One of the best yet most challenging parts of this course is the sheer volume of knowledge that can be gained in these four weeks. I learned a spectacular amount of information about the human body during the course, giving me a greater appreciation for the ingenuity of evolution and the delicate intricacy of the body’s structures and mechanisms. In addition, Dr. K has a knack for sprinkling little bits of knowledge throughout his lectures that, when given time to soak in, can stimulate a great deal of critical thinking.
For example, when Dr. K lectured on the respiratory system, he briefly mentioned that fetal hemoglobin has higher oxygen saturation than adult hemoglobin does at the same oxygen levels. While this assertion can be explained by the fact that the fetus has higher demand for oxygen and must compete for oxygen in slightly deoxygenated blood, it reminded me of an article I read in a previous biology class on imprinted genes.
Imprinted genes are genes which are “marked” by the maternal or paternal parent and which are expressed over other versions of the same gene. Mechanisms of imprinted gene expression and evolutionary reasons for their existence are mostly obscure due to their relatively recent discovery. In fact, the existence of imprinted genes was only verified through cloning experiments in the late 80s. Scientists attempting to create a uniparental mouse (a mouse with two paternal or two maternal sets of DNA) found that it was impossible to create a fully-developed uniparental embryo. When the embryo was created from two maternal sets of DNA, its cells were properly organized, but the placenta was insufficient. When the embryo was created from two paternal sets of DNA, it was able to form a very healthy placenta, but the fetus itself was a disorganized mass of cells.
These results flew in the face of Mendelian genetics, which suggested that genes are merely strands of information with no history of origin. To the contrary, genes do, in a sense, remember their parental origins. The studies in the 80s suggested that the expression of certain genes in the paternal genome is responsible for making the placenta, while the expression of certain genes in the maternal genome is responsible for organizing the embryo. One of the first explanations posited that the placenta should be thought of not as a maternal organ designed to support the fetus, but rather as a fetal organ designed to parasitize the mother. While the mother and the fetus both have the common purpose of perpetuating the continued survival of the fetus, they disagree over how much of the mother’s resources should be dedicated to the fetus. In a sense, maternal genes are “selfish” and only the genes necessary to organize the fetus are expressed. Hence, the uniparental mouse embryos made of two maternal sets of DNA were unable to create a sufficient placenta.
This competition for resources between the fetus and the mother, clearly observable through research on imprinted genes, is strikingly similar to the competition for oxygen between the fetus and the mother. As previously mentioned, fetal hemoglobin has a higher oxygen affinity than adult hemoglobin does. To ensure its own survival, it is entirely conceivable that the fetus robs oxygen from the mother’s bloodstream. Perhaps this is but another example of a battle of wills between the fetus and the mother.