Unilateral injury of sensorimotor cortex of the dominant or subdominant hemispheres of rats-mothers and emotional behavior of their offsprings in the "open field"

Neurohumoral disorders in mothers caused by brain injury, infection, hypoxia, and other pathological factors result in motor and psychoemotional disorders in children. Emotional behavior of 30-day-old offsprings of female rats with unilateral sensorimotor brain injury was studied in the "open field". Individual behavior was estimated (the probability of certain acts and significant transfers between them). Behavioral disorders in rat offsprings depended on the side (left of right) of mother's brain injury and "handedness". The right-side mother's injury turned to be more deleterious. Behavioral alterations were stronger in offsprings of ambidextral and left-handed females than in those born by right-handed males with the same sensorimotor injury.     

Perinatal supplementation with thymoquinone improves diabetic complications and T cell immune responses in rat offspring

Background

Epidemiological studies have shown that the offspring of mothers who experience diabetes mellitus during pregnancy are seven times more likely to develop health complications later in life compared to offspring born to nondiabetic mothers.

Aim of the study

We investigated whether supplementation with a natural antioxidant (thymoquinone; TQ) in female rats with streptozotocin (STZ)-induced gestational diabetes (GD) improved diabetic complications and T cell immune responses in their offspring.

Methods

Three groups of female rats were tested: nondiabetics, diabetics treated with TQ during pregnancy and lactation periods and diabetics that were not treated with TQ (n = 10 female rats in each group).

Results

Our data demonstrated a significant decrease in the numbers of neonates born to diabetic rats compared with those born to control rats. GD led to macrosomic pups with several postpartum complications, such as a significant increase in plasma levels of the pro-inflammatory cytokines IL-1β, IL-6, and TNF-α (but not of IL-10); a marked decrease in the plasma level of IL-2; a marked reduction in the proliferative capacity of superantigen (SEB)-stimulated T-lymphocytes; and an obvious reduction in the number of circulating and thymus homing T cells. TQ supplementation of diabetic mothers during pregnancy and lactation periods had an obvious and significant effect on the number and mean body weight of neonates. Furthermore, TQ significantly restored the IL-2 level and T cell proliferation and subsequently rescued both circulating and thymus homing T cells in the offspring.

Conclusions

Our data suggest that nutritional supplementation of GD mothers with the natural antioxidant TQ during pregnancy and lactation periods improves diabetic complications and maintains an efficient T cell immune response in their offspring, providing a protective effect in later life.     

Exposure to maternal overnutrition and a high-fat diet during early postnatal development increases susceptibility to renal and metabolic injury later in life

Overnutrition during pre- and postnatal development both confer increased susceptibility to renal and metabolic risks later in life; however, whether they have an additive effect on the severity of renal and metabolic injury remains unknown. The present study tested the hypothesis that a combination of a pre- and postnatal diet high in fat/fructose would exacerbate renal and metabolic injury in male offspring later in life. Male offspring born to high fat/high-fructose-fed mothers and fed a high-fat/high-fructose diet postnatally (HF-HF) had increased urine albumin excretion (450%), glomerulosclerosis (190%), and tubulointerstitial fibrosis (101%) compared with offspring born to mothers fed a standard diet and fed a standard diet postnatally (NF-NF). No changes in blood pressure or glomerular filtration were observed between any of the treatment groups. The HF-HF offspring weighed ～23% more than offspring born to mothers fed a high-fat/high-fructose diet and fed a normal diet postnatally (HF-NF), as well as offspring born to mothers fed a standard diet regardless of their postnatal diet. The HF-HF rats also had increased (and more variable) blood glucose levels over 12 wk of being fed a high-fat/high-fructose diet. A combination of exposure to a high-fat/high-fructose diet in utero and postnatally increased plasma insulin levels by 140% compared with NF-NF offspring. Our data suggest that the combined exposure to overnutrition during fetal development and early postnatal development potentiate the susceptibility to renal and metabolic disturbances later in life.     

Altered dopamine signaling in naturally occurring maternal neglect

Background

Child neglect is the most common form of child maltreatment, yet the biological basis of maternal neglect is poorly understood and a rodent model is lacking.

Methodology/Principal Findings

The current study characterizes a population of mice (MaD1) which naturally exhibit maternal neglect (little or no care of offspring) at an average rate of 17% per generation. We identified a set of risk factors that can predict future neglect of offspring, including decreased self-grooming and elevated activity. At the time of neglect, neglectful mothers swam significantly more in a forced swim test relative to nurturing mothers. Cross-fostered offspring raised by neglectful mothers in turn exhibit increased expression of risk factors for maternal neglect and decreased maternal care as adults, suggestive of possible epigenetic contributions to neglect. Unexpectedly, offspring from neglectful mothers elicited maternal neglect from cross-fostered nurturing mothers, suggesting that factors regulating neglect are not solely within the mother. To identify a neurological pathway underlying maternal neglect, we examined brain activity in neglectful and nurturing mice. c-Fos expression was significantly elevated in neglectful relative to nurturing mothers in the CNS, particularly within dopamine associated areas, such as the zona incerta (ZI), ventral tegmental area (VTA), and nucleus accumbens. Phosphorylated tyrosine hydroxylase (a marker for dopamine production) was significantly elevated in ZI and higher in VTA (although not significantly) in neglectful mice. Tyrosine hydroxylase levels were unaltered, suggesting a dysregulation of dopamine activity rather than cell number. Phosphorylation of DARPP-32, a marker for dopamine D1-like receptor activation, was elevated within nucleus accumbens and caudate-putamen in neglectful versus nurturing dams.

Conclusions/Significance

These findings suggest that atypical dopamine activity within the maternal brain, especially within regions involved in reward, is involved in naturally occurring neglect and that MaD1 mice are a useful model for understanding the basis of naturally occurring neglect.     

Motor Disturbances in Offspring of Female Ambidexter Rats with Psychogenic Trauma

The vital stress experienced by mothers both during and before their pregnancy produced motor disturbances in their offspring. By parameters of the EMG activity of the low extremities, more pronounced motor disturbances are revealed in the young 35-day old rat pups whose mothers were exposed to the acute psychogenic trauma during pregnancy. Asymmetry of the motor disturbances is the most prominent in the 45-day old rat pups born from the mothers exposed to the psychogenic trauma one month before pregnancy. In the process of ontogenetic development the revealed deviations are better compensated in the rat pups of the “neonatal stress” group than in the case of their mothers' preconception psychogenic trauma.     

Co-administration of Creatine Plus Pyruvate Prevents the Effects of Phenylalanine Administration to Female Rats During Pregnancy and Lactation on Enzymes Activity of Energy Metabolism in Cerebral Cortex and Hippocampus of the Offspring

Phenylketonuria (PKU) is the most frequent inborn error of metabolism. It is caused by deficiency in the activity of phenylalanine hydroxylase, leading to accumulation of phenylalanine and its metabolites. Untreated maternal PKU or hyperphenylalaninemia may result in nonphenylketonuric offspring with low birth weight and neonatal sequelae, especially microcephaly and intellectual disability. The mechanisms underlying the neuropathology of brain injury in maternal PKU syndrome are poorly understood. In the present study, we evaluated the possible preventive effect of the co-administration of creatine plus pyruvate on the effects elicited by phenylalanine administration to female Wistar rats during pregnancy and lactation on some enzymes involved in the phosphoryltransfer network in the brain cortex and hippocampus of the offspring at 21 days of age. Phenylalanine administration provoked diminution of body, brain cortex an hippocampus weight and decrease of adenylate kinase, mitochondrial and cytosolic creatine kinase activities. Co-administration of creatine plus pyruvate was effective in the prevention of those alterations provoked by phenylalanine, suggesting that altered energy metabolism may be important in the pathophysiology of maternal PKU. If these alterations also occur in maternal PKU, it is possible that pyruvate and creatine supplementation to the phenylalanine-restricted diet might be beneficial to phenylketonuric mothers.     

Maternal diabetes up‐regulates NOX2 and enhances myocardial ischaemia/reperfusion injury in adult offspring

Offspring of diabetic mothers are at risk of cardiovascular diseases in adulthood. However, the underlying molecular mechanisms are not clear. We hypothesize that prenatal exposure to maternal diabetes up‐regulates myocardial NOX2 expression and enhances ischaemia/reperfusion (I/R) injury in the adult offspring. Maternal diabetes was induced in C57BL/6 mice by streptozotocin. Glucose‐tolerant adult offspring of diabetic mothers and normal controls were subjected to myocardial I/R injury. Vascular endothelial growth factor (VEGF) expression, ROS generation, myocardial apoptosis and infarct size were assessed. The VEGF‐Akt (protein kinase B)‐mammalian target of rapamycin (mTOR)‐NOX2 signalling pathway was also studied in cultured cardiomyocytes in response to high glucose level. In the hearts of adult offspring from diabetic mothers, increases were observed in VEGF expression, NOX2 protein levels and both Akt and mTOR phosphorylation levels as compared to the offspring of control mothers. After I/R, ROS generation, myocardial apoptosis and infarct size were all significantly higher in the offspring of diabetic mothers relative to offspring of control mothers, and these differences were diminished by in vivo treatment with the NADPH oxidase inhibitor apocynin. In cultured cardiomyocytes, high glucose increased mTOR phosphorylation, which was inhibited by the PI3 kinase inhibitor LY294002. Notably, high glucose‐induced NOX2 protein expression and ROS production were inhibited by rapamycin. In conclusion, maternal diabetes promotes VEGF‐Akt‐mTOR‐NOX2 signalling and enhances myocardial I/R injury in the adult offspring. Increased ROS production from NOX2 is a possible molecular mechanism responsible for developmental origins of cardiovascular disease in offspring of diabetic mothers.     

Onset of the hormone-sensitive perinatal period for sexual differentiation of the sexually dimorphic nucleus of the preoptic area in female rats

The volume of the sexually dimorphic nucleus of the preoptic area (SDN-POA) of the rat brain is severalfold larger in males than in females. The volume of the SDN-POA can be influenced significantly by the hormonal milieu during the perinatal "critical period" of sexual differentiation of the brain. The purpose of the present study was to determine the onset of this period of sexual differentiation of the SDN-POA. Pregnant rats received no treatment or were injected subcutaneously with oil on day 17, 18, or 20, or testosterone (T;5 mg) on days 16-22 of gestation. On postnatal day 15, unilateral SDN-POA volumes from female offspring prenatally exposed to testosterone on day 16 or 17 were not different from values of control (untreated or oil-injected) offspring. Female offspring from mothers treated with testosterone on day 18, 19, or 20 of gestation showed a significant and similar increase in SDN-POA volume over values from control animals. SDN-POA volumes from female offspring exposed to testosterone on day 21 or 22, although larger than those of controls, were not different statistically. We conclude that with the specific paradigm used in this study SDN-POA development is insensitive prior to day 18 of gestation, the day on which the onset of the hormone-sensitive period occurs.     

Parental Diabetes: The Akita Mouse as a Model of the Effects of Maternal and Paternal Hyperglycemia in Wildtype Offspring

Aim/Hypothesis

Maternal diabetes and high-fat feeding during pregnancy have been linked to later life outcomes in offspring. To investigate the effects of both maternal and paternal hyperglycemia on offspring phenotypes, we utilized an autosomal dominant mouse model of diabetes (hypoinsulinemic hyperglycemia in Akita mice). We determined metabolic and skeletal phenotypes in wildtype offspring of Akita mothers and fathers.

Results

Both maternal and paternal diabetes resulted in phenotypic changes in wildtype offspring. Phenotypic changes were more pronounced in male offspring than in female offspring. Maternal hyperglycemia resulted in metabolic and skeletal phenotypes in male wildtype offspring. Decreased bodyweight and impaired glucose tolerance were observed as were reduced whole body bone mineral density and reduced trabecular bone mass.Phenotypic changes in offspring of diabetic fathers differed in effect size from changes in offspring of diabetic mothers. Male wildtype offspring developed a milder metabolic phenotype, but a more severe skeletal phenotype. Female wildtype offspring of diabetic fathers were least affected.

Conclusions

Both maternal and paternal diabetes led to the development of metabolic and skeletal changes in wildtype offspring, with a greater effect of maternal diabetes on metabolic parameters and of paternal diabetes on skeletal development. The observed changes are unlikely to derive from Mendelian inheritance, since the investigated offspring did not inherit the Akita mutation. While fetal programming may explain the phenotypic changes in offspring exposed to maternal diabetes in-utero, the mechanism underlying the effect of paternal diabetes on wildtype offspring is unclear.     

Electromyographic activity in the shoulder-neck region according to arm position and glenohumeral torque

The electromyographical (EMG) response to isometric ramp contractions of the right arm, the left arm, and both arms was studied using four pairs of surface electrodes above the right upper trapezius muscle (UT) of six men and six women. Contractions were made against gravity with the active arm(s) in eight positions, ranging from flexion to abduction. To describe arm positions, new, simple terminology was developed. Root mean square (rms)-converted EMG-signals were normalized (EMGnorm) with respect to a reference contraction. The EMGnorm corresponding to a 15 N.m torque in the right glenohumeral (GH) joint was strongly related to the position of the right arm (P less than 0.001). The shape of this relationship depended on the electrode position (P less than 0.001). The ratio between EMGnorm at 30 N.m and 15 N.m GH torques was related to arm position (P less than 0.001) and differed between electrodes (P less than 0.001). A left-side GH torque resulted in right-side (contralateral) EMG activity, typically corresponding to 20%-30% of that obtained during similar right-side GH torque. Bilateral GH torque implied 0%-50% increase in EMG activity as compared to that obtained with the right arm alone. The results have shown that signals from one pair of surface electrodes above UT cannot be taken as representative of the EMG activity from electrodes located elsewhere above UT. The EMG recordings reflected a complex pattern of muscular activation, significantly related to both outwardly visible factors (arm position, GH torque), and within-body servosystems (motor control reflexes).     

Maternal effects in the soft scale insect Saissetia coffeae (Hemiptera: Coccidae)

Effects of maternal environment on offspring performance have been documented frequently in herbivorous insects. Despite this, very few cases exist in which exposure of parent insects to a resource causes the phenotype of their offspring to be adjusted in a manner that is adaptive for that resource, a phenomenon called adaptive transgenerational phenotypic plasticity. I performed a two-generation reciprocal cross-transplant experiment in the field with the soft scale insect Saissetia coffeae (Hemiptera: Coccidae) on two disparate host plant species in order to separate genetic effects from possible transgenerational plasticity. Despite striking differences in quality between host species, maternal host had no effect on overall offspring performance, and I detected no "acclimatization" to the maternal host species. However, there was a significant negative association between maternal and offspring development times, with potentially adaptive implications. Furthermore, offspring of mothers reared in an environment where scale densities were higher and scales were more frequently killed by fungi were significantly less likely to suffer from fungal attack than were offspring of mothers reared in an environment where densities were low and fungal attack was rare. Although S. coffeae does not appear to alter offspring phenotype to increase offspring fitness on these two distinct plant species, it does appear that offspring phenotype may be responding to some subtler aspects of maternal environment. In particular, the possibility of induced transgenerational prophylaxis in S. coffeae deserves further investigation.     

Diabetic pregnancy in rats leads to impaired glucose metabolism in offspring involving tissue-specific dysregulation of 11beta-hydroxysteroid dehydrogenase type 1 expression

Population-based studies have shown that the offspring of diabetic mothers have an increased risk of developing obesity, insulin resistance, type 2 diabetes and hypertension in later life. To investigate mechanism for the high incidence of metabolic diseases in the offspring of diabetic mothers, we focused on the tissue-specific glucocorticoid regulation by 11beta-hydroxysteroid dehydrogenase type 1 (11beta-HSD1) and studied offspring born to streptozotocin-induced diabetic rats. The body weights of newborn rats from diabetic mothers were heavier than those from control mothers. Offspring born to diabetic mothers demonstrated insulin resistance and mild glucose intolerance after glucose loading at 10 weeks and showed significantly increased 11beta-HSD1 mRNA and enzyme activity in adipose tissue at 12 weeks of age without obvious obesity. Hepatic 11beta-HSD1 mRNA was also elevated. We propose that the 11beta-HSD1 in adipose tissue and liver may play a key role in the development of metabolic syndrome in the offspring of diabetic mothers. Tissue-specific glucocorticoid dysregulation provides a candidate mechanism for the high incidence of metabolic diseases in the offspring of diabetic mothers. Therefore early analyses before apparent obesity are needed to elucidate the molecular mechanisms that may be programmed during the fetal period.     

Impact of daily work-load during pregnancy on the microstructure of the rat heart in male offspring.

In two series of experiments the development of body weight, heart weight and the microstructure of the rat heart in the male offspring from exercised and control inactive mothers was followed. In 50-day-old male offspring the total body weight and heart weight did not differ; in 100-day-old male offspring the heart weight was significantly higher in those from mothers exercising daily for 1 hr (run on a treat-mill with the speed 14 to 16 m/min, i.e. mild exercise of an aerobic character) throughout pregnancy. As regards microstructure of the heart, the differences were significant both in younger and older animals. The number of exercised mothers. The capillary: fiber ratio was significantly higher and the diffusion distance significantly shorter in male offspring of exercised mothers. During the prenatal period a favorable effect of work-load for the offspring could be induced more easily even with mild aerobic and quite short daily exercise than later during postnatal life as shown by experiments reported previously.     

Maternal exposure to predation risk decreases offspring antipredator behaviour and survival in threespined stickleback

1. Adaptive maternal programming occurs when mothers alter their offspring's phenotype in response to environmental information such that it improves offspring fitness. When a mother's environment is predictive of the conditions her offspring are likely to encounter, such transgenerational plasticity enables offspring to be better-prepared for this particular environment. However, maternal effects can also have deleterious effects on fitness.2. Here, we test whether female threespined stickleback fish exposed to predation risk adaptively prepare their offspring to cope with predators. We either exposed gravid females to a model predator or not, and compared their offspring's antipredator behaviour and survival when alone with a live predator. Importantly, we measured offspring behaviour and survival in the face of the same type of predator that threatened their mothers (Northern pike).3. We did not find evidence for adaptive maternal programming; offspring of predator-exposed mothers were less likely to orient to the predator than offspring from unexposed mothers. In our predation assay, orienting to the predator was an effective antipredator behaviour and those that oriented, survived for longer.4. In addition, offspring from predator-exposed mothers were caught more quickly by the predator on average than offspring from unexposed mothers. The difference in antipredator behaviour between the maternal predator-exposure treatments offers a potential behavioural mechanism contributing to the difference in survival between maternal treatments.5. However, the strength and direction of the maternal effect on offspring survival depended on offspring size. Specifically, the larger the offspring from predator-exposed mothers, the more vulnerable they were to predation compared to offspring from unexposed mothers.6. Our results suggest that the predation risk perceived by mothers can have long-term behavioural and fitness consequences for offspring in response to the same predator. These stress-mediated maternal effects can have nonadaptive consequences for offspring when they find themselves alone with a predator. In addition, complex interactions between such maternal effects and offspring traits such as size can influence our conclusions about the adaptive nature of maternal effects.     

Mothers influence offspring body size through post-oviposition maternal effects in the redbacked salamander, Plethodon cinereus

In the terrestrial salamander (Plethodon cinereus), previous work has shown that mothers body size is positively correlated to offspring size at the time of hatching even after controlling for the effects of egg size. This study was designed to determine whether maternal body size affects offspring size via pre-oviposition factors (e.g., yolk quality, jelly coat composition, or maternal genes) or post-oviposition factors (e.g., parental care behaviors, parental modification of environment). Gravid females were captured and induced to lay eggs in experimental chambers in which the environment was standardized. Fifteen clutches were exchanged, or cross-fostered, between female pairs differing in body size. Ten females whose eggs were taken away and then returned served as controls for the crossing treatment. Foster mothers did not significantly differ from control mothers in the time spent with eggs, body position, or number of egg movements during brooding. Average egg mass measured midway through development was not significantly correlated to the body size of either the genetic or foster mother, but was correlated to pre-oviposition oocyte size. At hatching, offspring body length was positively correlated to egg size and the foster mothers body size. This correlation suggests that in P. cinereus post-oviposition maternal effects have a greater impact on offspring size than other maternal factors incorporated into the egg prior to oviposition. While our study showed that larger mothers moved their eggs less often and tended to spend more time in contact with their eggs, further work needs to be done to identify the specific mechanisms through which larger mothers influence the body size of their offspring. This is the first experimental demonstration of post-oviposition maternal effects for any amphibian with parental care.     

Maternal Exercise during Pregnancy Increases BDNF Levels and Cell Numbers in the Hippocampal Formation but Not in the Cerebral Cortex of Adult Rat Offspring

Clinical evidence has shown that physical exercise during pregnancy may alter brain development and improve cognitive function of offspring. However, the mechanisms through which maternal exercise might promote such effects are not well understood. The present study examined levels of brain-derived neurotrophic factor (BDNF) and absolute cell numbers in the hippocampal formation and cerebral cortex of rat pups born from mothers exercised during pregnancy. Additionally, we evaluated the cognitive abilities of adult offspring in different behavioral paradigms (exploratory activity and habituation in open field tests, spatial memory in a water maze test, and aversive memory in a step-down inhibitory avoidance task). Results showed that maternal exercise during pregnancy increased BDNF levels and absolute numbers of neuronal and non-neuronal cells in the hippocampal formation of offspring. No differences in BDNF levels or cell numbers were detected in the cerebral cortex. It was also observed that offspring from exercised mothers exhibited better cognitive performance in nonassociative (habituation) and associative (spatial learning) mnemonic tasks than did offspring from sedentary mothers. Our findings indicate that maternal exercise during pregnancy enhances offspring cognitive function (habituation behavior and spatial learning) and increases BDNF levels and cell numbers in the hippocampal formation of offspring.     

Developmental changes in mother-offspring grooming in Japanese macaques

A cross-sectional analysis was made of developmental changes in mother-offspring grooming in Japanese macaques, Macaca,. fuscata. When offspring were immature, time spent grooming by their mothers decreased with offspring age. Soliciting by offspring increased steadily with age, in contrast to their successful soliciting, which decreased gradually until early adolescence. This is in accord with the hypothesis that grooming is one form of post-weaning maternal investment, which may entail behavioral conflict between mothers and immature offspring. On the other hand, mothers spent much more time for grooming of their adult female offspring than for their adolescent male and female offspring. It is argued that grooming by mothers may shift from a form of maternal investment in their offspring to a benefit to be exchanged reciprocally with them. © 1995 Wiley-Liss, Inc.     

Effects of maternal age and environment on offspring vital rates in the oleander aphid (Hemiptera: Aphididae)

Maternal effects have the potential to affect population dynamics and evolution. To affect population dynamics, maternal effects must influence offspring vital rates (birth, death, or movement). Here, we explore the magnitude of nongenetic maternal influence on the vital rates of an insect herbivore and explore predictability of maternal effects with reference to published studies. We experimentally studied the effects of maternal age, host plant species (two Asclepias spp.), and density on offspring vital rates in Aphis nerii, the oleander aphid. Older mothers produced offspring that lived shorter lives, consistent with the "Lansing Effect." Older mothers also produced offspring that matured at a younger age. As maternal age increased, offspring mass at maturity decreased when mothers were on Asclepias syriaca. However, offspring mass was highest from intermediate aged mothers on A. viridis. The absence of maternal density effects seems to exclude maternal density as a potential source of delayed density dependence in A. nerii. Our results indicate that maternal effects have some influence on A. nerii vital rates. However, references to published studies suggest that only the Lansing Effect is a predictable response to maternal age in insects. Moreover, the magnitude of observed effects was generally low.     

Rapid Onset of Maternal Vocal Recognition in a Colonially Breeding Mammal,the Australian Sea Lion

Background

In many gregarious mammals, mothers and offspring have developed the abilities to recognise each other using acoustic signals. Such capacity may develop at different rates after birth/parturition, varying between species and between the participants, i.e., mothers and young. Differences in selective pressures between species, and between mothers and offspring, are likely to drive the timing of the onset of mother-young recognition. We tested the ability of Australian sea lion mothers to identify their offspring by vocalisation, and examined the onset of this behaviour in these females. We hypothesise that a rapid onset of recognition may reflect an adaptation to a colonial lifestyle.

Principal Findings

In a playback study maternal responses to own pup and non-filial vocalisations were compared at 12, 24 and every subsequent 24 hours until the females'' first departure post-partum. Mothers showed a clear ability to recognise their pup''s voice by 48 hours of age. At 24 hours mothers called more, at 48 hours they called sooner and at 72 hours they looked sooner in response to their own pup''s vocalisations compared to those of non-filial pups.

Conclusions

We demonstrate that Australian sea lion females can vocally identify offspring within two days of birth and before mothers leave to forage post-partum. We suggest that this rapid onset is a result of selection pressures imposed by a colonial lifestyle and may be seen in other colonial vertebrates. This is the first demonstration of the timing of the onset of maternal vocal recognition in a pinniped species.     

The Influence of Maternal Quality on Brood Sex Allocation in the Small Carpenter Bee,Ceratina calcarata

In the twig‐nesting carpenter bee, Ceratina calcarata, body size is an important component of maternal quality, smaller mothers producing significantly fewer and smaller offspring than larger mothers. As mothers precisely control the sex and size of each offspring, smaller mothers might compensate by preferentially allocating their investment towards sons. We investigated whether variation in maternal quality leads to variation in sex allocation patterns. At the population level, the numerical sex ratio was 57% male‐biased (1.31 M/F), but the investment between the sexes was balanced (1.02 M/F), because females are 38% larger than males (1.28 F/M). Maternal body size explained both sex allocation pattern and size variation among offspring: larger mothers invested more in individual progeny and produced more female offspring than smaller mothers. Maternal investment in offspring of both sexes decreased throughout the season, probably as a result of increasing maternal wear and age. The exception to this pattern was the curious production of dwarf females in the first two brood cell positions. We suggest that the sex ratio distribution reflects the maternal body size distribution and a constraint on small mothers to produce small broods. This leads to male‐biased allocation by small females, to which large mothers respond by biasing their allocation towards daughters.