Monday, May 21, 2007

Battle of sexes

Human Beings are diploid – that is each of us contains a copy of chromosome from our Mom and one from Dad. This gives us the advantage of having a spare copy of any given gene. However, there are certain genes that are "marked"in the embryo in such a way that either the Mom's or the Dad's copy is selectively silenced. The end result is that some genes in our body come with instructions attached, I am from Mom, Use only me! or vice- versa. The process that does this is called imprinting – either maternal ( for use only Mom’s gene) or paternal ( for use only Dad’s gene).

Why develop this curious phenomenon? On the surface it seems to be counter productive to us humans. If the marked/imprinted gene is defective then there is no working copy left since the silenced copy form the other parent can never be used. So why evolve such a complex yet dangerous mechanism? Since the process became known to scientists in the early 60s, several hypotheses have been put forth as to why this must occur. One of the most popular one shows the peculiar nature of inherent in a gene – its selfishness.

The Haig hypothesis is simple - it relates the development of a baby to the parent's inherent fidelity. The hypothesis, put forth by David Haig, predicts that Mom and Dad have different interests when in it comes to the development of their baby in any non-monogamous species, and hence imprint genes that are involved in growth of the embryo. Simply put both Mom and Dad fight a genetic war when it comes to the baby, more so if either one of them is prone to promiscuous!

Is there evidence for this prediction?
There is an excellent study done with the “deer mice” Peromyscus. This is a perfect species genus as we have both monogamous and polygamous species that can interbreed namely, P. maniculatus and P. polionotus. The females of the dark brown Peromyscus maniculatus species are promiscuous (babies within a single litter often have different fathers). Peromyscus polionotus, the sandy mouse, however pairs for life.

Check scenario one - Dad screws around but Mom is faithful.
In this case, the dad knows that the chances that all the offspring that she might carry are all his is slim. So he has to think of a way to make sure his baby grows faster at the cost off all other siblings and even mom.

This is exactly what you see when mate the faithful Peromyscus polionotus female with the
P. maniculatus male.The pups obtained are huge and mothers die giving birth.
Reason ? Well, the Peromyscus maniculatus dad has put a copy of a gene that ensures his baby grows faster since the female of his species is promiscuous. But the poor faithful Peromyscus polionotus mom is not used to playing this war and hence has no defense against the signals he is sending in. So the babies, prompted by Dad's genes grow unchecked, use up the mom’s resources and kill mom.

Check Scenario two - Mom is promiscuous but Dad is not.
The mom knows that since all the litter she carries has her genes, she can spread her genes in the population if she can restrict the growth of any one fetus, to conserve resources for her offspring with other males. So the genes she imprints will slow fetal growth.
That is what happens when you mate the promiscous P. maniculatus females with a steadfast Peromyscus polionotus male - you get tiny pups.
What happens? In this case, the mom is using her imprinted copy to slow down growth of the babies but the counterpart signal to grow is never received from the dad. The result is puny babies.

What if both parents are not promiscuous or vice versa?
The offsprings from a P. maniculatus cross or from a Peromyscus polionotus cross are healthy and similar in size. Reason? Each partner has co-evolved the defenses. In case of the promiscuous pair, the dad signals the babies to grow faster and mom to grow slower. In the other pair, each parent has the same vested interest in the offspring. End result is a normal sized litter.

What about humans?
So far about 80 of the 30,000 or so genes in the human genome are currently known to be imprinted. More importantly, most of these genes seem to play a role in directing fetal growth! And in the expected direction if humans were not considered to be monogamous-- genes expressed from the dad’s copy generally increase resource transfer to the child, whereas maternally expressed genes reduce it. So our genes behave much in the same way as the promiscuous mice! However there are imprinted loci are also implicated in behaviour/ neurological cases (Prader -Willi Syndrome) indicating that there is more to understand about this phenomenon.

More support for the theory comes from early indications that of very little imprinting in in fish, amphibians, reptiles and birds. Since the hypothesis states that imprinted genes are linked with acquiring resources from parents, this makes sense. But imprinting does also exist in seed plants where the endosperm tissue acts as the placenta to feed the embryo. Why this is the case is still unclear. There is lot of research that is ongoing and more that needs to be done. As molecular tools improve, we will be dissecting roles of imprinted genes much easily.

1. Dawson, W.D. Fertility and size inheritance in a Peromyscus species cross. Evolution 19, 44−55.
2. Vrana Et. al., Genomic imprinting is disrupted in interspecific Peromyscus hybrids, Nature Genetics, 20, 362 - 365


Prashanth said...

I thought we were talking about imprinting... where does promiscuity come into this??

Sakshi said...

Haig's theory states that promiscuity could be the reason why imprinting occurs.
(Imprinting - marking a gene to define it's source)

Anonymous said...

Thank you for this article, as a student of biology, ironically I rarely get to read about such interesting phenomena.

Anyway, just a side question, won't the sexes each have developed somekind of mechanism against imprinting? or it's just all a red queen's race, going nowhere with all the evolution?

-- reika

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