ck Center For Behavioral Biology

Raleigh, NC, United States

ck Center For Behavioral Biology

Raleigh, NC, United States
Time filter
Source Type

Diamond S.E.,North Carolina State University | Diamond S.E.,ck Center For Behavioral Biology | Nichols L.M.,North Carolina State University | McCoy N.,North Carolina State University | And 8 more authors.
Ecology | Year: 2012

Physiological tolerance of environmental conditions can influence species-level responses to climate change. Here, we used species-specific thermal tolerances to predict the community responses of ant species to experimental forest-floor warming at the northern and southern boundaries of temperate hardwood forests in eastern North America. We then compared the predictive ability of thermal tolerance vs. correlative species distribution models (SDMs) which are popular forecasting tools for modeling the effects of climate change. Thermal tolerances predicted the responses of 19 ant species to experimental climate warming at the southern site, where environmental conditions are relatively close to the ants' upper thermal limits. In contrast, thermal tolerances did not predict the responses of the six species in the northern site, where environmental conditions are relatively far from the ants' upper thermal limits. Correlative SDMs were not predictive at either site. Our results suggest that, in environments close to a species' physiological limits, physiological trait-based measurements can successfully forecast the responses of species to future conditions. Although correlative SDMs may predict large-scale responses, such models may not be accurate for predicting sitelevel responses. © 2012 by the Ecological Society of America.

Diamond S.E.,North Carolina State University | Diamond S.E.,ck Center For Behavioral Biology | Sorger D.M.,North Carolina State University | Sorger D.M.,ck Center For Behavioral Biology | And 8 more authors.
Global Change Biology | Year: 2012

Effects of climate warming on wild populations of organisms are expected to be greatest at higher latitudes, paralleling greater anticipated increases in temperature in these regions. Yet, these expectations assume that populations in different regions are equally susceptible to the effects of warming. This is unlikely to be the case. Here, we develop a series of predictive models for physiological thermal tolerances in ants based on current and future climates. We found that tropical ants have lower warming tolerances, a metric of susceptibility to climate warming, than temperate ants despite greater increases in temperature at higher latitudes. Using climatic, ecological and phylogenetic data, we refine our predictions of which ants (across all regions) were most susceptible to climate warming. We found that ants occupying warmer and more mesic forested habitats at lower elevations are the most physiologically susceptible to deleterious effects of climate warming. Phylogenetic history was also a strong indicator of physiological susceptibility. In short, we find that ants that live in the canopies of hot, tropical forest are the most at risk, globally, from climate warming. Unfortunately this is where many, perhaps most, ant and other species on Earth live. © 2011 Blackwell Publishing Ltd.

Losa-Ward S.M.,North Carolina State University | Todd K.L.,North Carolina State University | McCaffrey K.A.,North Carolina State University | Tsutsui K.,Waseda University | And 2 more authors.
Biology of Reproduction | Year: 2012

Hypothalamic neurons, which produce the kisspeptin family of peptide hormones (Kp), are critical for initiating puberty and maintaining estrous cyclicity by stimulating gonadotropinreleasing hormone (GnRH) release. Conversely, RFamide-related peptide-3 (RFRP3) neurons inhibit GnRH activity. It has previously been shown that neonatal exposure to bisphenol A (BPA) can alter the timing of female pubertal onset and induce irregular estrous cycles or premature anestrus. Here we tested the hypothesis that disrupted ontogeny of RFamide signaling pathways may be a mechanism underlying advanced puberty. To test this, we used a transgenic strain of Wistar rats whose GnRH neurons express enhanced green fluorescent protein. Pups were exposed by daily subcutaneous injection to vehicle, 17betaestradiol (E2), 50 lg/kg BPA, or 50 mg/kg BPA, from Postnatal Day (PND) 0 through PND 3, and then cohorts were euthanized on PNDs 17, 21, 24, 28, and 33 (5-8 animals per age per exposure; males were collected on PNDs 21 and 33). Vaginal opening was advanced by E2 and 50 lg/kg BPA. On PND 28, females exposed to E2 and 50 lg/kg BPA had decreased RFRP-3 fiber density and contacts on GnRH neurons. RFRP3 perikarya were also decreased in females exposed to 50 lg/kg BPA. Data suggest that BPA-induced premature puberty results from decreased inhibition of GnRH neurons. © 2012 by the Society for the Study of Reproduction, Inc.

Hicks K.D.,North Carolina State University | Sullivan A.W.,North Carolina State University | Sullivan A.W.,ck Center For Behavioral Biology | Cao J.,North Carolina State University | And 4 more authors.
Hormones and Behavior | Year: 2016

Concerns have been raised regarding the potential for endocrine disrupting compounds (EDCs) to alter brain development and behavior. Developmental exposure to bisphenol A (BPA), a ubiquitous EDC, has been linked to altered sociosexual and mood-related behaviors in various animal models and children but effects are inconsistent across laboratories and animal models creating confusion about potential risk in humans. Exposure to endocrine active diets, such as soy, which is rich in phytoestrogens, may contribute to this variability. Here, we tested the individual and combined effects of low dose oral BPA and soy diet or the individual isoflavone genistein (GEN; administered as the aglycone genistin (GIN)) on rat sociosexual behaviors with the hypothesis that soy would obfuscate any BPA-related effects. Social and activity levels were unchanged by developmental exposure to BPA but soy diet had sex specific effects including suppressed novelty preference, and open field exploration in females. The data presented here reinforce that environmental factors, including anthropogenic chemical exposure and hormone active diets, can shape complex behaviors and even reverse expected sex differences. © 2016 Elsevier Inc.

Lopez-Uribe M.M.,North Carolina State University | Lopez-Uribe M.M.,ck Center For Behavioral Biology | Sconiers W.B.,North Carolina State University | Frank S.D.,North Carolina State University | And 5 more authors.
Biology Letters | Year: 2016

Social living poses challenges for individual fitness because of the increased risk of disease transmission among conspecifics. Despite this challenge, sociality is an evolutionarily successful lifestyle, occurring in the most abundant and diverse group of organisms on earth-the social insects. Two contrasting hypotheses predict the evolutionary consequences of sociality on immune systems. The social group hypothesis posits that sociality leads to stronger individual immune systems because of the higher risk of disease transmission in social species. By contrast, the relaxed selection hypothesis proposes that social species have evolved behavioural immune defences that lower disease risk within the group, resulting in lower immunity at the individual level. We tested these hypotheses bymeasuring the encapsulation response in 11 eusocial and non-eusocial insect lineages.We built phylogenetic mixed linear models to investigate the effect of behaviour, colony size and body size on cellular immune response. We found a significantly negative effect of colony size on encapsulation response (Markov chain Monte Carlo generalized linear mixed model (mcmcGLMM) p < 0.05; phylogenetic generalized least squares (PGLS) p < 0.05). Our findings suggest that insects living in large societies may rely more on behavioural mechanisms, such as hygienic behaviours, than on immune function to reduce the risk of disease transmission among nest-mates. © 2016 The Author(s) Published by the Royal Society. All rights reserved.

He X.,South China Agricultural University | Zhou S.,ck Center For Behavioral Biology | St. Armour G.E.,ck Center For Behavioral Biology | Mackay T.F.C.,ck Center For Behavioral Biology | Anholt R.R.H.,ck Center For Behavioral Biology
Genes, Brain and Behavior | Year: 2016

The extent to which epistasis affects the genetic architecture of complex traits is difficult to quantify, and identifying variants in natural populations with epistatic interactions is challenging. Previous studies in Drosophila implicated extensive epistasis between variants in genes that affect neural connectivity and contribute to natural variation in olfactory response to benzaldehyde. In this study, we implemented a powerful screen to quantify the extent of epistasis as well as identify candidate interacting variants using 203 inbred wild-derived lines with sequenced genomes of the Drosophila melanogaster Genetic Reference Panel (DGRP). We crossed the DGRP lines to P[GT1]-element insertion mutants in Sema-5c and neuralized (neur), two neurodevelopmental loci which affect olfactory behavior, and to their coisogenic wild-type control. We observed significant variation in olfactory responses to benzaldehyde among F1 genotypes and for the DGRP line by mutant genotype interactions for both loci, showing extensive nonadditive genetic variation. We performed genome-wide association analyses to identify the candidate modifier loci. None of these polymorphisms were in or near the focal genes; therefore, epistasis is the cause of the nonadditive genetic variance. Candidate genes could be placed in interaction networks. Several candidate modifiers are associated with neural development. Analyses of mutants of candidate epistatic partners with neur (merry-go-round (mgr), prospero (pros), CG10098, Alhambra (Alh) and CG12535) and Sema-5c (CG42540 and bruchpilot (brp)) showed aberrant olfactory responses compared with coisogenic controls. Thus, integrating genome-wide analyses of natural variants with mutations at defined genomic locations in a common coisogenic background can unmask specific epistatic modifiers of behavioral phenotypes. Integrating analysis of natural variants with mutations at defined genomic locations can unmask epistatic modifiers of behaviors. © 2016 John Wiley & Sons Ltd and International Behavioural and Neural Genetics Society.

Loading ck Center For Behavioral Biology collaborators
Loading ck Center For Behavioral Biology collaborators