Why You (Don’t) Like Parma Violets

Whilst some may unanimously agree on the perception of a specific flavour (or combination of flavours) most will dispute variances in its intensity and inclination to like it: but why? As it’s (partially) due to your genes, of course!

Before exploring such variations let’s first establish that our flavour perception is about 80% reliant on out perception of smells at how we actually smell. So how we do smell? Well firstly, molecules from the surrounding air are inhaled through the nostrils and filtered by hairs within it. They then reach the back of the nose where the olfactory epithelium is located. Here is where odour detection occurs.

This is due to the odour molecules dissolving in a layer of mucus which lines the olfactory epithelium, binding to certain receptors on olfactory sensory neurons as they do so.  When these neurons reach their necessary threshold, action potentials are created which travel up their axons, through the ethmoid bone to the olfactory bulb in the brain. Here, within the glomeruli (bundles which the olfactory receptor neurons converge into) the olfactory neurons meet with the dendrites of a mitral cell, passing the signal onto them and then through the olfactory tract to the olfactory cortex in the brain.

The brain then processes the smell in two ways: one is that the signal is then passed on to be consciously interpreted by the frontal cortex; the other is that the signal is transferred to the amygdala, parts of the neocortex and the rest of the limbic system, triggering an emotional response (this is partly why smells are so closely linked to our memories). This processing of the sense of smell differs from the processing of sound and sight in that the impulse stimulated by odour detection takes a more direct route through the brain as opposed to going to a relay centre in the middle of the cerebral hemisphere first.

But how can we distinguish between odours? This is due to the combination of chemicals that we smell creating an overall depiction of an odour, with different odorants activating different odorant receptors. Though the olfactory epithelium in humans is only about the size of a postage stamp (with a dog’s 20 times larger, explaining their better sense of smell), 396 unique scent receptors have been identified in reference human genome, hence allowing us to detect over 1 trillion different odours, despite each olfactory neuron having receptors for only one kind of smell, as a result of combinational coding.

However, variations in our genes can cause variations in the perceptions of odours. After all, 1 out of every 50 of our genes is dedicated to smell. Such variations in perception include that of β-Ionone, a chemical that gives violets their distinctive smell and as such are used in the sweets Parma Violets. Though studies (such as http://www.cell.com/current-biology/fulltext/S0960-9822(13)00853-1 ) have shown that the sensitivity in perception of this smell greatly varies in individuals, with some being able to detect the floral tone whilst others detect a smell that more pungent than flowery or are unable to detect the smell at all (known as specific anosmia).

When they sequenced the genomes of the individuals tested they found a correlation between their perception of β-Ionone and the variant of the gene OR5A1 that the individual had, with this difference accounting for 96% of the variation in perception. Furthermore, when the researchers gave the participants a choice of juices, the group of people who were more sensitive to β-Ionone chose the option without β-Ionone added whilst the less sensitive group preferred the option with β-Ionone added.

This, therefore, shows how our genes can influence our inclination to certain food and drinks. Various industries have acknowledged this and as such have changed their composition or production methods. Let’s look at the chemical androstenone, 5-α-androst-16-en-3-one, which to some smells like vanilla though to others smells like sweaty urine. With this chemical being a pheromone in boars, male pigs which are bred for pork production are castrated to prevent androstenone production, to account for those who would smell sweaty urine. Sorry, boars.

And with Christmas approaching, you’re probably wondering about those Brussels sprouts. Well this time taste has a big role to play in our perception of their flavour, with variations in the TAS2R38 gene influencing our sensitivity to bitter tastes caused by the chemical phenylthiocarbamide (PTC). With Brussels sprouts containing very similar chemicals and about 50% of people having the variation of the gene which makes them less sensitive to such chemicals, you’ve got a roughly 50-50 chance of liking them.

So next time your parents criticise your profound disliking of certain foods, just let them know that you can’t help it: it’s in your genes!  

Lie In’s In Our Genes

The connection between sleep and your genes goes much deeper...

The connection between sleep and your genes goes much deeper...

Regularly staying up late and hitting that snooze button on mornings? Well if so, you’re most likely a “night owl” and before blaming this solely on environmental conditions, it’s worth pointing out that this is also partially as a result of your genes.

Previous studies, such as that made by Aachen University a few years ago, proved that there were physical differences between those who naturally feel more awake at different times of the day. In the study they observed that “night owls” had reduced integrity of white matter in multiple areas of the brain compared to their earlier-awaking counterparts: a quality that has been linked to depression (https://www.ncbi.nlm.nih.gov/pubmed/21170955) and thought to be as a result of “social jetlag”, where someone’s biological and social time are not aligned.

Though this was proven to be not the only reason when last month the 2017 Nobel Prize for physiology or medicine went to Jeffrey Hall, Michael Rosbash and Michael Young for explaining the reason for circadian rhythm (our body clock- a cycle by which physiological processes are regulated). Whilst this process may be controlled by external factors, such as the concentration of blue light, which suppresses melatonin and so sleep as the concentration increases, the three US scientists also proved that it can be influenced by genes.

Before getting to your lie-ins, let’s first look at the experiment they did. Using fruit flies, Rosbash and Hall isolated the section of DNA responsible for circadian rhythm called the period gene, which codes for the protein PER. Over a 24 hour cycle levels of this protein vary, decreasing during the day and increasing at night, switching off its own genetic instructions as it increases (a negative feedback loop).

 

Don't blame the traffic, blame the comfort of your bed!

Don't blame the traffic, blame the comfort of your bed!

However, Young discovered that genes “timeless” (tim) and “double-time” (dbt) each encode proteins which have varying effects on the stability of PER. This causes an organism’s internal clock to be slower or faster when PER is more stable or less stable respectively, hence causing us to have different chronotypes (times of the day when we are naturally inclined to feel more alert or tired): some being “morning larks” (early chronotypes); others “night owls” (late chronotypes) and the rest somewhere in between (intermediate chronotypes).

So if you find yourself constantly going late to school or work because you want “just 5 more minutes” in bed, then instead of blaming the horrendous traffic- which you could have avoided by leaving on time- remember to say that you can’t help it: it’s is in your genes! (Note that whilst this may be partly due to a predisposition you have no control over, there are ways to manage it and so it’s unlikely that your teacher or boss will allow this excuse… Sorry!)

How Chromosomes Cheat

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Cheating is wrong and something that we, as humans, should avoid: it’s unfair. Though for some chromosomes this is just in their nature.

Recently a team from the University of Pennsylvania conducted a study entitled “Spindle asymmetry drives non-Mendelian chromosome segregation” (http://science.sciencemag.org/content/358/6363/668 ). This basically means that they discovered how chromosomes “cheat” to have a rate of making it into the functional ovum, as opposed to a polar body, which is much higher than chance would predict (a polar body being one of three smaller cells that buds off from an oocyte, a cell in the ovary which undergoes meiosis to form an ovum, at the oocyte’s two meiotic divisions and degrades as opposed to developing into an ovum). This process in which certain alleles are favourably transmitted to the gamete is known as “meiotic drive”.

 

Spindle asymmetry drives non-Mendelian chromosome segregation  Source |   https://www.genengnews.com/gen-news-highlights/cheating-chromosomes-vault-past-competitors-to-reach-egg-cell-first/81255126   [University of Pennsylvania]

Spindle asymmetry drives non-Mendelian chromosome segregation

Source | https://www.genengnews.com/gen-news-highlights/cheating-chromosomes-vault-past-competitors-to-reach-egg-cell-first/81255126 [University of Pennsylvania]

The study involving mouse oocytes detected molecular signals which were shown to create an asymmetry in the machinery driving meiosis. To investigate the cause of this, the researchers focused on the meiotic spindle: the structure which pulls the pair of chromosomes apart to opposite poles of the cell by their centromere during anaphase I and later pulls the sister chromatids apart to opposite poles of the cell during anaphase II (anaphase I and II being stages during meiosis). The team looked at microtubules, which the meiotic spindle consists of, and found a lower distribution of a modification called tyrosination in the egg side of the cell as opposed to the opposite side, the cortex. However, this asymmetry in the distribution of tyrosination was only present during the stage of meiosis when the spindle moves from the equator, the middle of the cell, towards the cortex. This therefore shows that the cortex is the origin of the signal which sets up the modification of tyrosine.

With this established the researchers then tested their hypothesis of whether a molecule called CDC42, Cell Division Control Protein 42 homolog, contributed to tyrosination being asymmetrical. Members of the team, Lampson and Chenoweth, created an experimental system to test this by using a light-sensitive assay (an investigative procedure to determine the functional activity of CDC42) to selectively enrich CDC42 on one side of the pole (the signals shown as green in the diagram with the microtubule tyrosination in white). From this they inferred that CDC42 was at least partly responsible for inducing the tyrosination asymmetry and so the spindle’s asymmetry in the dividing cell.

 

Meiotic Drive | Source ~ http://web.sas.upenn.edu/lampson-lab/research/cell-biology-of-meiotic-drive/

Meiotic Drive | Source ~ http://web.sas.upenn.edu/lampson-lab/research/cell-biology-of-meiotic-drive/

Now- bear with me I’m almost there- having now discovered that the asymmetry exists and how it is caused, they then focused on how chromosomes can “cheat” as a result of this”.  They did so by comparing the effect of having larger, “stronger” centromeres or smaller, “weaker” centromeres during meiosis. With the use of live imaging of mouse oocytes they were able to discover that “stronger” centromeres were more likely to detach themselves from the spindle, especially when orientated to the cortical side of the cell, than the weaker ones which didn’t really seem to mind being in either side of the cell. They believe that the stronger ones do so in order flip themselves so that they are they are positioned to the pole of the cell which will later develop into the ovum ( see diagram) as “if you’re a selfish centromere and you’re facing the wrong way… that’s how you win”, as said by Lampson.

Whilst Lampson and his team’s work has shed more light into the segregation of chromosomes to gametes, and so helped further the understanding of certain conditions like Down’s syndrome where there are errors in this, there are still “ a ton” of other questions, like how “centromeres evolve to win these competitions” Lampson has said. Questions which explore why we are who we are:  questions which Lampson and his team hope to later investigate.

So there you have it. The combination of chromosomes we received from our parents may not be so random after all; thanks to how some chromosomes “cheat” to influence this process… or rather “make better use of circumstances than others”, some may prefer to say.