Maternal effect
These typically involve examining the phenotype of the organisms one generation later than in a conventional (zygotic) screen, as their mothers will be potentially homozygous for maternal effect mutations that arise.
Many maternal effect Drosophila mutants have been found that affect the early steps in embryogenesis such as axis determination, including bicoid, dorsal, gurken and oskar.
[9] Other maternal effect mutants either affect products that are similarly produced in the nurse cells and act in the oocyte, or parts of the transportation machinery that are required for this relocalization.
[13][14][15][16] In this body of work, Archer argued that accumulative maternal effects via the non-genetic evolution of matrilineal nutrient metabolism is responsible for the increased global prevalence of obesity and diabetes mellitus type 2.
The environmental cues such as light, temperature, soil moisture and nutrients that the mother plant encounters can cause variations in seed quality, even within the same genotype.
[23] In general, adaptive maternal effects are a mechanism to cope with factors that work to reduce offspring fitness;[24] they are also environment specific.
The phenotypic changes that arise from adaptive maternal effects are a result of the mother sensing that a certain aspect of the environment may decrease the survival of her offspring.
The adaptive maternal effect was induced by the mothers sensing the high population density and correlating it to low food availability per individual.
Ultimately, the squirrels born during this period of high population density showed an increased survival rate (and therefore fitness) during their first winter.
Ultimately these experiments showed the plasticity of egg size production in the beetle, as well as the influence of the maternal environment on the survivorship of the offspring.
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.
The medical field is working on methods to detect these diseases, some of which have been discovered to be heavily driven by epigenetic alterations due to maternal dietary effects.
The reversal of epigenetic effects will utilize the pharmaceutical field in an attempt to create drugs which target the specific genes and genomic alterations.
The general public can be aware of the risks of certain dietary behaviors during pregnancy in an attempt to curb the negative consequences which may arise in offspring later in their lives.
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.
Hyperglycemia during pregnancy is thought to cause epigenetic changes in the leptin gene of newborns leading to a potential increased risk for obesity and heart disease.
The decrease in these hormones caused fat mass gain, glucose intolerance, hypertriglyceridemia, abnormal adiponectin and leptin levels, and hypertension throughout the animal's lifetime.
However, it has been shown that decreased adiponectin levels are associated with obesity, insulin resistance, type II diabetes, and coronary artery disease in humans.
[34] In addition, high fat diets cause chronic low-grade inflammation in the placenta, adipose, liver, brain, and vascular system.
[36] A study done after the Dutch Hunger Winter of 1944-1945 showed that undernutrition during the early stages of pregnancy are associated with hypomethylation of the insulin-like growth factor II (IGF2) gene even after six decades.
Similar results have been demonstrated in the Nr3c1 and Ppara genes of the offspring of rats fed on an isocaloric protein-deficient diet before starting pregnancy.
Epigenetic alterations that occur during embryogenesis and early fetal development have greater physiologic and metabolic effects because they are transmitted over more mitotic divisions.
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.
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.
Increased methylation in the 11β-hydroxysteroid dehydrogenase type 2 (HSD2), glucocorticoid receptor (GR), and H19 ICR were positively correlated with adiposity and blood pressure in adulthood.
[39] Strong evidence in rats supports the conclusion that neonatal estrogen exposure plays a role in the development of prostate cancer.
Additionally, researchers looked at key genes involved in prostatic glandular and stromal growth, cell-cycle progression, apoptosis, hormone receptors, and tumor suppressors using a custom PCR array.
Epigenetic changes in moth offspring affect the production of phenoloxidase, an enzyme involved with melanization and correlated with resistance of certain pathogens in many invertebrate species.
[43] Ecologically, this is an example of the mother utilizing her environment and determining the best method to maximize offspring survival, without actually making a conscious effort to do so.
If a mother is able to gather a plentiful amount of resources, she will have a higher fecundity and produce offspring who are able to grow quickly to avoid predation.
