English bulldogs are at a genetic dead end, study finds
By Josh Hrala

Researchers have found evidence to suggest that English bulldogs – a breed known for short snouts and tiny, wrinkled bodies – are so genetically similar to one another, it’s impossible for breeders to make them healthier.

This ‘genetic dead end’ means that breeders will likely have to breed bulldogs - the fourth most popular breed in America - with different breeds if they want future generations to continue without major health issues.

“The English bulldog has reached the point where popularity can no longer excuse the health problems that the average bulldog endures in its often brief lifetime,” team leader Niels Pedersen from the University of California, Davis School of Veterinary Medicine, said in a statement.

“More people seemed to be enamoured with its appearance than concerned about its health. Improving health through genetic manipulations presumes that enough diversity still exists to improve the breed from within, and if not, to add diversity by outcrossing to other breeds,” he said. “We found that little genetic 'wiggle room’ still exists in the breed to make additional genetic changes.”

The team examined 102 English bulldogs - 87 from the US and 15 from elsewhere around the world - and made genetic comparisons to a set of 37 other English bulldogs that were brought to the UC Davis School of Veterinary Medicine because of health issues.

They found that the bulldogs lacked that genetic diversity needed for breeders to selectively breed individuals with healthier phenotypes, which means there’s little hope for breeders to create a healthier bulldog unless they crossbreed them.

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Scientists say money from ALS Ice Bucket Challenge led to new gene discovery
Scientists hope discovery will provide another potential target for therapy development

The Ice Bucket Challenge that went viral two years ago, raising hundreds of millions of dollars, has helped identify a new gene behind the neurodegenerative disease ALS, or Lou Gehrig’s disease, researchers say.

The challenge involved people pouring ice-cold water over their heads, posting video on social media, and donating funds for research on the condition, whose sufferers include British physicist Stephen Hawking.

Millions of people worldwide took part in the challenge in 2014, attracting more than 400 million views on social media.

The challenge raised $220 million US worldwide, according to the Washington-based ALS Association.

News of the gene discovery again sent Ice Bucket Challenge viral, proving one of the top trending topics on Twitter on Wednesday.

The money funded the largest ever study of inherited ALS and identified a new gene, NEK1, that ranks among the most common genes that contribute to amyotrophic lateral sclerosis, the ALS Association said in a statement.

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Gene Editing Is Now Cheap and Easy—and No One Is Prepared for the Consequences
No one is prepared for an era when editing DNA is as easy as editing a Microsoft Word document.

In April 2015, a paper by Chinese scientists about their attempts to edit the DNA of a human embryo rocked the scientific world and set off a furious debate. Leading scientists warned that altering the human germ line without studying the consequences could have horrific consequences. Geneticists with good intentions could mistakenly engineer changes in DNA that generate dangerous mutations and cause painful deaths. Scientists — and countries — with less noble intentions could again try to build a race of superhumans.


How a single gene can influence your emotional reactions

Serotonin is one of the major neurotransmitters (i.e. chemicals) in the brain. It’s very connected to our emotions and so it’s not a coincidence that a lot of the drugs that are used to treat depression and anxiety act on the serotonin system in the brain. This is clearly a very important chemical for determining the nature of our emotional lives.

The serotonin transporter gene is involved with the regulation of serotonin in the brain. People are born with variations of this gene. The long variation (or “allele”) clears serotonin out of the neural synapse more efficiently. The short variation is less efficient, which lets the serotonin hang around a little bit longer in the synapse.

The short variation was originally considered a risk gene because it was associated with depression and anxiety — but it’s now being thought of as a sensitivity gene.

Do you have the emotional sensitivity gene?

How elephants avoid cancer

Elephants have evolved extra copies of a gene that fights tumour cells, according to two independent studies1, 2 — offering an explanation for why the animals so rarely develop cancer.

Why elephants do not get cancer is a famous conundrum that was posed — in a different form — by epidemiologist Richard Peto of the University of Oxford, UK, in the 1970s3. Peto noted that, in general, there is little relationship between cancer rates and the body size or age of animals. That is surprising: the cells of large-bodied or older animals should have divided many more times than those of smaller or younger ones, so should possess more random mutations predisposing them to cancer. Peto speculated that there might be an intrinsic biological mechanism that protects cells from cancer as they age and expand.

At least one solution to Peto’s paradox may now have been found, according to a pair of papers independently published this week. Elephants have 20 copies of a gene called p53 (or, more properly, TP53), in their genome, where humans and other mammals have only one. The gene is known as a tumour suppressor, and it snaps to action when cells suffer DNA damage, churning out copies of its associated p53 protein and either repairing the damage or killing off the cell.

Abegglen, L. M. et al. J. Am. Med. Assoc. (2015).

Sulak, M. et al. Preprint at bioRxiv (2015).

Multiple copies of a tumour-suppressor gene help elephants avoid cancer. Theo Allofs/Minden Pictures/FLPA

Color Wheel Expansion

Thanks for joining us for the fun tonight! I think we’ve kept the lid on this for long enough…

Our engineering team has been working on new tools to help us generate and implement genes in a much faster and more efficient manner that does not sacrifice the image and color quality we’ve come to value as part of our site’s style. These tools are being developed to make future gene implementation much easier, but also come with the added benefit of allowing us to expand our color wheel without also increasing artist workload exponentially.

We are currently working on converting our existing breed art templates into ones that will be compatible with our new tools. Every time we finish 10, we will be revealing a color. Some will be old, some will be new.

To answer your questions:

  • We are intending to only expand the color wheel once, as we would like to minimize the disruption to player’s breeding ranges.
  • New colors will go between existing colors on the wheel so that they are in places that make sense for their range. We will not reshuffle the wheel, and your ranges will remain close to the same, but expanded.
  • New colors will ONLY be able to be bred, hatched, and scattered for.
  • Example: If you had a Rose to Magenta range, you’re not suddenly going to have a green in there. It will be more pinks.
  • To remain fair to all of our players, only the original 67 colors will be available during account registration and new dragon creation.

Fake Tertiary Gene: Leaf

- The Leaf tertiary grants a dragon extra camouflage from enemy’s and prey. It has only recently been breed for a wider range of colors in designer dragons. Dragons in colder climates shed their leaves during the winter. For the leaves to remain lush and colorful these dragons must supplement their diet with iron and potassium. 

I drew this gene while in class and thought “oh if their can be gems on dragons, why not leaves?” I have to admit the line art is a bit rough but overall wouldn’t a leaf gene be the coolest?

Neanderthal genes could be to blame for a number of health problems

Interbreeding between our early human ancestors and Neanderthals happened a lot. As a result, up to 4% of modern non-African people’s DNA is inherited from Neanderthals — a discovery made in 2010.

Still, scientists didn’t know how that lingering Neanderthal DNA affected our present biology — until now. It turns out, having that DNA could make you more prone to a number of health problems, including depression, heart attacks and one form of addiction.

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Mom’s in control – even before you’re born

Researchers have uncovered a way in which information contained in unfertilised eggs influences the development of the fetus and placenta during pregnancy. 

The research, performed in mice, indicates that even before conception a mother’s health may influence the health of her fetus. 

Epigenetic information is critical for determining which genes are turned on and off in our DNA. 

The researchers discovered that some epigenetic ‘marks’ laid down in eggs during their development in the ovaries and after fertilisation are passed onto the fetus and placenta. 

The findings suggest that mothers have the genetic tools to control the growth of their offspring during pregnancy by instructing placental development.

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Image credit: lunar caustic 

Scientists identify schizophrenia’s “Rosetta Stone” gene

Scientists have identified a critical function of what they believe to be schizophrenia’s “Rosetta Stone” gene that could hold the key to decoding the function of all genes involved in the disease.

The breakthrough has revealed a vulnerable period in the early stages of the brain’s development that researchers hope can be targeted for future efforts in reversing schizophrenia.

In a paper published today in the journal Science, neuroscientists from Cardiff describe having uncovered the previously unknown influence of a gene in ensuring healthy brain development.

The gene is known as ‘disrupted in schizophrenia-1’ (DISC-1). Past studies have shown that when mutated, the gene is a high risk factor for mental illness including schizophrenia, major clinical depression and bipolar disorder.

The aim of this latest study was to determine whether DISC-1’s interactions with other proteins, early on in the brain’s development, had a bearing on the brain’s ability to adapt its structure and function (also known as ‘plasticity’) later on in adulthood.

Many genes responsible for the creation of synaptic proteins have previously shown to be strongly linked to schizophrenia and other brain disorders, but until now the reasons have not been understood.

The team, led by Professor Kevin Fox from the University’s School of Biosciences, found that in order for healthy development of the brain’s synapses to take place, the DISC-1 gene first needs to bind with two other molecules known as ‘Lis’ and ‘Nudel’.

Their experiments in mice revealed that by preventing DISC-1 from binding with these molecules - using a protein-releasing drug called Tamoxifen at an early stage of the brain’s development – it would lack plasticity once it grows to its adult state, preventing cells (cortical neurons) in the brain’s largest region from being able to form synapses.

The ability to form coherent thoughts and to properly perceive the world is damaged as a consequence of this.

Preventing DISC-1 from binding with ‘Lis’ and ‘Nudel’ molecules, when the brain was fully formed, showed no effect on its plasticity. However, the researchers were able to pinpoint a seven-day window early on in the brain’s development - one week after birth - where failure to bind had an irreversible effect on the brain’s plasticity later on in life.

“We believe that DISC-1 is schizophrenia’s Rosetta Stone gene and could hold the master key to help us unlock our understanding of the role played by all risk genes involved in the disease,” said Professor Fox.

“The potential of what we now know about this gene is immense. We have identified a critical period during brain development that directs us to test whether other schizophrenia risk genes affecting different regions of the brain create their malfunction during their own critical period.

“The challenge ahead lies in finding a way of treating people during this critical period or in finding ways of reversing the problem during adulthood by returning plasticity to the brain. This, we hope, could one day help to prevent the manifestation or recurrence of schizophrenia symptoms altogether.”

Professor Jeremy Hall, an academic mental health clinician and director of the University’s Neuroscience and Mental Health Research Institute, said:

“This paper provides strong experimental evidence that subtle changes early on in life can lead to much bigger effects in adulthood. This helps explain how early life events can increase the risk of adult mental health disorders like schizophrenia.”

Schizophrenia affects around 1% of the global population and an estimated 635,000 people in the UK will at some stage in their lives be affected by the condition. The projected cost of schizophrenia to society is around £11.8 billion a year.

The symptoms of schizophrenia can be extremely disruptive, and have a large impact on a person’s ability to carry out everyday tasks, such as going to work, maintaining relationships and caring for themselves or others.