Maternal effect

A maternal effect is a situation where the phenotype of an organism is determined not only by the environment it experiences and its genotype, but also by the environment and genotype of its mother. In genetics, maternal effects occur when an organism shows the phenotype expected from the genotype of the mother, irrespective of its own genotype, often due to the mother supplying messenger RNA or proteins to the egg. Maternal effects can also be caused by the maternal environment independent of genotype, sometimes controlling the size, sex, or behaviour of the offspring. These adaptive maternal effects lead to phenotypes of offspring that increase their fitness. Further, it introduces the concept of phenotypic plasticity, an important evolutionary concept. It has been proposed that maternal effects are important for the evolution of adaptive responses to environmental heterogeneity.

A Drosophila melanogaster oocyte develops in an egg chamber in close association with a set of cells called nurse cells. Both the oocyte and the nurse cells are descended from a single germline stem cell, however cytokinesis is incomplete in these cell divisions, and the cytoplasm of the nurse cells and the oocyte is connected by structures known as ring canals. Only the oocyte undergoes meiosis and contributes DNA to the next generation.

Maternal effect genes are expresses during oogenesis by the mother (expressed prior to fertilization) and develop the anterior-posterior and dorsal ventral polarity of the egg. The anterior end of the egg becomes the head; posterior end becomes the tail. the dorsal side is on the top; the ventral side is in underneath. The products of maternal effect genes called maternal m RNAs are produced by nurse cell and follice cells and deposited in the egg cells (oocytes). At the start of development process, m RNA gradients are formed in oocytes along anterior-posterior and dorsal ventral axes.

It can sometimes be difficult to differentiate between maternal and adaptive maternal effects. Consider the following: Gypsy moths reared on foliage of black oak, rather than chestnut oak, had offspring that developed faster. This is a maternal, not an adaptive maternal effect. In order to be an adaptive maternal effect, the mother’s environment would have to have led to a change in the eating habits or behavior of the offspring. The key difference between the two therefore, is that adaptive maternal effects are environment specific. The phenotypes that arise are in response to the mother sensing an environment that would reduce the fitness of her offspring. By accounting for this environment she is then able to alter the phenotypes to actually increase the offspring’s fitness. Maternal effects are not in response to an environmental cue, and further they have the potential to increase offspring fitness, but they may not.

Currently, researchers are examining the correlations between maternal diet during pregnancy and its effect on the offspring’s susceptibility for chronic diseases later in life. The fetal programming hypothesis highlights the idea that environmental stimuli during critical periods of fetal development can have lifelong effects on body structure and health and in a sense they prepare offspring for the environment they will be born into. Many of these variations are thought to be due to epigenetic mechanisms brought on by maternal environment such as stress, diet, gestational diabetes, and exposure to tobacco and alcohol. These factors are thought to be contributing factors to obesity and cardiovascular disease, neural tube defects, cancer, diabetes, etc. Studies to determine these epigenetic mechanisms are usually performed through laboratory studies of rodents and epidemiological studies of humans.

The effect of maternal diet in species other than humans is also relevant. Many of the long term effects of global climate change are unknown. Knowledge of epigenetic mechanisms can help scientists better predict the impacts of changing community structures on species which are ecologically, economically, and/or culturally important around the world. Since many ecosystems will see changes in species structures, the nutrient availability will also be altered, ultimately affecting the available food choices for reproducing females. Maternal dietary effects may also be used to improve agricultural and aquaculture practices. Breeders may be able to utilize scientific data to create more sustainable practices, saving money for themselves, as well as the consumers.

In another study, researchers discovered that perinatal nutrient restriction resulting in intrauterine growth restriction (IUGR) contributes to diabetes mellitus type 2 (DM2). IUGR refers to the poor growth of the baby in utero. In the pancreas, IUGR caused a reduction in the expression of the promoter of the gene encoding a critical transcription factor for beta cell function and development. Pancreatic beta cells are responsible for making insulin; decreased beta cell activity is associated with DM2 in adulthood. In skeletal muscle, IUGR caused a decrease in expression of the Glut-4 gene. The Glut-4 gene controls the production of the Glut-4 transporter; this transporter is specifically sensitive to insulin. Thus, when insulin levels rise, more glut-4 transporters are brought to the cell membrane to increase the uptake of glucose into the cell. This change is caused by histone modifications in the cells of skeletal muscle that decrease the effectiveness of the glucose transport system into the muscle. Because the main glucose transporters are not operating at optimal capacity, these individuals are more likely to develop insulin resistance with energy rich diets later in life, contributing to DM2.

In utero or neonatal exposure to bisphenol A (BPA), a chemical used in manufacturing polycarbonate plastic, is correlated with higher body weight, breast cancer, prostate cancer, and an altered reproductive function. In a mice model, the mice fed on a BPA diet were more likely to have a yellow coat corresponding to their lower methylation state in the promoter regions of the retrotransposon upstream of the Agouti gene. The Agouti gene is responsible for determining whether an animal’s coat will be banded (agouti) or solid (non-agouti). However, supplementation with methyl donors like folic acid or phytoestrogen abolished the hypomethylating effect. This demonstrates that the epigenetic changes can be reversed through diet and supplementation.

Parental-mediated dietary epigenetic effects on immunity has a broader significance on wild organisms. Changes in immunity throughout an entire population may make the population more susceptible to an environmental disturbance, such as the introduction of a pathogen. Therefore, these transgenerational epigenetic effects can influence the population dynamics by decreasing the stability of populations who inhabit environments different from the parental environment that offspring are epigenetically modified for.