Link to paper: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3923652/
ERIKSSON, JOHAN G., et al. “Boys Live Dangerously in the Womb.” American journal of human biology : the official journal of the Human Biology Council, U.S. National Library of Medicine, 13 Feb. 2014, www.ncbi.nlm.nih.gov/pmc/articles/PMC3923652/.
There is not very much known on this topic, which expresses the possibility of boys being at a greater risk than girls in the mother’s womb. This paper begins to shed some light on the differences that have risen and theories about why this might be.
There are a few distinguishing characteristics that differentiate boys and girls while in the mother’s womb. As a result, researchers have claimed that this puts boys at a risk of hypertension, along with other diseases later in life. Boys, have been found to grow faster in the womb than girls, due to this, they demand more from the placenta for nutrients to compensate, but during late gestation this can cause the placenta to grow more than it needs to – “compensatory placental enlargement”.
The paper emphasizes the importance of the mother’s diet, especially when they’re having a boy. The mother can improve her diet, however, her metabolism and how her body stores the ingested nutrients is also a contributing factor, as well as how well the placenta can “transport nutrients…to [the] fetus”.
Researchers found that the placentas of boys were more efficient, but they did not have a very large reserve capacity, which can be threatening if the mother’s diet does not fulfill the fetus’ nutritional needs.
A fascinating theory presented in the paper suggests that there is a “trade-off [of] visceral development to protect brain growth”! Although, this sounds like a very strategic trade-off, it can have serious effects on the physical health of the child in later years, that put them at risk of diseases characteristic of malnutrition in the womb. The paper describes that hypertension can be a result of a “lifetime reduction in the number of nephrons” because of the trade-off to protect the cranium, less significance is placed on other body parts.
Researchers found that a shorter length of the placenta “predicted later hypertension in women”. And it was not how high the birthweight of the men with a high placental weight, it was the “disproportion between the growth of the lesser diameter [of the placenta] and the fetus that predicted the disorder”. The greater the difference between the two, the greater the risk of hypertension in later years of their lives.
The researchers did not find a strong correlation between the placental weights and the men’s risk of hypertension. As well, a low birth weight linked to hypertension was found to be statistically significant in males and females, as described in Figure 1 and Table 2. Figure 1 presents the odds ratio for the association between placental area and hypertension, while controlling for the low birth weight. They did find that the boy’s placenta’s were smaller when they also considered the weight of the child at birth, “suggesting that boys placentas are more efficient than girls’ placentas”.
They also suggested that there may be a relation between the size of the placenta and pregnancy complications, such as preeclampsia, this may be a result of a change in the tissue development on one side of the placenta.
Researchers believe that boys are “more responsive to their mother’s current diet than girls” while girls focus more on the history of their mother’s health habits and homeostatic mechanisms, such as metabolism.
This research is of interest, a) because this area of research (obstetrics and gynaecology) is my future career path and I want to learn everything there is to know about fetal development and this paper puts a slight twist to the field of study and b) it is one of the papers that I have been assigned to review for a research project for the summer. We will be examining the differences between boys and girls in the womb and the effects of this on pregnancy outcomes.
By: Simran Grewal
Summary: ATP-Binding Cassette Transporter G26 Is Required for Male Fertility and Pollen Exine Formation in Arabidopsis.
Pollen, the male reproductive gamete, requires high durability for its travels from the plant’s male reproductive organ called the stamen, to the stigma, the female organ. During the journey, the tough outer wall of pollen grains, called the exine, keeps pollen grains safe from nature’s elements by acting as a physical shield.
Four researchers at the University of British Columbia in 2010 uncovered the function of a gene they call ABCG26. The gene helps develop the the exine and plays an important role in male fertility of Arabidopsis, a small flowering plant.
A complex compound called sporopollenin gives the exine its incredible strength. Previous research suggests that sporopollenin is formed in the tapetum, a part of the stamen that produces nutrients for developing pollen grains. The precursors to pollen grains are called micropores, and require an assortment of molecules, including sporopollenin components, to be brought to them from the tapetum. However, the components of sporopollenin and the specific proteins that transport them aren’t well known.
To discover a protein involved in transporting sporopollenin constituents from the tapetum to the anther locule – an area of sacs where microspores form – the researchers looked at a group of proteins called ATP-binding cassette (ABC) transporters. Arabidopsis was examined for ABC transporter proteins made in the tapetum at the same time as proteins already known to be needed for sporopollenin formation. They uncovered protein ABCG26, and the gene responsible for its production ABCG26.
For the study, normal Arabidopsis with ABCG26 and Arabidopsis created with only a mutated form of the gene, abcg26-1 that didn’t code for the ABCG26, were used.
It was found that ABCG26 is required for male fertility. 85% of the normal Arabidopsis observed produced seeds and had large, yellow anthers, the part of the stamen responsible for producing microspores. Meanwhile, 99% of mutants failed to produce seeds and developed small dry anthers, without pollen, making them incapable of fertilizing the stigma.
To understand this loss of fertility, microscopy was used to look at the development of pollen grains in normal Arabidopsis and mutant Arabidopsis. The data explains that a lack of ABCG26 caused poor exine formation, thereby causing infertility.
As shown in Figure 6A, normal pollen grains had round oblong shapes, while Figure 6B shows the deformity of mutant pollen grains.
Moreover, Figure 6E shows normal microspores with an arch shaped protrusion labeled Te and Ba indicating the exine structure, while no protrusions can be observed in the mutant of Figure 6F. The consequence of this difference is seen in Figure 6C where a normal exine is present indicated by Ex, and in Figure 6D where the mutant lacks a proper exine, indicated as DEx.
Most of the misshapen mutant microspores that lacked proper exines were degraded in later stages of anther development and did not mature into pollen grains. The ones that matured had extremely weak and thin exines, making most ineffective in fertilization.
These findings not only significantly improve the scientific community’s understanding of exine formation, but also have potential applications to agriculture where reduced male plant fertility could be desirable in preventing certain GMOs from reproducing with and modifying naturally occurring populations.
I chose to summarize this article as I had to read it for a biology class and found it interesting learning about the anatomy of plants, as I hadn’t done much previous study in plant biology.