•Urban lizards had higher ectoparasite loads and laid a higher proportion of unfertilized eggs.•Eggs from urban lizards had higher immune parameters in the yolk.•Egg mass and egg viability are ...important predictors of egg yolk physiology.•Maternal immune challenge altered egg yolk oxidative status in urban animals.
Urbanization can cause innumerable abiotic and biotic changes that have the potential to influence the ecology, behavior, and physiology of native resident organisms. Relative to their rural conspecifics, urban Side-blotched Lizard (Uta stansburiana) populations in southern Utah have lower survival prospects and maximize reproductive investment via producing larger eggs and larger clutch sizes. While egg size is an important predictor of offspring quality, physiological factors within the egg yolk are reflective of the maternal environment and can alter offspring traits, especially during energetically costly processes, such as reproduction or immunity. Therefore, maternal effects may represent an adaptive mechanism by which urban-dwelling species can persist within a variable landscape. In this study, we assess urban and rural differences in egg yolk bacterial killing ability (BKA), corticosterone (CORT), oxidative status (d-ROMs), and energy metabolites (free glycerol and triglycerides), and their association with female immune status and egg quality. Within a laboratory setting, we immune challenged urban lizards via lipopolysaccharide injection (LPS) to test whether physiological changes associated with immune system activity impacted egg yolk investment. We found urban females had higher mite loads than rural females, however mite burden was related to yolk BKA in rural eggs, but not urban eggs. While yolk BKA differed between urban and rural sites, egg mass and egg viability (fertilized vs. unfertilized) were strong predictors of yolk physiology and may imply tradeoffs exist between maintenance and reproduction. LPS treatment caused a decrease in egg yolk d-ROMs relative to the control treatments, supporting results from previous research. Finally, urban lizards laid a higher proportion of unfertilized eggs, which differed in egg yolk BKA, CORT, and triglycerides in comparison to fertilized eggs. Because rural lizards laid only viable eggs during this study, these results suggest that reduced egg viability is a potential cost of living in an urban environment. Furthermore, these results help us better understand potential downstream impacts of urbanization on offspring survival, fitness, and overall population health.
The coqui frog (Eleutherodactylus coqui) was introduced to the island of Hawai'i in the 1980s and has spread across much of the island. Concern remains that this frog will continue to expand its ...range and invade higher elevation habitats where much of the island's endemic species are found. We determined whether coqui thermal tolerance and physiology change along Hawai'i’s elevational gradients. We measured physiological responses using a short-term experiment to determine baseline tolerance and physiology by elevation, and a long-term experiment to determine the coqui's ability to acclimate to different temperatures. We collected frogs from low, medium, and high elevations. After both the short and long-term experiments, we measured critical thermal minimum (CTmin), blood glucose, oxidative stress, and corticosterone levels. CTmin was lower in high elevation frogs than low elevation frogs after the short acclimation experiment, signifying that they acclimate to local conditions. After the extended acclimation, CTmin was lower in frogs acclimated to cold temperatures compared to warm-acclimated frogs and no longer varied by elevation. Blood glucose levels were positively correlated with elevation even after the extended acclimation, suggesting glucose may also be related to lower temperatures. Oxidative stress was higher in females than males, and corticosterone was not significantly related to any predictor variables. The extended acclimation experiment showed that coquis can adjust their thermal tolerance to different temperatures over a 3-week period, suggesting the expansion of coqui into higher elevation habitats may still be possible, and they may not be as restricted by cold temperatures as previously thought.
•Coqui frogs are an invasive species in Hawai'i and threaten high elevation species.•High elevation frogs were more cold-tolerant than low elevation frogs.•Cold tolerance was higher in cold-acclimated frogs after 3 weeks.•Frogs collected at higher elevations have more glucose.•These traits might allow coqui to survive at higher elevations.
The coqui frog (Eleutherodactylus coqui) was introduced to the island of Hawai'i in the 1980s, and has spread across much of the island. There is concern they will invade higher elevation areas where ...negative impacts on native species are expected. It is not known if coqui change behavior and baseline physiology in ways that allow them to invade higher elevations. We investigated where coqui are found across the island and whether that includes recent invasion into higher elevations. We also investigated whether elevation is related to coqui's microhabitat use, including substrate use and height off the forest floor, and physiological metrics, including plasma osmolality, oxidative status, glucose, free glycerol, and triglycerides, that might be associated with invading higher elevations. We found coqui have increased the area they occupy along roads from 31% to 50% and have moved into more high‐elevation locations (16% vs. 1%) compared to where they were found 14 years ago. We also found frogs at high elevation on different substrates and closer to the forest floor than frogs at lower elevations—perhaps in response to air temperatures which tended to be warmer close to the forest floor. We observed that blood glucose and triglycerides increase in frogs with elevation. An increase in glucose is likely an acclimation response to cold temperatures while triglycerides may also help frogs cope with the energetic demands of suboptimal temperatures. Finally, we found that female coqui have higher plasma osmolality, reactive oxygen metabolites (dROMs), free glycerol, and triglycerides than males. Our study suggests coqui behavior and physiology in Hawai'i may be influenced by elevation in ways that allow them to cope with lower temperatures and invade higher elevations.
Research Highlights: Coqui frogs in Hawai'i were present in more areas and higher elevations compared to a survey 14 years prior. Frogs at high elevation use different microhabitats and have higher energy metabolite levels than frogs from lower elevations.
•Approaches used to measure germ cell genotoxicity for health risk assessment were evaluated.•Further integration of germ cell assays with somatic cell genotoxicity tests was ...recommended.•Reproductive toxicology endpoints that may indicate germ cell genotoxicity were discussed.•The need for research on the use of global genomic approaches in this field was highlighted.•Approaches to measure newly recognized types of genomic changes were recommended.
This workshop reviewed the current science to inform and recommend the best evidence-based approaches on the use of germ cell genotoxicity tests. The workshop questions and key outcomes were as follows. (1) Do genotoxicity and mutagenicity assays in somatic cells predict germ cell effects? Limited data suggest that somatic cell tests detect most germ cell mutagens, but there are strong concerns that dictate caution in drawing conclusions. (2) Should germ cell tests be done, and when? If there is evidence that a chemical or its metabolite(s) will not reach target germ cells or gonadal tissue, it is not necessary to conduct germ cell tests, notwithstanding somatic outcomes. However, it was recommended that negative somatic cell mutagens with clear evidence for gonadal exposure and evidence of toxicity in germ cells could be considered for germ cell mutagenicity testing. For somatic mutagens that are known to reach the gonadal compartments and expose germ cells, the chemical could be assumed to be a germ cell mutagen without further testing. Nevertheless, germ cell mutagenicity testing would be needed for quantitative risk assessment. (3) What new assays should be implemented and how? There is an immediate need for research on the application of whole genome sequencing in heritable mutation analysis in humans and animals, and integration of germ cell assays with somatic cell genotoxicity tests. Focus should be on environmental exposures that can cause de novo mutations, particularly newly recognized types of genomic changes. Mutational events, which may occur by exposure of germ cells during embryonic development, should also be investigated. Finally, where there are indications of germ cell toxicity in repeat dose or reproductive toxicology tests, consideration should be given to leveraging those studies to inform of possible germ cell genotoxicity.
Next-generation sequencing technologies can now be used to directly measure heritable de novo DNA sequence mutations in humans. However, these techniques have not been used to examine environmental ...factors that induce such mutations and their associated diseases. To address this issue, a working group on environmentally induced germline mutation analysis (ENIGMA) met in October 2011 to propose the necessary foundational studies, which include sequencing of parent–offspring trios from highly exposed human populations, and controlled dose–response experiments in animals. These studies will establish background levels of variability in germline mutation rates and identify environmental agents that influence these rates and heritable disease. Guidance for the types of exposures to examine come from rodent studies that have identified agents such as cancer chemotherapeutic drugs, ionizing radiation, cigarette smoke, and air pollution as germ-cell mutagens. Research is urgently needed to establish the health consequences of parental exposures on subsequent generations.
Birth defects, de novo genetic diseases, and chromosomal abnormality syndromes occur in ∼5% of all live births, and affected children suffer from a broad range of lifelong health consequences. ...Despite the social and medical impact of these defects, and the 8 decades of research in animal systems that have identified numerous germ‐cell mutagens, no human germ‐cell mutagen has been confirmed to date. There is now a growing consensus that the inability to detect human germ‐cell mutagens is due to technological limitations in the detection of random mutations rather than biological differences between animal and human susceptibility. A multidisciplinary workshop responding to this challenge convened at The Jackson Laboratory in Bar Harbor, Maine. The purpose of the workshop was to assess the applicability of an emerging repertoire of genomic technologies to studies of human germ‐cell mutagenesis. Workshop participants recommended large‐scale human germ‐cell mutation studies be conducted using samples from donors with high‐dose exposures, such as cancer survivors. Within this high‐risk cohort, parents and children could be evaluated for heritable changes in (a) DNA sequence and chromosomal structure, (b) repeat sequences and minisatellites, and (c) global gene expression profiles and pathways. Participants also advocated the establishment of a bio‐bank of human tissue samples from donors with well‐characterized exposure, including medical and reproductive histories. This mutational resource could support large‐scale, multiple‐endpoint studies. Additional studies could involve the examination of transgenerational effects associated with changes in imprinting and methylation patterns, nucleotide repeats, and mitochondrial DNA mutations. The further development of animal models and the integration of these with human studies are necessary to provide molecular insights into the mechanisms of germ‐cell mutations and to identify prevention strategies. Furthermore, scientific specialty groups should be convened to review and prioritize the evidence for germ‐cell mutagenicity from common environmental, occupational, medical, and lifestyle exposures. Workshop attendees agreed on the need for a full‐scale assault to address key fundamental questions in human germ‐cell environmental mutagenesis. These include, but are not limited to, the following: Do human germ‐cell mutagens exist? What are the risks to future generations? Are some parents at higher risk than others for acquiring and transmitting germ‐cell mutations? Obtaining answers to these, and other critical questions, will require strong support from relevant funding agencies, in addition to the engagement of scientists outside the fields of genomics and germ‐cell mutagenesis. Environ. Mol. Mutagen., 2007. Published 2007 Wiley‐Liss, Inc.
PDF
