Open main menu
Home
Random
Recent changes
Special pages
Community portal
Preferences
About Wikipedia
Disclaimers
Incubator escapee wiki
Search
User menu
Talk
Dark mode
Contributions
Create account
Log in
Editing
Maternal effect
(section)
Warning:
You are not logged in. Your IP address will be publicly visible if you make any edits. If you
log in
or
create an account
, your edits will be attributed to your username, along with other benefits.
Anti-spam check. Do
not
fill this in!
==Maternal diet and environment influence epigenetic effects== {{further|Epigenetics}} Related to adaptive maternal effects are epigenetic effects. [[Epigenetics]] is the study of long lasting changes in [[gene expression]] that are produced by modifications to chromatin instead of changes in DNA sequence, as is seen in DNA mutation. This "change" refers to [[DNA methylation]], [[Histone acetylation and deacetylation|histone acetylation]], or the interaction of [[non-coding RNA]]s with DNA. DNA methylation is the addition of methyl groups to the DNA. When DNA is methylated in mammals, the transcription of the gene at that location is turned down or turned off entirely. The induction of DNA methylation is highly influenced by the maternal environment. Some maternal environments can lead to a higher methylation of an offspring's DNA, while others lower methylation.[22]{{citation needed|date=September 2017}} The fact that methylation can be influenced by the maternal environment, makes it similar to adaptive maternal effects. Further similarities are seen by the fact that methylation can often increase the fitness of the offspring. Additionally, epigenetics can refer to histone modifications or non-coding RNAs that create a sort of [[Epigenetics|cellular memory]]. Cellular memory refers to a cell's ability to pass nongenetic information to its daughter cell during replication. For example, after differentiation, a liver cell performs different functions than a brain cell; cellular memory allows these cells to "remember" what functions they are supposed to perform after replication. Some of these epigenetic changes can be passed down to future generations, while others are reversible within a particular individual's lifetime. This can explain why individuals with identical DNA can differ in their susceptibility to certain chronic diseases. 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 [[Prenatal nutrition|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.<ref>{{cite journal |vauthors=Barua S, Junaid MA |title=Lifestyle, pregnancy and epigenetic effects |journal=Epigenomics |volume=7 |issue=1 |pages=85β102 |year=2015 |pmid=25687469 |doi=10.2217/epi.14.71 }}</ref> Studies to determine these epigenetic mechanisms are usually performed through laboratory studies of rodents and epidemiological studies of humans.
Edit summary
(Briefly describe your changes)
By publishing changes, you agree to the
Terms of Use
, and you irrevocably agree to release your contribution under the
CC BY-SA 4.0 License
and the
GFDL
. You agree that a hyperlink or URL is sufficient attribution under the Creative Commons license.
Cancel
Editing help
(opens in new window)