Did you know we prefer to make friends with people that have similar genes to ourselves?

This study compared the genome sequences of people who are friends versus people who are strangers.

People who are friends share more similar genes than strangers (~0.1%).

The genomes of friends are as similar as fourth cousins (~0.2%).

Genes associated with the olfactory system are similar in friends, suggesting that smelling our friends might be important.

Conversely, friends tend to have different immune systems, which might help to protect a large population against infection.

Do you want more information?

Background

Friendship is very important in human culture and society.

Humans are better than any other species at making and keeping friends.

We prefer friends that are similar to ourselves (e.g. same area, race, etc).

People from similar areas, races share similar genes.

Following this logic, do we prefer to make friends with people that have similar genes?

Materials and Methods

The authors conducted a genome-wide association study (GWAS) to compare SNPs (single nucleotide polymorphisms) between pairs of friends (n= 1,367) or pairs of strangers (n= 1,196,429). No pairs were related to each other. Most subjects were of European ancestry.

SNPs are single bases in DNA that vary between individuals in a population. E.g. a gene might have the same DNA sequence in all people, except for a single base at position X that varies between people. Not a mutation, just different for different people. This study analysed 466,608 SNPs to determine how similar/different people’s genomes are.

Results

The genomes of friends are more similar than people who are strangers.

The genomes of friends are as similar as fourth cousins (~0.2%).

Genes associated with the olfactory system were found to be important for forming friendships, suggesting that smelling our friends might be important (or they like the same smells).

Conversely, friends tend to have different immune systems that might help to protect a large population against infection.

Discussion

One theory suggests that our care/nurture for family members and descendants is proportional to the number of genes we share with them. For example, we share 50% of our genes with our children, 25% with grandchildren, 12.5% with first cousins, etc. We put great effort into nurturing these relations so that our genes are successfully passed on to future generations. This pattern could extend to friends, even though they share a much lower percentage of genes (~0.2%).

The control group in this study were strangers. It is conceivable that these pairs could be friends if they had known each other. Perhaps a better control group would be people that don’t like each other.

Future Directions

Future studies might specify particular genes important for friendships.

Also, do spouses (e.g. husbands, girlfriends) prefer partners with genomes that are similar (like friends) or different (opposites attract).

Article

Friendship and natural selection

Christakis and Fowler, 2014 Proc. Natl. Acad. Sci. USA 111 S3:10796

Keywords

Gene, genome, genetic, SNP, polymorphism, mutation, sequence, sequencing, GWAS, DNA, friend, stranger, people, human

Subject

Science, Biology, Genetics, SC4-14LW, ACSSU150, ACSHE119, ACSHE134, SC5-15LW, ACSSU184

There’s a well-known saying that goes; Coughs and sneezes spread diseases.

But what about the other end? Do farts also spread diseases?

Here, a man farted onto agar plates wearing either underpants and jeans or nothing at all.

Bacteria grew on the agar plate that was farted on by the bare bottom, but not the covered bottom.

The bacteria was E.coli, which is commonly found in human faeces.

This means that farts can transmit faecal bacteria, although underpants and trousers provide effective protection by filtering out the bacteria.

Do you want more information?

Background

Coughs and sneezes spread diseases, so a subscriber to this website/podcast posed the question, is the same true for emissions from the bottom?

That is, do farts carry bacteria?

They visited microbiologist Dr. Simon Park at the University of Surrey, UK who devised the experiment below.

Materials and Methods

An (unnamed) man was asked to fart onto agar plates wearing either underpants and jeans or nothing at all (bare bottom). The air emitted from the bottom hits the agar plates and if there’s any bacteria in it, they will land on the agar plates and grow. The number of bacterial colonies can then be countered/compared a few days later.

(Agar is like jelly containing food, sugars, etc. to support bacterial growth).

Results

The plate exposed to the fart from the bare bottom showed a number of colonies of bacteria.

These colonies were identified as E.coli – a common strain of bacteria commonly found in human faeces.

The plate exposed to the fart from the covered bottom showed no bacterial colonies at all.

This indicates that underpants and jeans provide effective protection by filtering out faecal bacteria from farts.

Article

Would filtering farts prevent hospital acquired infections?

The Naked Scientist Website/Podcast, University of Cambridge

(http://www.thenakedscientists.com/HTML/questions/question/3333/)

Keywords

Microbiology, microbiologist, bacteria, germ, E.coli, microbiome, gut, bottom, bum, anus, faeces, fart, flatulence, infection, infectious, disease, transmission, cough, sneeze

Subject

Science, Biology, Microbiology, ST1-11LW, ACSSU211, ST2-11LW, ACSSU073, ST3-11LW, ACSSU094, SC4-14LW, ACSSU111

Did you know that 97% of bird species don’t have penises?

This study shows that during development in the egg, birds begin to develop a small penis, but a hormone called Bmp kills the cells and makes the penis regress.

Biologists don’t know why birds evolved to lose their penis. It might make copulating or flying easier for the birds.

In contrast, those species that do develop penises can have enormous penises. For example, ducks can have penises longer than their bodies and they spiral in an anticlockwise direction.

Do you want more information?

Background

All bird species (~10,000) reproduce by internal fertilization (like humans). That is, male penis inserts into female vagina to fertilize eggs.

Some bird species have huge penises. E.g. the duck penis can be longer than its own body and spirals in an anticlockwise direction.

However, the vast majority of species (97%) don’t have a protruding penis at all.

Instead their penises barely protrude from the body and can’t insert into a female’s vagina (non-intromittent phallus).

Biologists don’t know why birds evolved to lose their penis.

However, this study shows how penis growth is blocked in birds.

Materials and Methods

Penis growth in the embryo (egg) was compared in birds that have protruding penises (ducks, emus) versus those that don’t (chickens) using high-powered electron microscopes (their penises were very small).

Expression of molecules controlling penis growth was visualised using light microscopy (in situ hybridization for mRNA, immunohistochemistry for proteins).

Results

Penises grow in both types of birds, however the growth is halted and regresses in chickens (but not ducks and emus).

A hormone called Bmp is expressed in the chicken that causes cells to die, thus blocking penis growth.

Blocking Bmp production caused the chicken embryos to grow small penises.

The Bmp hormone is also involved in loss of teeth, beak shape and growth of feathers in birds.

Discussion

Biologists can’t explain why most bird species have lost their penises. Possible explanations include:

1) Reproduction of males without a penis requires cooperation with the female. Thus, females have greater control over reproduction.

2) Might make copulating faster or easier.

3) Not having a large penis might increase flight performance.

4) Might reduce the risk of contracting STDs from female birds.

Article

Developmental basis of phallus reduction during bird evolution

Herrera et al., 2013 Current Biology 23:1065-74

Keywords

Evolution, natural, selection, animal, species, bird, chicken, duck, aves, emu, develop, development, organ, genital, penis, vagina, male, female, reproduction, sex, copulation, flight, fertilization, embryo, Bmp

Subject

Science, Biology, Zoology, ST1-10LW, ACSSU017, ST2-10LW, ACSSU044, ST3-10LW, ACSSU043, SC4-14LW, ACSSU111, ACSSU150, SC5-15LW, ACSSU175, ACSSU185

Did you know that vials containing one of the World’s deadliest viruses were accidently discovered in a storeroom near Washington in 2014?

The vials contained Smallpox (variola virus); one of the most deadly diseases in history.

Worldwide vaccinations eradicated the disease in the late 1970s.

The virus was thought to only exist in 2 super-secure labs in Atlanta (USA) and Siberia (Russia).

However, 6 vials were accidently found in a storage room near Washington in 2014.

They were immediately tested then destroyed by government officials.

This very scary virus could be used as a biological weapon if it got into the wrong hands.

Some people argue the stocks in the super-secure labs should also be destroyed, completely wiping out the virus from the planet – what do you think?

Do you want more information?

Background

Smallpox killed a third of people it infected for many centuries, even as recently as the 1960s when it infected 12 million people and killed 2 million.

It is a highly contagious disease caused by the variola virus.

It causes horrible blisters on the skin that leave permanent scars. It is deadly if it infects the circulatory or respiratory systems.

A worldwide vaccination program completely eradicated smallpox (declared eradicated by WHO in 1979).

The only known stocks of smallpox (kept in liquid nitrogen at -200ºC) exist at 2 super-secure laboratories: the CDC in Atlanta (USA) and VECTOR in Novosibirsk, Siberia (Russia). Until now……

Results

On July 1 2014, scientists were cleaning out a storage room at the NIH (National Institute of Health) at Bethesda, USA near Washington DC.

They found 6 glass vials containing freeze-dried variola virus (smallpox) in a cardboard box, dating back to the 1950s.

Their origin is completely unknown.

No staff were exposed to the deadly virus.

The vials were securely transported to the CDC in Atlanta by law enforcement officers and confirmed to be smallpox (PCR assay).

They were then destroyed.

Discussion

Discussion point: Some people argue that smallpox should be completely wiped off the planet by destroying the stocks at the super-secure labs in Atlanta and Siberia. Others argue they should be kept for research purposes to improve vaccines.

Article

Media statement on newly discovered Smallpox specimens, July 8, 2014

Centers for Disease Control and Prevention, Atlanta, USA

Further Reading

Smallpox was instrumental in the development of vaccines.

English doctor Edward Jenner noticed that milkmaids rarely contracted the deadly smallpox virus.

He hypothesised that prior infection with the closely-related but less harmful cowpox virus might make them immune to smallpox.

In 1796, he scraped pus from the blistered hands of a milkmaid infected with cowpox. He injected the pus into an 8-year-old called James Phipps.

He then exposed James to smallpox, but he did not become infected.

Thus, Jenner had successfully vaccinated James against smallpox.

A crater on the moon is named in Edward Jenner’s honour.

Keywords

Infection, infectious, disease, virus, contagious, smallpox, cowpox, variola, vaccine, vaccination, immune, immunity, immune system

Subject

Science, Biology, ST2-10LW, ACSSU044, ACSSU072, SC4-15LW, ACSHE119, ACSHE134, SC5-15LW, ACSSU175, ACSSU184

Did you know there’s a genetic disease that causes extremely long eyelashes?

It’s a rare hereditary condition called Trichomegaly that causes growth of ‘movie lashes’.

This study discovered it’s caused by mutation of the FGF5 gene.

Affected patients have 2 mutant copies (alleles) of FGF5 (recessive).

FGF5 protein is a growth factor (hormone) that normally blocks hair growth. Mutations reduce the activity of FGF5, relieving this block and allowing excessive growth of eyelashes.

It’s possible that drugs targeting FGF5 could be extremely lucrative in the cosmetics industry (e.g. remove women’s moustaches, men’s monobrows).

This study serves as an interesting case study for Mendelian genetics.

Do you want more information?

Background

Trichomegaly is a rare hereditary condition that causes growth of extremely long eyelashes.

Also called ‘movie lashes’.

First discovered/described in 1944 by Gray.

The genetic mutation that causes trichomegaly is not known.

Materials and Methods

This study performed genome sequencing of 2 affected families from Pakistan and compared it to the genomes of unaffected people to identify the genetic mutation causing trichomegaly.

Results

Mutations in a gene called FGF5 were discovered in patients with trichomegaly, but not in unaffected people.

All affected patients had 2 copies of the mutated FGF5 gene, hence they were homozygous for this allele and the condition is recessive.

Scalp hair, nails and teeth are not affected in these patients, however the length of forearm hair is also increased.

Adding FGF5 protein to hair cells blocked hair growth.

Discussion

FGF5 protein is a growth factor (hormone) that normally blocks hair growth. Mutations reducing FGF5 activity relieve this block, promoting excessive growth of eyelashes.

It primarily affects eyelashes and forearm hair because these normally grow for a short amount time, then are turned off by FGF5. Mutation of FGF5 prevents this block and instead these hairs continue to grow.

In contrast, scalp hair continually grows and is not turned off by FGF5. Therefore, mutation of FGF5 has little affect on scalp hair.

FGF5 mutations also increase hair growth in mice, cats, dogs, rabbits.

Future Directions

Drugs targeting FGF5 could be worth $billions to the cosmetics industry, whereby FGF5 agonists could remove unwanted hair growth (e.g. women’s moustaches, men’s monobrows), while FGF5 antagonists could induce hair growth (e.g. women’s ‘movie’ eyelashes).

Article

FGF5 is a crucial regulator of hair length in humans

Higgins et al., 2014 Proc. Natl. Acad. Sci. USA 111:10648-53

Further Reading

Positive selection of the FGF5 gene during evolution helped marine mammals (e.g. dolphins, whales) to lose their hair for improved streamlining in water (Chen et al., 2013 BMC Evol. Biol. 13:34).

Keywords

Gene, genome, genetic, sequencing, mutation, polymorphism, inherited, recessive, homozygous, allele, DNA, hereditary

Subject

Science, Biology, Genetics, SC5-15LW, ACSSU184

Did you know that all animals over 3 kg urinate for 21 seconds?

It doesn’t matter how big the animal is (0.03kg cat to 8,000kg elephant) or how big its bladder is (5ml-cat to 18L-elephant).

Rather, it is dependent on the diameter of the urethra.

In general, humans and animals urinate 5.6 times per day for 21 seconds, giving a total of 2 minutes per day urinating (0.2% of the day).

NOTE: This study was performed on a small number of animals and needs to be replicated before solid conclusions can be drawn.

Do you want more information?

Background

All animals urinate to remove excess fluid and waste products.

The ability to store urine in the bladder means animals don’t constantly urinate, including in their own homes.

Their ability to control the release of urine allows animals to use it for communication purposes and even self-defence.

Urinary problems can be caused by prostate cancer in males (enlargement of the prostate restricts flow through the urethra). Also incontinence caused by increased abdominal pressure in obesity.

Very little is known about similarities/differences in urination by different animal species.

Materials and Methods

The authors filmed 16 animals urinating using high-speed cameras, and studied 28 urination videos from YouTube. They also collected the urine expelled by the animals using “containers of appropriate size.”

Results

Large animals (>3kg) urinate for the same amount of time (21 +/- 13 seconds).

The constant urination time was independent of body mass, which ranged from 0.03kg (cat) to 8,000kg (elephant).

It was also independent of bladder volume, ranging from 5ml (cat) to 18L (elephant).

Instead, constant urination time was dependent on the diameter of the urethra, which was proportional to body size.

Small animals (<1kg) do not generate ‘jets’ of urine like larger animals. Instead, they produce droplets in a short amount of time (0.01-2 sec).

General rules across animal species: bladder volume = 4.6 ml/kg body mass. Daily urination is 26 ml/kg body mass and 5.6 times per day. Total time spent urinating is 5.6 x 21 sec = 2 minutes per day (0.2% of the day).

Discussion

The urethra is generally directed downwards to increase the gravitational force on the urine to expel it quicker from the body.

The diameter of the urethra increases proportionally with the size of the animal, allowing a constant urination time of ~21 second (for animals >3kg).

Future Studies

Note that these studies were performed using a small number of animals using ‘less-than-perfect’ data (e.g. YouTube videos), so these results should probably be replicated by other studies before solid conclusions can be drawn.

Article

Duration of urination does not change with body size

Yang et al., 2014 Proc. Natl. Acad. Sci. USA 111:11932-7

Keywords

Animal, species, comparison, mammal, urine, urination, wee, urethra, bladder, genital, waste, fluid, ecology, zoology

Subject

Science, biology, ST2-10LW, ACSSU044, SC4-14LW, ACSSU111, ACSSU150, SC5-14LW, ACSSU175

Did you know that scientists are using genetic engineering to turbo charge photosynthesis in plants?

World population is increasing and the UN predicts food production needs to double by 2050. Therefore, need to increase yield of crops.

Rubisco, possibly the most abundant enzyme on Earth, is critical for fixing CO₂ from the air and converting it to sugar (photosynthesis).

However, rubisco in crops is quite slow and inefficient.

Here they replaced the slow form of rubisco in crops (tobacco plants) with a much faster form from cyanobacteria using genetic engineering.

When CO₂ levels were high, this new form of rubisco provided much higher rates of CO₂ fixation (photosynthesis) than normal plants.

If the new form of rubisco could be combined with ways of increasing CO₂ levels in chloroplasts, this would effectively ‘turbocharge’ the rate of photosynthesis, greatly increasing crop yields and food production.

Do you want more information?

Background

World population is increasing and the UN predicts food production needs to double by 2050.

Therefore, need to increase the efficiency and yield of plant crops.

Photosynthesis in plants converts CO₂ from the air to sugar (glucose).

Rubisco, possibly the most abundant enzyme on Earth, is a key rate-limiting step for fixing CO₂ for photosynthesis.

However, rubisco can’t discriminate between CO₂ and O₂ in the air.

This wasn’t a problem when plants first evolved billions of years ago, when Earth’s atmosphere had high CO₂/low O₂ levels.

But now, O₂ levels are high (20%), reducing fixation of CO₂ into sugar.

Plants evolved two different ways to fix this problem:

1) Crop plants changed rubsico so that it uses CO₂ but not O₂, although it works much slower (30% reduction of photosynthetic efficiency).

2) Cyanobacteria, microalgae and weeds kept the faster form of rubisco, but developed CO₂-concentrating mechanisms (CCMs) that increase the local concentration of CO₂ around rubisco, increasing its efficiency.

Could the faster form of rubisco and CCMs be introduced into crop plants to increase photosynthetic efficiency and crop yields?

Materials and Methods

Here, scientists from the US and UK performed the first step. They used genetic engineering to replace the slow form of rubisco in a crop plant (tobacco) with a faster form from cyanobacteria.

Results

The authors successfully removed the tobacco plant’s own rubisco gene and replaced it with the rubisco from cyanobacteria.

The new plants couldn’t survive in normal air, because their new rubisco (from cyanobacteria) couldn’t distinguish between CO₂ and O₂. Therefore, the O₂ interfered with fixing CO₂ into sugar.

However, when CO₂ levels were increased (adding sodium carbonate), the plants survived and actually had higher rates of CO₂ fixation (photosynthesis) than normal plants.

Discussion

Introducing a faster, more efficient rubisco is the first step.

Second step is to introduce CCMs. That is, mechanisms for increasing the local concentration of CO₂ around rubisco in chloroplasts to drive the reaction faster.

If both were combined, this would ‘turbocharge’ photosynthesis in plants, greatly increasing crop yields and food production.

Article

A faster Rubisco with potential to increase photosynthesis in crops

Lin et al., 2014 Nature 513:547-50

Keywords

Plant, crop, cyanobacteria, tobacco, leaf, leaves, chloroplast, photosynthesis, rubisco, CO₂, carbon dioxide, O₂, oxygen, enzyme, catalyst, sugar, glucose, food, genetic, engineering, gene

Subject

Science, botany, agriculture, SC4-13ES, ACSSU116, SC5-13ES, ACSSU189, SC5-14LW, ACSSU176, SC5-15LW, ACSSU184, ACSSU185, SC5-17CW, ACSSU178, ACSSU179, ACSSU187

White tigers have been bred for circus/magician shows for over 50 years.

They have white fur, dark stripes, blue eyes, pink nose and pink paw pads.

Now, scientists have discovered the mutation that causes the white colour.

Mutation of a gene called SLC45A2 reduces the production of pheomelanine (red/yellow), but not eumelanin (brown/black).

Therefore, the tigers retain their dark stripes, but do not produce the characteristic orange colour of a tiger and are instead white.

This mutation is recessive, so the tigers must have 2 mutant genes (alleles) to become white.

This study serves as an interesting case study for Mendelian genetics.

Do you want more information?

Background

White tigers have been seen in the wilds of India for the past 500 years.

They have white fur, dark stripes, blue eyes, pink nose and pink paw pads.

The last one seen in the wild was shot dead by hunters in 1958.

A white tiger captured in 1951 was bred to create other white tigers that have been kept as exotic pets in captivity (e.g. circus/magician shows).

These captive white tigers have several health defects, such as stillbirths and deformities. Therefore, it was assumed it was a genetic deformity.

White tigers are not albinos. Their colour (like many animals) is due to a change in the balance of levels of pheomelanin (red/yellow) and eumelanin (brown/black).

So what is the genetic mutation that causes tigers to be white?

Materials and Methods

The authors analysed the genome of 16 captive white tigers and compared it to 130 non-white tigers, looking for differences between the 2 groups that might cause the white colour.

Results

The major/causative difference in genomes between white and control tigers was discovered in a gene called SLC45A2.

This mutation is recessive. That is, a tiger must have 2 mutant forms (alleles) of the gene to become white (ww). If they have 1 mutant allele and 1 normal (Ww), they will not be white.

The protein produced by the SLC45A2 gene is found in cell membranes and has a central pore/channel for transporting sugars/protons.

The genetic mutation changes the amino acid at position 477 from an alanine to a valine.

This partially blocks the channel, reducing transport of sugars/protons.

This reduces production of pheomelanin (red/yellow), but not eumelanin (brown/black).

Discussion

Since the A477V mutation in SLC45A2 reduces production of pheomelanin (red/yellow), but not eumelanin (brown/black), the white tigers retain their dark stripes, but do not produce the characteristic orange colour of a tiger and are instead white.

Article

The genetic basis of white tigers

Xu et al., 2013 Current Biology 23:1031-5

Keywords

Gene, genetic, genome, GWAS, sequencing, mutation, polymorphism, SNP, DNA, melanin, colour, tiger, cat, pigment

Subject

Science, biology, ST1-10LW, ACSSU017, SC5-15LW, ACSSU184