Summary: Researchers uncovered a fascinating link between “imprinted genes” and parenting behaviors in mice. Unlike typical genes where both maternal and paternal copies are expressed, imprinted genes allow only one parent’s copy to be active.
Through sequencing, the team identified the gene Magel2 as being imprinted and influencing parental care. Mice with inactive Magel2 were found to be neglectful parents, further emphasizing the gene’s role in parenting.
Key Facts:
- Genomic imprinting in mammals can affect parental behavior, with only one copy of the gene (either from mother or father) being expressed.
- Magel2 was identified as a significant imprinted gene affecting parenting behavior, with inactive Magel2 leading to neglectful parenting in mice.
- The findings indicate that imprinted genes might have evolved to synchronize parenting activities between mother and offspring.
Source: PLOS
Whether a mouse is a good or bad parent can be traced back to imprinted genes in key neurons in the “parenting hub” in the brain, according to a new study by Anthony Isles of Cardiff University and colleagues, published October 19 in the journal PLOS Genetics.
In mice, there is some evidence that an unusual phenomenon in mammals called genomic imprinting impacts parenting behavior. Mammals inherit two copies of each gene – one from each parent – and usually, each copy is expressed equally in the cell.
With imprinted genes, however, only one copy is expressed, either the one inherited from the father or the mother.
To confirm that imprinted genes play a role in parenting, Isles’ team used sequencing data from neurons in the parenting hub in the hypothalamus of mice. They found that imprinted genes are especially common among the genes expressed in these cells, including Magel2, a novel imprinted gene that was not previously linked to parenting.
Further experiments showed that mice lacking an active form of Magel2 were inattentive parents that made subpar nests.
The new findings show that genomic imprinting plays an important role in controlling parenting behavior in mice. Interestingly, previous research has shown that if mouse pups lose the paternal version of Magel2, they make fewer ultrasonic vocalizations, which they use to get their mother’s attention.
Together, these results support the idea that genomic imprinting has evolved to coordinate parenting activities between a mother and her pups.
The authors add: “Our study demonstrates the importance of imprinted genes as a group in neural circuitry that controls parenting behavior in mammals. These findings imply that the maternal and paternal genomes may differentially manipulate parental care for their own ends, and thus shaping the evolution of parenting behavior in mammals.”
About this genetics research news
Author: Charlotte Bhaskar
Source: PLOS
Contact: Charlotte Bhaskar – PLOS
Image: The image is credited to Neuroscience News
Original Research: Open access.
“The parenting hub of the hypothalamus is a focus of imprinted gene action” by Higgs MJ et al. PLOS Genetics
Abstract
The parenting hub of the hypothalamus is a focus of imprinted gene action
Imprinted genes are subject to germline epigenetic modification resulting in parental-specific allelic silencing. Although genomic imprinting is thought to be important for maternal behaviour, this idea is based on serendipitous findings from a small number of imprinted genes.
Here, we undertook an unbiased systems biology approach, taking advantage of the recent delineation of specific neuronal populations responsible for controlling parental care, to test whether imprinted genes significantly converge to regulate parenting behaviour.
Using single-cell RNA sequencing datasets, we identified a specific enrichment of imprinted gene expression in a recognised “parenting hub”, the galanin-expressing neurons of the preoptic area.
We tested the validity of linking enriched expression in these neurons to function by focusing on MAGE family member L2 (Magel2), an imprinted gene not previously linked to parenting behaviour. We confirmed expression of Magel2 in the preoptic area galanin expressing neurons.
We then examined the parenting behaviour of Magel2-null(+/p) mice. Magel2-null mothers, fathers and virgin females demonstrated deficits in pup retrieval, nest building and pup-directed motivation, identifying a central role for this gene in parenting.
Finally, we show that Magel2-null mothers and fathers have a significant reduction in POA galanin expressing cells, which in turn contributes to a reduced c-Fos response in the POA upon exposure to pups.
Our findings identify a novel imprinted gene that impacts parenting behaviour and, moreover, demonstrates the utility of using single-cell RNA sequencing data to predict gene function from expression and in doing so here, have identified a purposeful role for genomic imprinting in mediating parental behaviour.
