Imprinted Genes and Infant Temperament: First Findings
A pioneering study links expression of imprinted genes to infant temperament.
Posted January 2, 2017
Appropriately for my opening post of 2017, “the first study to show a relationship between prenatal epigenetic regulation of imprinted genes and infant temperament” has just appeared.
According to the theory imprinted brain theory, paternal genes like IGF2 featured in the previous post tend to promote growth and consumption of the mother’s resources, while maternal ones tend to counter these demands on the mother. The theory is illustrated below by a painting by Collin Murphy commissioned by my friend, colleague, and a co-author of the study I am citing, Randy Jirtle :
The idea for this painting came to me in a dream, and appears to be inspired by The Creation of Adam painting in the Sistine Chapel by Michelangelo. The major differences are that the upper hand of God is female, whereas the lower hand is male. Additionally, in this painting there is no distance between the hands of God and the human brain.
As this study remarks,
The parent-of-origin-dependent manner in which this subset of genes is expressed is tightly regulated through epigenetic processes, including DNA methylation at differentially methylated regions (DMRs), which directly affects the genes’ expression. The ways in which imprinted gene regulation might affect brain development could be either by disrupting regulation of nutrient acquisition, hormones , or fetal growth, or, more directly, by influencing neuronal growth and pruning, or axonal sprouting and interconnections. IGF2 , eg, plays a major role in balancing nutrients for growth across the placental membranes, and altered regulation may indirectly affect brain development by influencing the supply of nutrients during critical stages of development. Other imprinted genes, such as neuronatin ( NNAT ), may play a more direct role, as this imprinted gene has been implicated in regulation of ion channels during brain development.
The study “investigated the associations between early childhood temperament and the DNA methylation status of umbilical cord blood leukocytes with reference to the nine DMRs in the imprinted genes that are important for embryonic growth regulation ( H19, IGF2, MEST, PLAGL1, and SGCE ) or brain development ( MEG3, MEG3-IG, NNAT, and PEG3 ).”
The paper adds that “others have shown that altered placental tissue DNA methylation in a cluster of imprinted genes, including MEG3 , was associated with reduced quality of movement in newborn infants.” MEG3 is an imprinted gene expressed from the maternal copy, and as I explained in detail in a recent post , quality of movement in infants is a key behavioral trait of Angelman syndrome children, who are hyperactive /sleepless and whose epigenetics features over-expression of paternal and reduced expression of maternal imprinted genes on chromosome 15. In contrast, Prader-Willi children are the reverse: inactive/ sleepy with enhanced expression of maternal and reduced expression of paternal genes in the same region. To the extent that hyperactive, sleepless children make more demands on the mother and inactive, sleepy ones less, this pattern could be seen as making sense in terms of conflict between resource-demanding paternal genes and resource-limiting maternal ones.
The same might be said of the findings of the new research that enhanced expression of maternally-active MEG3 “was positively related to greater expression of internalizing symptoms and surgency temperament,” The latter has been defined as “a personality trait that features cheerfulness, spontaneity, responsiveness and sociability.” All of these, but especially the latter two terms, correlate closely with what I would call mentalism , understood as an ability to get on with other people and to relate well to them mentally and socially. And according to the imprinted brain theory, mentalism is mainly facilitated by maternal genes (which include X chromosome ones, as explained in a previous post ).
Summarizing the study:
these early data support gene-specific associations between epigenetic differences in the regulatory regions of two imprinted domains at birth and later infant temperament, further justifying follow-up work on the role of imprinted genes in neurodevelopmental outcomes in children. Investigating imprinted genes in relation to neurodevelopmental outcomes may be a useful approach to understanding the role of DNA methylation on neurodevelopment because epigenetic mechanisms, and environmentally induced effects can have a significant impact on gene expression.
The authors add that “identifying epigenetic marks associated with temperament could be useful in risk assessment, thus providing a window of opportunity for prevention.” Indeed, and as I pointed out in a previous post , one such test already exists and has been patented to do exactly this.
Finally, as the authors conclude,
Epigenetic signatures are potentially reversible. Therefore, it may also be possible to discover ways to correct DNA methylation profiles, restore gene function, and optimize neurodevelopmental growth.
Collin Murphy’s striking depiction of the imprinted brain might have been inspired by Randy Jirtle’s dream, but clearly, he and his co-authors have now made a major step towards opening up a whole gallery of pictures depicting DNA and development, of which this landmark study is just the start.
(With thanks and acknowledgement to Randy Jirtle for his help.)
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Christopher Robert Badcock, Ph.D. , is the author of The Imprinted Brain: How Genes Set the Balance Between Autism and Psychosis.
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This article is part of the Bringwise Psychology Journal — daily insights on human behavior, mental health, and personal growth.