Respiration modulates oscillatory neural network activity at rest

Despite recent advances in understanding how respiration affects neural signalling to influence perception, cognition, and behaviour, it is yet unclear to what extent breathing modulates brain oscillations at rest. We acquired respiration and resting state magnetoencephalography (MEG) data from human participants to investigate if, where, and how respiration cyclically modulates oscillatory amplitudes (2 to 150 Hz). Using measures of phase–amplitude coupling, we show respiration-modulated brain oscillations (RMBOs) across all major frequency bands. Sources of these modulations spanned a widespread network of cortical and subcortical brain areas with distinct spectrotemporal modulation profiles. Globally, delta and gamma band modulations varied with distance to the head centre, with stronger modulations at distal (versus central) cortical sites. Overall, we provide the first comprehensive mapping of RMBOs across the entire brain, highlighting respiration–brain coupling as a fundamental mechanism to shape neural processing within canonical resting state and respiratory control networks (RCNs).

Despite recent advances, it remains unclear to what extent breathing modulates brain oscillations at rest. This magnetoencephalography study in human participants identifies a widespread brain network of neural oscillations that are coupled to the respiratory rhythm.     

Parasitism of Aganaspis daci against Ceratitis capitata under Mediterranean climate conditions

The effect of environmental factors is essential to the success of parasitoids as biological control agents, as it determines their foraging activity, development, and survival. The larval‐pupal parasitoid wasp Aganaspis daci (Weld) (Hymenoptera: Figitidae) is known to have a very low fertility (i.e., offspring production) in the field in certain Mediterranean areas, probably due to its inability to efficiently oviposit under such climatic conditions. In this study, the percentage of parasitism and induced mortality (mortality of host pupae attributed to parasitoids, from which adults do not emerge) caused by this wasp to the Mediterranean fruit fly (medfly), Ceratitis capitata (Wiedemann) (Diptera: Tephritidae), was assessed under field conditions across 1 year, using medfly‐infested apples and parasitoid‐confined release in a lemon orchard of southeastern Spain. As A. daci is known to have very few emergences in the field, fertility was assessed in the laboratory from parasitized pupae recovered from the field. We found average parasitism rates of 27% and high induced mortality rates of 66% under field conditions. Consequently, medfly population reduction (total mortality of C. capitata caused by A. daci, i.e., induced mortality + % parasitism) was, on average, 87%. Parasitism and induced mortality varied throughout the year, depending on the average temperature and relative humidity. The interaction of these factors resulted in the highest parasitism rates at low mean temperature and humidity values; likewise, the highest percentages of induced mortality were obtained with a combination of high mean temperature and low mean humidity values. In conclusion, A. daci may exert a strong impact on medfly populations, being a good candidate for inundative field releases for the management of C. capitata in the Mediterranean Basin.     

Hydrologic regimes as potential drivers of morphologic divergence in fish

Fishes often exhibit phenotypic divergence across gradients of abiotic and biotic selective pressures. In streams, many of the known selective pressures driving phenotypic differentiation are largely influenced by hydrologic regimes. Because flow regimes drive so many attributes of lotic systems, we hypothesized fish exhibit phenotypic divergence among streams with different flow regimes. We used a comparative field study to investigate the morphological divergence of Campostoma anomalom (central stonerollers) among streams characterized by highly variable, intermittent flow regimes and streams characterized by relatively stable, groundwater flow regimes. We also conducted a mesocosm experiment to compare the plastic effects of one component of flow regimes, water velocity, on morphology of fish from different flow regimes. We observed differences in shape between flow regimes likely driven by differences in allometric growth patterns. Although we observed differences in morphology across flow regimes in the field, C. anomalum did not exhibit morphologic plasticity in response to water velocity alone. This study contributes to the understanding of how complex environmental factors drive phenotypic divergence and may provide insight into the evolutionary consequences of disrupting natural hydrologic patterns, which are increasingly threatened by climate change and anthropogenic alterations.     

Bayesian mapping of genomewide interacting quantitative trait loci for ordinal traits

Development of statistical methods and software for mapping interacting QTL has been the focus of much recent research. We previously developed a Bayesian model selection framework, based on the composite model space approach, for mapping multiple epistatic QTL affecting continuous traits. In this study we extend the composite model space approach to complex ordinal traits in experimental crosses. We jointly model main and epistatic effects of QTL and environmental factors on the basis of the ordinal probit model (also called threshold model) that assumes a latent continuous trait underlies the generation of the ordinal phenotypes through a set of unknown thresholds. A data augmentation approach is developed to jointly generate the latent data and the thresholds. The proposed ordinal probit model, combined with the composite model space framework for continuous traits, offers a convenient way for genomewide interacting QTL analysis of ordinal traits. We illustrate the proposed method by detecting new QTL and epistatic effects for an ordinal trait, dead fetuses, in a F(2) intercross of mice. Utility and flexibility of the method are also demonstrated using a simulated data set. Our method has been implemented in the freely available package R/qtlbim, which greatly facilitates the general usage of the Bayesian methodology for genomewide interacting QTL analysis for continuous, binary, and ordinal traits in experimental crosses.     

Heparanase expression and function during early pregnancy in mice

Embryo implantation is a complex process that involves interactions between cell-surface and extracellular components of the blastocyst and the uterus, including blastocyst adhesion to the uterine luminal epithelium, epithelial basement membrane penetration and stromal extracellular matrix remodeling, angiogenesis, and decidualization. These processes all involve interactions with heparan sulfate (HS) proteoglycans, which harbor various growth factors and cytokines and support cell adhesion. Heparanase (HPSE) is an endo-beta-glucuronidase that cleaves HS at specific sites. HPSE also can act as an adhesion molecule independent of its catalytic activity. Thus, HPSE is a multifunctional molecule contributing to and modulating HS-dependent processes. Exogenously added HPSE improves embryo implantation in mice; however, no information is available regarding the normal pattern of HPSE expression and activity during the implantation process in any system. Using several approaches, including real-time RT-PCR, in situ hybridization, and immunohistochemistry, we determined that uterine HPSE expression increases dramatically during early pregnancy in mice. Heparanase mRNA and protein were primarily expressed in decidua and were rapidly induced at the implantation site. Uterine HPSE activity was characterized and demonstrated to increase >40-fold during early pregnancy. Finally, we demonstrate that the HPSE inhibitor PI-88 severely inhibits embryo implantation in vivo. Collectively, these results indicate that HPSE plays a role in blastocyst implantation and complements previous studies showing a role for HS-dependent interactions in this process.     

Effect of inositol hexakisphosphate kinase 2 on transforming growth factor beta-activated kinase 1 and NF-kappaB activation

We previously showed that inositol hexakisphosphate kinase 2 (IHPK2) functions as a growth-suppressive and apoptosis-enhancing kinase during cell stress. Overexpression of IHPK2 sensitized ovarian carcinoma cell lines to the growth-suppressive and apoptotic effects of interferon beta (IFN-beta), IFN-alpha2, and gamma-irradiation. Expression of a kinase-dead mutant abrogated 50% of the apoptosis induced by IFN-beta. Because the kinase-dead mutant retained significant response to cell stressors, we hypothesized that a portion of the death-promoting function of IHPK2 was independent of its kinase activity. We now demonstrate that IHPK2 binds to tumor necrosis factor (TNF) receptor-associated factor (TRAF) 2 and interferes with phosphorylation of transforming growth factor beta-activated kinase 1 (TAK1), thereby inhibiting NF-kappaB signaling. IHPK2 contains two sites required for TRAF2 binding, Ser-347 and Ser-359. Compared with wild type IHPK2-transfected cells, cells expressing S347A and S359A mutations displayed 3.5-fold greater TAK1 activation following TNF-alpha. This mutant demonstrated a 6-10-fold increase in NF-kappaB DNA binding following TNF-alpha compared with wild type IHPK2-expressing cells in which NF-kappaB DNA binding was inhibited. Cells transfected with wild type IHPK2 or IHPK2 mutants that lacked S347A and S359A mutations displayed enhanced terminal deoxynucleotidyltransferase-mediated dUTP nick end-labeling staining following TNF-alpha. We believe that IHPK2-TRAF2 binding leads to attenuation of TAK1- and NF-kappaB-mediated signaling and is partially responsible for the apoptotic activity of IHPK2.