Editing Maternal effect (section)

==Maternal diet effects and ecology==
{{more citations needed section|date=September 2017}}

Maternal dietary effects are not just seen in humans, but throughout many taxa in the animal kingdom. These maternal dietary effects can result in ecological changes on a larger scale throughout populations and from generation to generation. The plasticity involved in these epigenetic changes due to maternal diet represents the environment into which the offspring will be born. Many times, epigenetic effects on offspring from the maternal diet during development will genetically prepare the offspring to be better adapted for the environment in which they will first encounter. The epigenetic effects of maternal diet can be seen in many species, utilizing different ecological cues and epigenetic mechanisms to provide an adaptive advantage to future generations.

Within the field of ecology, there are many examples of maternal dietary effects. Unfortunately, the epigenetic mechanisms underlying these phenotypic changes are rarely investigated. In the future, it would be beneficial for ecological scientists as well as epigenetic and genomic scientists to work together to fill the holes within the ecology field to produce a complete picture of environmental cues and epigenetic alterations producing phenotypic diversity.

===Parental diet affects offspring immunity===
A [[Pyralidae|pyralid moth species]], ''[[Plodia interpunctella]]'', commonly found in food storage areas, exhibits maternal dietary effects, as well as paternal dietary effects, on its offspring. 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. In this study, parent moths were housed in food rich or food poor environments during their reproductive period. Moths who were housed in food poor environments produced offspring with less phenoloxidase, and thus had a weaker immune system, than moths who reproduced in food rich environments. This is believed to be adaptive because the offspring develop while receiving cues of scarce nutritional opportunities. These cues allow the moth to allocate energy differentially, decreasing energy allocated for the immune system and devoting more energy towards growth and reproduction to increase fitness and insure future generations. One explanation for this effect may be imprinting, the expression of only one parental gene over the other, but further research has yet to be done.<ref>{{cite journal | vauthors = Vargas G, Michaud JP, Nechols JR, Moreno CA |title=Age-specific maternal effects interact with larval food supply to modulate life history in Coleomegilla maculata |journal=Ecological Entomology |volume=39 |issue=1 |year=2014 |pages=39–46 |doi=10.1111/een.12065 |bibcode=2014EcoEn..39...39V |s2cid=54585960 |hdl=2097/17235 |hdl-access=free }}</ref>

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.

===Maternal diet affects offspring growth rate===

Food availability also influences the epigenetic mechanisms driving growth rate in the [[Mouthbrooder|mouthbrooding cichlid]], ''Simochromis pleurospilus''. When nutrient availability is high, reproducing females will produce many small eggs, versus fewer, larger eggs in nutrient poor environments. Egg size often correlates with fish larvae body size at hatching: smaller larvae hatch from smaller eggs. In the case of the cichlid, small larvae grow at a faster rate than their larger egg counterparts. This is due to the increased expression of GHR, the growth hormone receptor. Increased transcription levels of GHR genes increase the receptors available to bind with [[growth hormone]], GH, leading to an increased growth rate in smaller fish. Fish of larger size are less likely to be eaten by predators, therefore it is advantageous to grow quickly in early life stages to insure survival. The mechanism by which GHR transcription is regulated is unknown, but it may be due to hormones within the yolk produced by the mother, or just by the yolk quantity itself. This may lead to DNA methylation or histone modifications which control genic transcription levels.<ref>{{cite journal | vauthors = Triggs AM, Knell RJ |title=Parental diet has strong transgenerational effects on offspring immunity |journal=Functional Ecology |volume=26 |issue=6 |year=2012 |pages=1409–17 |doi=10.1111/j.1365-2435.2012.02051.x |doi-access=free |bibcode=2012FuEco..26.1409T }}</ref>

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. Ecology is generally driven by the ability of an organism to compete to obtain nutrients and successfully reproduce. 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. Mothers who are unable to obtain as many nutrients will produce fewer offspring, but the offspring will be larger in hopes that their large size will help insure survival into sexual maturation. Unlike the moth example, the maternal effects provided to the cichlid offspring do not prepare the cichlids for the environment that they will be born into; this is because mouth brooding cichlids provide parental care to their offspring, providing a stable environment for the offspring to develop. Offspring who have a greater growth rate can become independent more quickly than slow growing counterparts, therefore decreasing the amount of energy spent by the parents during the parental care period.

A similar phenomenon occurs in the [[sea urchin]], ''Strongylocentrotus droebachiensis''. Urchin mothers in nutrient rich environments produce a large number of small eggs. Offspring from these small eggs grow at a faster rate than their large egg counterparts from nutrient poor mothers. Again, it is beneficial for sea urchin larvae, known as [[planula]], to grow quickly to decrease the duration of their larval phase and metamorphose into a juvenile to decrease predation risks. Sea urchin larvae have the ability to develop into one of two phenotypes, based on their maternal and larval nutrition. Larvae who grow at a fast rate from high nutrition, are able to devote more of their energy towards development into the juvenile phenotype. Larvae who grow at a slower rate with low nutrition, devote more energy towards growing spine-like appendages to protect themselves from predators in an attempt to increase survival into the juvenile phase. The determination of these phenotypes is based on both the maternal and the juvenile nutrition. The epigenetic mechanisms behind these phenotypic changes is unknown, but it is believed that there may be a nutritional threshold that triggers epigenetic changes affecting development and, ultimately, the larval phenotype.<ref>{{cite journal | vauthors = Bertram DF, Strathmann RR |title=Effects of Maternal and Larval Nutrition on Growth and Form of Planktotrophic Larvae |journal=Ecology |volume=79 |issue=1 |year=1998 |pages=315–27 |jstor=176885 |doi=10.1890/0012-9658(1998)079[0315:EOMALN]2.0.CO;2 |s2cid=85923751 }}</ref>