(Edited down from a BBC
website)
1. There’s a gene that
makes you more likely to become overweight.
Many of us put on
weight during the pandemic, but can we blame our genes if we no longer fit into
our jeans? The answer is, maybe. The fat mass and obesity related gene, FTO, is
a regular gene which all of us have. However, one version of FTO makes you more
likely to be obese, and one version makes you less likely to be obese. Obesity
expert Dr Giles Yeo explains: “Around half of the world’s population have one
copy of this version of FTO that makes you slightly likely to be heavier, and
this makes you on average one and a half kilos heavier and 20 percent more
likely to become obese over your lifetime.” A sixth of the world population,
more than a billion people, will have two copies of this version of the gene
and be 50 percent more likely to be obese.
2. The “Warrior gene” has been used in court as a defence for brutal crimes. MAO-A or Monoamine oxidase A to be precise, is a gene that breaks down serotonin, a chemical in our brain that we need to feel good. When MAO-A is less active, explains Dr Sally McSwiggan, the result is a higher concentration of serotonin in our grey matter. Some think this results in us becoming more impulsive, more emotional and more aggressive. Up to 60% of us are walking around with the low activity “warrior” version of MAO-A and most will never commit a crime.
A study compared
800 violent and non-violent prisoners to look for a link between this gene and
violent behaviour. It found that inmates carrying a certain version of MAO-A
were indeed more likely to commit violent crimes. But this doesn’t mean anyone
who carries the gene is destined for a life of brutality. In fact, up to 60% of
us are walking around with the low activity “warrior” version of MAO-A, and
most will never commit a crime. This hasn’t stopped lawyers bringing their
client’s DNA in to the courtroom, however, in the hope of getting them off the
hook.
3. We share the “eyeball
gene” with every living creature.
PAX6 is the gene that tells an embryo to build an eye. It is expressed very early on, as Professor Veronica van Heyningen explains, only a week or two after fertilisation in the human embryo. Before the brain is even really a brain – more a tube of nerve cells – the eyes begin to “bud out”. PAX6 is then expressed in all different layers of the eye from the retina to the cornea to the lens.
PAX6 is the gene that tells an embryo to build an eye. It is expressed very early on, as Professor Veronica van Heyningen explains, only a week or two after fertilisation in the human embryo. Before the brain is even really a brain – more a tube of nerve cells – the eyes begin to “bud out”. PAX6 is then expressed in all different layers of the eye from the retina to the cornea to the lens.
It isn’t easy for
scientists to study PAX6, but one study has revealed an unlikely connection
with another creature’s eye growing gene; the fruit fly. Dr Patrick Callaerts
ran experiments where he activated the gene in flies’ legs. He found that they
would start growing eyes right there on their limbs. His team then put the
human PAX6 gene into the flies and, incredibly, the same thing happened: the
flies grew normal fly eyes. In transpired that PAX6 is the master control gene,
which tells an embryo to build an eye, whether it’s in a fly or a human.
And they learned
something even more fundamental - wherever you find eyes, you find PAX6. From
fish to flatworms, pandas to parakeets, wallabies to water fleas – it’s
ubiquitous. The same gene that makes our peepers is behind the eyes of every
other animal, from a tiny fruit fly to a gigantic blue whale.
4. Only one in ten
of people genetically at risk of Huntington’s Disease choose to get tested.
Huntington’s disease is an inherited neurological disorder which stops parts of the brain working properly over time. Initial symptoms can include difficulty concentrating and involuntary movements of the limbs and body. There's currently no cure for Huntington's disease or any way to stop it getting worse.
Huntington’s disease is an inherited neurological disorder which stops parts of the brain working properly over time. Initial symptoms can include difficulty concentrating and involuntary movements of the limbs and body. There's currently no cure for Huntington's disease or any way to stop it getting worse.
The gene
responsible is called Huntington. As with all genes for diseases, we all have
two copies of Huntington, one from our mum and one from our dad. But in people
who develop Huntington’s disease, at least one of those copies has an unusual
glitch. The fault is in a repeating sequence in the gene called a CAG. Normally
there are twenty of these repeats but in Huntington’s disease the CAG expands.
“When you get to 40 of the CAG repeats you will definitely develop the disease
if you live long enough,” explains Dr Sarah Tabrizi.
Since the 1980s
it’s been possible for people in affected families to get tested for the
Huntington’s gene, which reveals their risk of developing the disease and the
chance of passing it on to their children. But it’s not a simple decision. In
fact, only about one in ten people at risk choose to get tested. Perhaps
understandable given the fact there is currently no cure. A large-scale trial
for a new drug raised hopes, but it did not halt symptoms in sufferers and the
trial was stopped. However, Dr Tabrizi remains hopeful. “We will find treatments,” says the neuroscientist.
5. One in a hundred
of us are naturally immune to HIV
Stephen Krone lived
in New York through the heyday of the gay scene in the 1970s and early 80s. He
watched as one after another of his friends, including his boyfriend, were
struck down by the mysterious disease that was ravaging their community. But
Krone was never affected.
Scientists learnt
that a gene called CCR5 is the crucial portal by which HIV infects immune
cells. And a specific version of the gene, called delta 32, seemed to protect
against the virus. Dr Stephen O’Brien discovered that people who had two copies
of CCR5-delta32 were never found among HIV infected individuals, which he
describes as “remarkable statistically.” It seemed that if you carried this genotype,
you could not be infected, ever. It was because these individuals simply had no
doorway by which HIV could enter cells. “They were walking around as this rare
but very, very noticeable group who were genetically resistant to the infection
of HIV,” says Stephen. It was a ground-breaking discovery: “It was really the
first time that anybody had identified a human mutation which was good for you
in the sense that it protected you from a deadly infectious disease – AIDS.”
I'm listening to David Bowie's The Jean Genie
(Ha ha!). You can listen here.
