Stick insects frequently reproduce this way. They are using a mechanism known as parthenogenesis, from the Greek for ‘virgin birth’. Females lay fertile eggs without ever mating with a male, and perfectly healthy little stick insects emerge from these eggs. These insects have evolved with special mechanisms to ensure that the offspring have the correct number of chromosomes. But these chromosomes all came from the mother.
This is very different from mice and humans, as we saw in the last chapter. For us and our rodent relatives, the only way to generate live young is by having DNA from both a mother and a father. It’s tempting to speculate that stick insects are highly unusual but they’re not. We mammals are the exceptions. Insects, fish, amphibians, reptiles and even birds all have a few species that can reproduce parthenogenetically. It’s we mammals who can’t. It’s our class in the animal kingdom which is the odd one out, so it makes sense to ask why this is the case. We can begin by looking at the features which are found only in mammals. Well, we have hair, and we have three bones in our middle ear. Neither of these characteristics is found in the other classes, but it seems unlikely these are the key features that have led us to abandon virgin birth. For this issue there is a much more important characteristic.
The most primitive examples of mammals are the small number of creatures like the duck-billed platypus and the echidna, which lay eggs. After them, in terms of reproductive complexity, are the marsupials such as the kangaroo and the Tasmanian devil, which give birth to very under-developed young. The young of these species go through most of their developmental stages outside the mother’s body, in her pouch. The pouch is a glorified pocket on the outside of the body.
By far the greatest numbers of our class are called placental (or eutherian) mammals. Humans, tigers, mice, blue whales – we all nourish our young in the same way. Our offspring undergo a really long developmental phase inside the mother, in the uterus. During this developmental stage, the young get their nourishment via the placenta. This large, pancake-shaped structure acts as an interface between the blood system of the foetus and the blood system of the mother. Blood doesn’t actually flow from one to the other. Instead the two blood systems pass so closely to one another that nutrients such as sugars, vitamins, minerals and amino acids can pass from the mother to the foetus. Oxygen also passes from the mother’s blood to the foetal blood supply. In exchange, the foetus gets rid of waste gases and other potentially harmful toxins by passing them back into the mother’s circulation.
It’s a very impressive system, and allows mammals to nurture their young for long periods during early development. A new placenta is created in each pregnancy and the code for its production isn’t carried by the mother. It’s all coded for by the foetus. Think back yet again to our model of the early blastocyst in Chapter 2. All the cells of the blastocyst are descendants of the fertilised single-cell zygote. The cells that will ultimately become the placenta are the tennis ball cells on the outside of the blastocyst. In fact, one of the earliest decisions that cells make as they begin to roll down Waddington’s epigenetic landscape is whether they are turning into future placental cells, or future body cells.
While the placenta is a great method for nourishing a foetus, the system has ‘issues’. To use business or political speech, there’s a conflict of interest, because in evolutionary terms, our bodies are faced with a dilemma.
This is the evolutionary imperative for the male mammal, phrased anthropomorphically:
This pregnant female is carrying my genes in the form of this foetus. I may never mate with her again. I want my foetus to get as big as possible so that it has the greatest chance of passing on my genes.
For the female mammal, the evolutionary imperative is rather different:
I want this foetus to survive and pass on my genes. But I don’t want it to be at the cost of draining me so much that I never reproduce again. I want more than this one chance to pass on my genes.
This battle of the sexes in mammals has reached an evolutionary Mexican stand-off. A series of checks and balances ensures that neither the maternal nor the paternal genome gets the upper hand. We can get a better understanding of how this works if we look once again at the experiments of Azim Surani, Davor Sobel and Bruce Cattanach. These are the scientists who created the mouse zygotes that contained only paternal DNA or only maternal DNA.
After they had created these test tube zygotes, the scientists implanted them into the uterus of mice. None of the labs ever generated living mice from these zygotes. However, the zygotes did develop for a while in the womb, but very abnormally. The abnormal development was quite different, depending on whether all the chromosomes had come from the mother or the father.
In both cases the few embryos that did form were small and retarded in growth. Where all the chromosomes had come from the mother, the placental tissues were very underdeveloped[62]. If all the chromosomes came from the father, the embryo was even more retarded but there was much better production of the placental tissues[63]. Scientists created embryos from a mix of these cells – cells which had only maternally inherited or paternally inherited chromosomes. These embryos still couldn’t develop all the way to birth. When examined, the researchers found that all the tissues in the embryo were from the maternal-only cells whereas the cells of the placental tissues were the paternal-only type[64].
All these data suggested that something in the male chromosomes pushes the developmental programme in favour of the placenta, whereas a maternally-derived genome has less of a drive towards the placenta, and more towards the embryo itself. How is this consistent with the conflict or evolutionary imperative laid out earlier in this chapter? Well, the placenta is the portal for taking nutrients out of the mother and transferring them into the foetus. The paternally-derived chromosomes promote placental development, and thereby create mechanisms for diverting as much nutrition as possible from the mother’s bloodstream. The maternal chromosomes act in the opposite way, and a finely poised stalemate develops in normal pregnancies.
One obvious question is whether all the chromosomes are important for these effects. Bruce Cattanach used complex genetic experiments on mice to investigate this. The mice contained chromosomes that had been rearranged in different ways. The simplest way to explain this is that each mouse had the right amount of chromosomes, but they’d been ‘stuck together’ in unusual ways. He was able to create mice which had precise abnormalities in the inheritance of their chromosomes. For example, he could create mice which inherited both copies of a specific chromosome from just one parent.
The first experiments he reported were using mouse chromosome 11. For all the other pairs of chromosomes, the mice inherited one of each pair maternally, and one paternally. But for chromosome 11, Bruce Cattanach created mice that had inherited two copies from their mother and none from their father, or vice versa. Figure 8.1 represents the results[65].
Figure 8.1 Bruce Cattanach created genetically modified mice, in which he could control how they inherited a particular region of chromosome 11. The middle mouse inherited one copy from each parent. Mice which inherited both copies from their mother were smaller than this normal mouse. In contrast, mice which inherited both copies from their father were larger than normal.