changes in standard functional measures.

Waterbirds have a major functional role in wetlands, and understanding how functional traits of waterbirds depend on environmental characteristics can facilitate management of ecosystems and their services. We investigate how the waterbird community in a Neotropical river-floodplain system responds to environmental gradients, identifying how they affect waterbird species richness, functional diversity (measured as functional dispersion) and functional composition (specific functional traits). We sampled 22 lakes in the Upper Paraná floodplain system in southern Brazil, and modelled avian functional diversity and species richness as a function of environmental variables. Then we used a unified RLQ and fourth-corner analysis to evaluate environment-trait relationships. Waterbird species richness and functional diversity varied according to different environmental variables. Lake area and diversity of aquatic vegetation were associated with avian species richness, while relative abundance of grass and emergent macrophytes and mean and variation of depth were related to functional diversity. Furthermore, changes in functional diversity seemed to be mainly driven by presence of species that depend on perches for foraging (e.g. kingfishers, cormorants, and kites), whose presence was mainly associated with deep water and emergent macrophytes. Nevertheless, changes in functional diversity and functional composition did not depend on exactly the same set of environmental variables, suggesting that trait combinations (e.g. below surface feeders who feed on fish), not only specific traits, are important drivers of the variation in functional diversity between lakes. Given the observed differences in responses of species richness and functional diversity, both these diversity metrics should be used as complementary tools in ecosystem management. Furthermore, our results show that functional diversity and composition are partially coupled, suggesting that although functional diversity is influenced by the environmental filtering of particular traits, it also reflects other ecological mechanisms (e.g. competitive interactions among species).

Biological networks pervade nature. They describe systems throughout all levels of biological organization, from molecules regulating metabolism to species interactions that shape ecosystem dynamics. The network thinking revealed recurrent organizational patterns in complex biological systems, such as the formation of semi-independent groups of connected elements (modularity) and non-random distributions of interactions among elements. Other structural patterns, such as nestedness, have been primarily assessed in ecological networks formed by two non-overlapping sets of elements; information on its occurrence on other levels of organization is lacking. Nestedness occurs when interactions of less connected elements form proper subsets of the interactions of more connected elements. Only recently these properties began to be appreciated in one-mode networks (where all elements can interact) which describe a much wider variety of biological phenomena. Here, we compute nestedness in a diverse collection of one-mode networked systems from six different levels of biological organization depicting gene and protein interactions, complex phenotypes, animal societies, metapopulations, food webs and vertebrate metacommunities. Our findings suggest that nestedness emerge independently of interaction type or biological scale and reveal that disparate systems can share nested organization features characterized by inclusive subsets of interacting elements with decreasing connectedness. We primarily explore the implications of a nested structure for each of these studied systems, then theorize on how nested networks are assembled. We hypothesize that nestedness emerges across scales due to processes that, although system-dependent, may share a general compromise between two features: specificity (the number of interactions the elements of the system can have) and affinity (how these elements can be connected to each other). Our findings suggesting occurrence of nestedness throughout biological scales can stimulate the debate on how pervasive nestedness may be in nature, while the theoretical emergent principles can aid further research on commonalities of biological networks.

The neuronal transporter GlyT2 is a polytopic, 12-transmembrane domain, plasma membrane glycoprotein involved in the removal and recycling of synaptic glycine from inhibitory synapses. Mutations in the human GlyT2 gene (SLC6A5) that cause deficient glycine transport or defective GlyT2 trafficking are the second most common cause of hyperekplexia or startle disease. In this study we examined several aspects of GlyT2 biogenesis that involve the endoplasmic reticulum chaperone calnexin (CNX). CNX binds transiently to an intermediate under-glycosylated transporter precursor and facilitates GlyT2 processing. In cells expressing GlyT2, transporter accumulation and transport activity were attenuated by siRNA-mediated CNX knockdown and enhanced by CNX overexpression. GlyT2 binding to CNX was mediated by glycan and polypeptide-based interactions as revealed by pharmacological approaches and the behavior of GlyT2 N-glycan-deficient mutants. Moreover, transporter folding appeared to be stabilized by N-glycans. Co-expression of CNX and a fully non-glycosylated mutant rescues glycine transport but not mutant surface expression. Hence, CNX discriminates between different conformational states of GlyT2 displaying a lectin-independent chaperone activity. GlyT2 wild-type and mutant transporters were finally degraded in the lysosome. Our findings provide further insight into GlyT2 biogenesis, and a useful framework for the study of newly synthesized GlyT2 transporters bearing hyperekplexia mutations.