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Transgenerational plasticity, the influence of the environment experienced by parents on the phenotype and fitness of subsequent generations, is being increasingly recognized. Human-altered environments, such as those resulting from the increasing use of pesticides, may be major drivers of such cross-generational influences, which in turn may have profound evolutionary and ecological repercussions. Most of these consequences are, however, unknown. Whether transgenerational plasticity elicited by pesticide exposure is common, and the consequences of its potential carryover effects on fitness and population dynamics, remains to be determined. Here, we investigate whether exposure of parents to a common pesticide elicits intra-, inter-, and transgenerational responses (in F0, F1, and F2 generations) in life history (fecundity, longevity, and lifetime reproductive success), in an insect model system, the seed beetle Callosobruchus maculatus. We also assessed sex specificity of the effects. We found sex-specific and hormetic intergenerational and transgenerational effects on longevity and lifetime reproductive success, manifested both in the form of maternal and paternal effects. In addition, the transgenerational effects via mothers detected in this study are consistent with a new concept: terminal investment transgenerational effects. Such effects could underlie cross-generational responses to environmental perturbation. Our results indicate that pesticide exposure leads to unanticipated effects on population dynamics and have far-reaching ecological and evolutionary implications.

The Fukushima nuclear accident in March 2011 caused biological impacts on the pale grass blue butterfly Zizeeria maha. At least some of the impacts are likely mediated by the host plant, resulting in “field effects”. However, to obtain the whole picture of the impacts, direct exposure effects should also be evaluated. Here, we examined the distribution of experimentally ingested anthropogenic cesium-137 (137Cs) in adult butterfly bodies using imaging plate autoradiography. We showed that 137Cs ingested by larvae was incorporated into adult bodies and was biased to females, although the majority of ingested 137Cs was excreted in the pupal cuticle and excretory material during eclosion. 137Cs accumulation in adult bodies was the highest in the abdomen, followed by the thorax and other organs. These results suggest that 137Cs accumulation in reproductive organs may cause adverse transgenerational or maternal effects mediated by reactive oxygen species (ROS) on germ cells. 137Cs accumulation was detected in field individuals collected in September 2011 and September 2016 but not in May 2011, which is consistent with the abnormality dynamics known from previous studies. Taken together, these results contribute to an integrative understanding of the multifaceted biological effects of the Fukushima nuclear accident in the field.

Mental disorders during pregnancy are common and affect the health of mother and child. Despite a relatively high prevalence rate, treatment options have not been investigated systematically. Particularly symptoms of posttraumatic stress disorder (PTSD) may increase significantly during the course of pregnancy. However, proper guidelines for psychotherapeutic treatment of PTSD during pregnancy do not exist. In this article, we aimed at discussing the effects of untreated PTSD on pregnancy and postpartum mother-child bonding as well as exposure therapy during pregnancy. To do so, we present the case of a pregnant woman with complex PTSD following childhood sexual abuse. At the time of hospitalization, the patient was pregnant in the second trimester and reported intrusive re-experiencing of the traumatic events, nightmares, anxiety and helplessness as well as an impairing level of irritability during social situations. After a careful discussion of the case within our department and at the annual conference of the German Association of Psychiatry, Psychotherapy and Psychosomatics, we decided to treat the patient with dialectical behavior therapy for PTSD (DBT-PTSD) including exposure therapy under the regular observation of a gynecologist. Psychometric measurements (Davidson Trauma Scale (DTS) and Borderline Symptom- List-23 (BSL-23) were used to observe the course of treatment regarding common PTSD-symptoms and disturbances in self-organization (DSO). The intensity of intrusions and hyperarousal increased from the date of admission, reached the maximum when exposure started and decreased below baseline-level at the end of treatment. Avoidance behavior continually decreased from the beginning until the end of therapy. Decreased BSL-23 values show major improvements regarding DSO. To our knowledge, the course of pregnancy was not affected by treatment-induced psychological and physical symptoms. : DBT- PTSD is a potential treatment option for patients suffering from PTSD during pregnancy. Yet, further (epigenetic) research in this field is urgently needed.

Whether environmentally-induced changes in phenotypes can be heritable is a topic with revived interest. In plants, heritable trait variation can occur without DNA sequence mutations through epigenetic mechanisms involving DNA methylation. However, it remains unknown if this other system of inheritance responds to environmental changes and if it can provide a rapid way for plants to generate adaptive heritable phenotypic variation. To obtain a comprehensive assessment of potential transgenerational effects induced by the environment, we subjected four natural accessions as well as the reference accession Col-0 of A. thaliana to mild drought in a multigenerational design. As expected, plastic responses to drought were observed in each accession, as well as a number of intergenerational effects of parental environments. However, after an intervening generation without stress, descendants of stressed and non-stressed plants were phenotypically indistinguishable, except for very few trait-based parental effects and irrespective of whether they were grown in control conditions or under water deficit. In addition, genome-wide analysis of DNA methylation and gene expression in the reference accession Col-0 demonstrated that, while mild drought induced changes in the DNA methylome of exposed plants, variants were not inherited. We conclude that mild drought stress does not induce transgenerational epigenetic effects.

BPA is one of the most common endocrine disruptors that is widely being manufactured daily nationwide. Although scientific evidence supports claims of negative effects of BPA on humans, there is also evidence suggesting that a low level of BPA is safe. However, numerous in vivo trials contraindicate with this claim and there is a high possibility of BPA exposure could lead to obesity. It has been speculated that this does not stop with the exposed subjects only, but may also cause transgenerational effects. Direct disruption of endocrine regulation, neuroimmune and signaling pathways, as well as gut microbiata, has been identified to be interrupted by BPA exposure, leading to overweight or obesity. In these instances, cardiovascular complications are one of the primary notable clinical signs. In regard to this claim, this review paper discusses the role of BPA on obesity in the perspective of endocrine disruptions and possible cardiovascular complications that may arise due to BPA. Thus, the aim of this review is to outline the changes in gut microbiota and neuroimmune or signaling mechanisms involved in obesity in relation to BPA. To identify potentially relevant articles, a depth search was done on the databases Nature, PubMed, Wiley Online Library, and Medline & Ovid from the past 5 years. According to Boolean operator guideline, selected keywords such as (1) BPA OR environmental chemical AND fat OR LDL OR obese AND transgenerational effects or phenocopy (2) Endocrine disruptors OR chemical AND lipodystrophy AND phenocopy (3) Lipid profile OR weight changes AND cardiovascular effect (4) BPA AND neuroimmune OR gene signaling, were used as search terms. Upon screening, 11 articles were finalized to be further reviewed and data extraction tables containing information on (1) the type of animal model (2) duration and dosage of BPA exposure (3) changes in the lipid profile or weight (4) genes, signaling mechanism, or any neuroimmune signal involved, and (5) transgenerational effects were created. In toto, the study indicates there are high chances of BPA exposure affecting lipid profile and gene associated with lipolysis, leading to obesity. Therefore, this scoping review recapitulates the possible effects of BPA that may lead to obesity with the evidence of current in vivo trials. The biomarkers, safety concerns, recommended dosage, and the impact of COVID-19 on BPA are also briefly described.

Oocytes and preimplantation embryos require careful regulation of the redox environment for optimal development both in vivo and in vitro. Reactive oxygen species (ROS) are generated throughout development as a result of cellular metabolism and enzyme reactions. ROS production can result in (i) oxidative eustress, where ROS are helpful signalling molecules with beneficial physiological functions and where the redox state of the cell is maintained within homeostatic range by a closely coupled system of antioxidants and antioxidant enzymes, or (ii) oxidative distress, where excess ROS are deleterious and impair normal cellular function. in vitro culture of embryos exacerbates ROS production due to a range of issues including culture-medium composition and laboratory culture conditions. This increase in ROS can be detrimental not only to assisted reproductive success rates but can also result in epigenetic and genetic changes in the embryo, resulting in transgenerational effects. This review examines the effects of oxidative stress in the oocyte and preimplantation embryo in both the in vivo and in vitro environment, identifies mechanisms responsible for oxidative stress in the oocyte/embryo in culture and approaches to reduce these problems, and briefly examines the potential impacts on future generations.

Queen health and quality play a significant role in the survival, expansion, and productivity of honey bee colonies. Nevertheless, modern beekeeping practices, intensified agriculture, and climate change can leave queens vulnerable to diverse stressors. These stressors can exert a negative impact on queens, resulting in a range of morphological and physiological abnormalities. The repercussions of queen stress may not only cause direct impacts on her survival and performance, but it may also extend to the offspring of surviving queens through transgenerational mechanisms. Here, we review the current knowledge regarding the effects of major abiotic stressors (namely, nutrition, pesticides, and extreme temperatures) on queen health and their potential impacts on the queen’s progeny. Gaining insight into the effects of these factors across individual and colony levels is vital for prioritizing further research on queen and colony health.

Domestication of wild animals induces a set of phenotypic characteristics collectively known as the domestication syndrome. However, how this syndrome emerges is still not clear. Recently, the neural crest cell deficit hypothesis proposed that it is generated by a mildly disrupted neural crest cell developmental program, but clear support is lacking due to the difficulties of distinguishing pure domestication effects from preexisting genetic differences between farmed and wild mammals and birds. Here, we use a farmed fish as model to investigate the role of persistent changes in DNA methylation (epimutations) in the process of domestication. We show that early domesticates of sea bass, with no genetic differences with wild counterparts, contain epimutations in tissues with different embryonic origins. About one fifth of epimutations that persist into adulthood are established by the time of gastrulation and affect genes involved in developmental processes that are expressed in embryonic structures, including the neural crest. Some of these genes are differentially expressed in sea bass with lower jaw malformations, a key feature of domestication syndrome. Interestingly, these epimutations significantly overlap with cytosine-to-thymine polymorphisms after 25 years of selective breeding. Furthermore, epimutated genes coincide with genes under positive selection in other domesticates. We argue that the initial stages of domestication include dynamic alterations in DNA methylation of developmental genes that affect the neural crest. Our results indicate a role for epimutations during the beginning of domestication that could be fixed as genetic variants and suggest a conserved molecular process to explain Darwin’s domestication syndrome across vertebrates.

Recent evidence suggests that stressed plants employ epigenetic mechanisms to transmit acquired resistance traits to their progeny. However, the evolutionary and ecological significance of transgenerational induced resistance (t-IR) is poorly understood because a clear understanding of how parents interpret environmental cues in relation to the effectiveness, stability, and anticipated ecological costs of t-IR is lacking. Here, we have used a full factorial design to study the specificity, costs, and transgenerational stability of t-IR following exposure of Arabidopsis thaliana to increasing stress intensities by a biotrophic pathogen, a necrotrophic pathogen, and salinity. We show that t-IR in response to infection by biotrophic or necrotrophic pathogens is effective against pathogens of the same lifestyle. This pathogen-mediated t-IR is associated with ecological costs, since progeny from biotroph-infected parents were more susceptible to both necrotrophic pathogens and salt stress, whereas progeny from necrotroph-infected parents were more susceptible to biotrophic pathogens. Hence, pathogen-mediated t-IR provides benefits when parents and progeny are in matched environments but is associated with costs that become apparent in mismatched environments. By contrast, soil salinity failed to mediate t-IR against salt stress in matched environments but caused non-specific t-IR against both biotrophic and necrotrophic pathogens in mismatched environments. However, the ecological relevance of this non-specific t-IR response remains questionable as its induction was offset by major reproductive costs arising from dramatically reduced seed production and viability. Finally, we show that the costs and transgenerational stability of pathogen-mediated t-IR are proportional to disease pressure experienced by the parents, suggesting that plants use disease severity as an environmental proxy to adjust investment in t-IR.

In our previous work, we reported alterations in protamines/histones ratio, in DNA binding of these proteins and their involvement in DNA oxidative damage in 84% of the young men living in the Land of Fires. In the present work, we extended our findings, evaluating any alterations in spermatozoa of a family case, a father and son, living in this area, to also give a first look at the possibility of transgenerational inherited effects of environmental contaminants on the molecular alterations of sperm nuclear basic proteins (SNBP), DNA and semen parameters. In the father and son, we found a diverse excess of copper and chromium in the semen, different alterations in SNBP content and low DNA binding affinity of these proteins. In addition, DNA damage, in the presence of CuCl2 and H2O2, increased by adding both the father and son SNBP. Interestingly, son SNBP, unlike his father, showed an unstable DNA binding and were able to produce DNA damage even without external addition of CuCl2, in line with a lower seminal antioxidant activity than the father. The peculiarity of some characteristics of son semen could be a basis for possible future studies on transgenerational effects of pollutants on fertility.