How effective are maternal effects at having effects?

The well studied trade-off between offspring size and offspring number assumes that offspring fitness increases with increasing per-offspring investment. Where mothers differ genetically or exhibit plastic variation in reproductive effort, there can be variation in per capita investment in offspring, and via this trade-off, variation in fecundity. Variation in per capita investment will affect juvenile performance directly—a classical maternal effect—while variation in fecundity will also affect offspring performance by altering the offsprings' competitive environment. The importance of this trade-off, while a focus of evolutionary research, is not often considered in discussions about population dynamics. Here, we use a factorial experiment to determine what proportion of variation in offspring performance can be ascribed to maternal effects and what proportion to the competitive environment linked to the size–number trade-off. Our results suggest that classical maternal effects are significant, but that in our system, the competitive environment, which is linked to maternal environments by fecundity, can be a far more substantial influence

Systematic review and meta-analysis: anxiety and depressive disorders in offspring of parents with anxiety disorders

Objective: We conducted meta-analyses to assess risk of anxiety disorders among offspring of parents with anxiety disorders and to establish whether there is evidence of specificity of risk for anxiety disorders as opposed to depression in offspring, and whether particular parent anxiety disorders confer risks for particular child anxiety disorders. We also examined whether risk was moderated by offspring age, gender, temperament and the presence of depressive disorders in parents. Method: We searched PsycINFO, PubMed and Web of Science in June, 2016 and July, 2017 (PROSPERO CRD42016048814). Study inclusion criteria: published in peer-reviewed journals; contained at least one group of parents with anxiety disorders and at least one comparison group of parents who did not have anxiety disorders; reported rates of anxiety disorders in offspring, and used validated diagnostic tools to ascertain diagnoses. We used random and mixed-effects models and evaluated study quality. Results: We included 25 studies (7285 offspring). Where parents had an anxiety disorder, offspring were significantly more likely to have anxiety (RR: 1.76, 95% CI = 1.58-1.96) and depressive disorders (RR: 1.31, 95% CI = 1.13-1.52) than offspring of parents without anxiety disorders. Parent Panic Disorder and Generalized Anxiety Disorder appeared to confer particular risk. Risk was greater for offspring anxiety than depressive disorders (RR: 2.50, 95% CI = 1.50-4.16), and specifically for offspring Generalized Anxiety Disorder, Separation Anxiety Disorder and Specific Phobia, but there was no evidence that children of parents with particular anxiety disorders were at increased risk for the same particular anxiety disorders. Moderation analyses were possible only for offspring age, gender and parental depressive disorder; none were significant. Conclusions: Parent anxiety disorders pose specific risks of anxiety disorders to offspring. However, there is limited support for transmission of the same particular anxiety disorder. These results support the potential for targeted prevention of anxiety disorders

Selection, inheritance, and the evolution of parent-offspring interactions

Very few studies have examined parent-offspring interactions from a quantitative genetic perspective. We used a cross-fostering design and measured genetic correlations and components of social selection arising from two parental and two offspring behaviors in the burying beetle Nicrophorus vespilloides. Genetic correlations were assessed by examining behavior of relatives independent of common social influences. We found positive genetic correlations between all pairs of behaviors, including between parent and offspring behaviors. Patterns of selection were assessed by standardized performance and selection gradients. Parental provisioning had positive effects on offspring performance and fitness, while remaining near the larvae without feeding them had negative effects. Begging had positive effects on offspring performance and fitness, while increased competition among siblings had negative effects. Coadaptations between parenting and offspring behavior appear to be maintained by genetic correlations and functional trade-offs; parents that feed their offspring more also spend more time in the area where they can forage for themselves. Families with high levels of begging have high levels of sibling competition. Integrating information from genetics and selection thus provides a general explanation for why variation persists in seemingly beneficial traits expressed in parent-offspring interactions and illustrates why it is important to measure functionally related suites of behaviors

Sex distribution of offspring-parents obesity: Angel's hypothesis revisited

This study, which is based on two cross sectional surveys' data, aims to establish any effect of parental obesity sex distribution of offspring and to replicate the results that led to the hypothesis that obesity may be associated with sex-linked recessive lethal gene. A representative sample of 4,064 couples living in Renfrew/Paisley, Scotland was surveyed 1972-1976. A total of 2,338 offspring from 1,477 of the couples screened in 1972-1976, living in Paisley, were surveyed in 1996. In this study, males represented 47.7% among the total offspring of the couples screened in 1972-1976. In the first survey there was a higher male proportion of offspring (53%, p < 0.05) from parents who were both obese, yet this was not significant after adjustment for age of parents. Also, there were no other significant differences in sex distribution of offspring according to body mass index, age, or social class of parents. The conditions of the original 1949 study of Angel (1949) (which proposed a sex-linked lethal recessive gene) were simulated by selecting couples with at least one obese daughter. In this subset, (n = 409), obesity in fathers and mothers was associated with 26% of offspring being male compared with 19% of offspring from a non-obese father and obese mother. Finally we conclude that families with an obese father have a higher proportion of male offspring. These results do not support the long-established hypotheses of a sex-linked recessive lethal gene in the etiology of obesity

Statistical methods for detecting genes associated with sperm competition in natural populations of Drosophila, using blocks of tightly linked single nucleotide polymorphisms : a thesis presented in partial fulfilment of the requirements for the degree of Master of Science in Statistics at Massey University, Albany, New Zealand

The purpose of the project is to develop statistical methods for detecting genes associated with sperm competition in natural populations of Drosophila (fruit flies). The flies' genotype information given by Fiumera et al. (2004) is used as the starting point of the analysis. This dataset utilizes blocks of tightly linked single nucleotide polymorphisms within genes suspected to affect sperm competition. The sperm competition detection process is completed in three different stages: maternal and offspring haplotypes reconstruction; paternal genotype and offspring fraction estimation; and preferred genotype detection. Software programs HAPLORE and PHASE 2.0 were implemented for maternal and offspring haplotype reconstruction. The software Parentage is applied on the reconstructed haplotypes for estimating paternal genotypes and the amount of offspring they produced. Lastly, the Kruskal Wallis and permutation tests were conducted to detect differences in offspring produced between groups of males with different genotypes

Evidence for inbreeding depression in a species with limited opportunity for maternal effects

It is often assumed that mating with close relatives reduces offspring fitness. In such cases, reduced offspring fitness may arise from inbreeding depression (i.e., genetic effects of elevated homozygosity) or from post-mating maternal investment. This can be due to a reduction in female investment after mating with genetically incompatible males ("differential allocation") or compensation for incompatibility ("reproductive compensation"). Here, we looked at the effects of mating with relatives on offspring fitness in mosquitofish, Gambusia holbrooki. In this species, females are assumed to be nonplacental and to allocate resources to eggs before fertilization, limiting differential allocation. We looked at the effects of mating with a brother or with an unrelated male on brood size, offspring size, gestation period, and early offspring growth. Mating with a relative reduced the number of offspring at birth, but there was no difference in the likelihood of breeding, gestation time, nor in the size or growth of these offspring. We suggest that due to limited potential for maternal effects to influence these traits that any reduction in offspring fitness, or lack thereof, can be explained by inbreeding depression rather than by maternal effects. We highlight the importance of considering the potential role of maternal effects when studying inbreeding depression and encourage further studies in other Poeciliid species with different degrees of placentation to test whether maternal effects mask or amplify any genetic effects of mating with relatives.This work was supported bythe Australian Research Council (DP120100339). R.V.-T. is supported by fellowships from Consejo Nacion-al de Ciencia y Tecnologıa-Mexico and the ResearchSchool of Biology

Offspring subcutaneous adipose markers are sensitive to the timing of maternal gestational weight gain

peer-reviewedBackground Excessive maternal weight gain during pregnancy impacts on offspring health. This study focused on the timing of maternal gestational weight gain, using a porcine model with mothers of normal pre-pregnancy weight. Methods Trial design ensured the trajectory of maternal gestational weight gain differed across treatments in early, mid and late gestation. Diet composition did not differ. On day 25 gestation, sows were assigned to one of five treatments: Control sows received a standard gestation diet of 2.3 kg/day (30 MJ DE/day) from early to late gestation (day 25–110 gestation). E sows received 4.6 kg food/day in early gestation (day 25–50 gestation). M sows doubled their food intake in mid gestation (day 50–80 gestation). EM sows doubled their food intake during both early and mid gestation (day 25–80 gestation). L sows consumed 3.5 kg food/day in late gestation (day 80–110 gestation). Offspring body weight and food intake levels were measured from birth to adolescence. Markers of lipid metabolism, hypertrophy and inflammation were investigated in subcutaneous adipose tissue of adolescent offspring. Results The trajectory of gestational weight gain differed across treatments. However total gestational weight gain did not differ except for EM sows who were the heaviest and fattest mothers at parturition. Offspring birth weight did not differ across treatments. Subcutaneous adipose tissue from EM offspring differed significantly from controls, with elevated mRNA levels of lipogenic (CD36, ACACB and LPL), nutrient transporters (FABP4 and GLUT4), lipolysis (HSL and ATGL), adipocyte size (MEST) and inflammation (PAI-1) indicators. The subcutaneous adipose depot from L offspring exhibited elevated levels of CD36, ACACB, LPL, GLUT4 and FABP4 mRNA transcripts compared to control offspring. Conclusions Increasing gestational weight gain in early gestation had the greatest impact on offspring postnatal growth rate. Increasing maternal food allowance in late gestation appeared to shift the offspring adipocyte focus towards accumulation of fat. Mothers who gained the most weight during gestation (EM mothers) gave birth to offspring whose subcutaneous adipose tissue, at adolescence, appeared hyperactive compared to controls. This study concluded that mothers, who gained more than the recommended weight gain in mid and late gestation, put their offspring adipose tissue at risk of dysfunction.This research was funded by Teagasc, under the National Development Plan. LBMcN was in receipt of a Teagasc Walsh Fellowship. Nestle hosted LG on a sabbatical and funded the RT-PCR cost