No evidence for sex-specific effects of the maternal social environment on offspring development in Japanese quail (Coturnix japonica)

The social environment of reproducing females can cause physiological changes, with consequences for reproductive investment and offspring development. These prenatal maternal effects are often found to be sexspecific and may have evolved as adaptations, maximizing fitness of male and female offspring for their future environment. Female hormone levels during reproduction are considered a potential mechanism regulating sex allocation in vertebrates: high maternal androgens have repeatedly been linked to increased investment in sons, whereas high glucocorticoid levels are usually related to increased investment in daughters. However, results are not consistent across studies and therefore still inconclusive. In Japanese quail (Coturnix japonica), we previously found that pair-housed females had higher plasma androgen levels and tended to have higher plasma corticosterone levels than group-housed females. In the current study we investigate whether these differences in maternal social environment and physiology affect offspring sex allocation and physiology. Counter to our expectations, we find no effects of the maternal social environment on offspring sex ratio, sex-specific mortality, growth, circulating androgen or corticosterone levels. Also, maternal corticosterone or androgen levels do not correlate with offspring sex ratio or mortality. The social environment during reproduction therefore does not necessarily modify sex allocation and offspring physiology, even if it causes differences in maternal physiology. We propose that maternal effects of the social environment strongly depend upon the type of social stimuli and the timing of changes in the social environment and hormones with respect to the reproductive cycle and meiosi

AMPA Receptors Commandeer an Ancient Cargo Exporter for Use as an Auxiliary Subunit for Signaling

Fast excitatory neurotransmission in the mammalian central nervous system is mainly mediated by ionotropic glutamate receptors of the AMPA subtype (AMPARs). AMPARs are protein complexes of the pore-lining α-subunits GluA1-4 and auxiliary β-subunits modulating their trafficking and gating. By a proteomic approach, two homologues of the cargo exporter cornichon, CNIH-2 and CNIH-3, have recently been identified as constituents of native AMPARs in mammalian brain. In heterologous reconstitution experiments, CNIH-2 promotes surface expression of GluAs and modulates their biophysical properties. However, its relevance in native AMPAR physiology remains controversial. Here, we have studied the role of CNIH-2 in GluA processing both in heterologous cells and primary rat neurons. Our data demonstrate that CNIH-2 serves an evolutionarily conserved role as a cargo exporter from the endoplasmic reticulum (ER). CNIH-2 cycles continuously between ER and Golgi complex to pick up cargo protein in the ER and then to mediate its preferential export in a coat protein complex (COP) II dependent manner. Interaction with GluA subunits breaks with this ancestral role of CNIH-2 confined to the early secretory pathway. While still taking advantage of being exported preferentially from the ER, GluAs recruit CNIH-2 to the cell surface. Thus, mammalian AMPARs commandeer CNIH-2 for use as a bona fide auxiliary subunit that is able to modify receptor signaling

Towards a Unified Theory of Health-Disease: I. Health as a complex model-object

Este trabalho apresenta uma abordagem sistemática para a modelagem de várias classes de enfermidade-moléstia-doença, designada como Holopatogênese. Holopatogênese é definido como um processo de sobre determinação de doenças e condições relacionadas, tomadas como um integral, compreendendo facetas selecionadas da saúde enquanto objeto complexo. Em primeiro lugar, o marco conceitual da Holopatogênese é apresentado como uma série de três interfaces significativas: biomolecular- imunológica, fisiopatológico-clínica e epidemiológico-ecossocial. Em segundo lugar, proposições derivadas da Holopatogênese são introduzidas a fim de permitir o desenho do complexo doença-enfermidade como uma rede hierárquica de redes. Em terceiro lugar, propõe-se uma formalização de correspondências intra e inter nível, processos de sobredeterminação, efeitos e laços componentes da Holopatogênese. Finalmente, o modelo Holopatogênese é avaliado como uma patologia teórica compreensiva tomada como passo preliminar para uma teoria unificada de saúde-doença