This time on Science interrupted I’m going to talk to you about how my adventures in science were interrupted by baby ducklings. And not just because we are in the time of year when Facebook spams me with cute videos of baby ducks following their mama duck around.
If you have taken a basic introduction to psychology course, then you have probably heard of Lorenz’s work with baby ducks1 -- specifically, that ducks are one of many species that imprint on others shortly after birth. It is this imprinting that then leads to attachment to the imprinted object. In normal scenarios, baby ducks imprint onto their moms and form attachments with their moms. But, with Lorenz’s work, baby ducks (ok it was really geese, but geese aren’t as cute as ducks) who saw Lorenz shortly after they hatched imprinted onto Lorenz, thought that he was their mom, and followed him everywhere (you can find out more here).
Besides being incredibly adorable, the concept of imprinting in attachment systems is a really good example for explaining how imprinting in genes works (I also want to thank a fellow NPR SciCommer for pointing out that I haven’t clearly explained imprinting in my other posts, and inspiring my obsession with baby ducks over the past few days).
Think of imprinted genes as baby ducks, and the parent of origin (PO for short because my husband vetoed using POO as an acronym) as the mother duck. When imprinted genes are “born” -- aka, they make it into sperm or egg cells -- they imprint on the first thing they “see” -- aka, they embody your gene’s fitness “interests”-- and behave in ways that are in alignment with these interests. In this case, it means that the imprinted genes remember their PO and behave in ways to help their PO’s interests, even when they have made it into a new individual.
All of this imprinting happens at the epigenetic level. This means that the interests of gene’s PO are not encoded in your DNA, but rather have “tags” that are used to interpret and change how DNA is read by the body2,3. Tags are kind of like stoplights and street signs -- they tell your body when to turn these genes on, when to turn them off, and what to let them do4. So, when imprinted genes are in a new individual, these epigenetic tags create a complex roadmap that the new individual’s body has to follow. Turn here… stop at this light… wait you missed the cross street. In addition to the roadmap, imprinted genes from different POs act as aggressive backseat drivers -- they fight with each other to try and turn each other’s expression off (with the exception of X chromosome inactivation, which is a fancy way of saying that only one X chromosome can be active in your cells at a given time5 -- if you are XY then your X chromosome from your mom is always active, but if you are XX then only one of your Xs is active in your cells at a given time).
This complex designing of roadmaps through genetic imprinting is a normal process in human development but there is little known about how it influences normal development. More attention has been devoted to the effects of genetic imprinting in diseases6 since there are clear associations between genetic imprinting and developmental problems. Genetic imprinting has been implicated in many diseases7, ranging from developmental diseases such as Angelman and Prader-Willi syndromes8 to lung cancer9.
If I were to try to summarize what we know about imprinting in normal growth and development, the summary would simultaneously be saturated and completely empty. Imprinting, and the genetic conflict that ensures from genes pursuing different interests, is responsible for our growth and development but we really don’t know how it works. Some researchers have been trying to figure some of this out by studying pregnancy and placental development10–15, but there are still way more questions than answers.
Anyway, back to the ducks. Lorenz’s research showed the importance of imprinting for attachment in ducks. I think the same thing is happening in humans. Our imprinted genes and genetic conflict might bias us towards different kinds of attachment strategies16,17. This isn’t a new prediction18, but I think it is one that researchers have largely ignored because it sounds a lot like biological determinism. I’m not saying our genes and genetic conflict determine what kind of attachment strategy you will have, but I’m suggesting that your genes might predispose you to certain kinds of attachment systems like risk factors for certain diseases predispose you to develop that disease. If this prediction is supported in future research, then it would mean that the development of attachment systems are a lot more complex than we’ve previously thought (and it would also alleviate a lot of mom-shaming, since current theories of attachment theory focus on how attentive the mother is to her child and how that shapes the child’s attachment). So, like ducks, who your genes imprinted onto matters and can have long-term and unintended effects.
Stay curious my friends,
JDA
In case you are interested, here are some of the articles that I read and thought about while writing this.
1. Lorenz, K. Der Kumpan in der Umwelt des Vogels. Journal für Ornithologie 83, 137–213 (1935).
2. CDC. What is Epigenetics? https://www.cdc.gov/genomics/disease/epigenetics.htm (2020).
3. Mazzio, E. A. & Soliman, K. F. A. Basic concepts of epigenetics: impact of environmental signals on gene expression. Epigenetics 7, 119–130 (2012).
4. Wright, J. Epigenetics: reversible tags. Nature 498, S10–1 (2013).
5. Genetic Imprinting and X Inactivation. https://www.nature.com/scitable/topicpage/genetic-imprinting-and-x-inactivation-1066/.
6. Falls, J. G., Pulford, D. J., Wylie, A. A. & Jirtle, R. L. Genomic imprinting: implications for human disease. Am. J. Pathol. 154, 635–647 (1999).
7. Lobo, I. Genomic Imprinting and Patterns of Disease Inheritance. Nature Education 1, 66 (2008).
8. Nicholls, R. D., Saitoh, S. & Horsthemke, B. Imprinting in Prader–Willi and Angelman syndromes. Trends Genet. 14, 194–200 (1998).
9. Kondo, M., Matsuoka, S. & Uchida, K. Selective maternal-allele loss in human lung cancers of the maternally expressed p57(KIP2) gene at 11p15.5. Lung Cancer 1, 110 (1996).
10. Haig, D. Genetic conflicts in human pregnancy. Q. Rev. Biol. 68, 495–532 (1993).
11. Boddy, A. M., Fortunato, A., Wilson Sayres, M. & Aktipis, A. Fetal microchimerism and maternal health: a review and evolutionary analysis of cooperation and conflict beyond the womb. Bioessays 37, 1106–1118 (2015).
12. Natri, H., Garcia, A. R., Buetow, K. H., Trumble, B. C. & Wilson, M. A. The Pregnancy Pickle: Evolved Immune Compensation Due to Pregnancy Underlies Sex Differences in Human Diseases. Trends Genet. 35, 478–488 (2019).
13. Moore, T. Review: Parent-offspring conflict and the control of placental function. Placenta 33 Suppl, S33–6 (2012).
14. Moore, T. & Reik, W. Genetic conflict in early development: parental imprinting in normal and abnormal growth. Rev. Reprod. 1, 73–77 (1996).
15. Fowden, A. L. & Moore, T. Maternal-fetal resource allocation: co-operation and conflict. Placenta 33 Suppl 2, e11–5 (2012).
16. Bowlby, J. Attachment and loss: retrospect and prospect. Am. J. Orthopsychiatry 52, 664–678 (1982).
17. Bowlby, J. Attachment: Attachment and loss. New York: Basic (1969).
18. Crespi, B. J. The Strategies of the Genes: Genomic Conflicts, Attachment Theory, and Development of the Social Brain. in Brain, Behavior and Epigenetics (eds. Petronis, A. & Mill, J.) 143–167 (Springer Berlin Heidelberg, 2011).
