Silver fox displaying ‘domestication syndrome’ (Photo credit: luz rovira via Flickr)
In the 1950s, Russian fox fur breeder Dmitri Belyaev embarked on a monumental experiment in the Siberian city of Novosibirsk. He wanted to see if he could domesticate wild foxes by selectively breeding only the tamest in each generation. He was essentially trying to re-run thousands of years of history — dogs and many of our farm animals were domesticated several thousand years ago, and scientists are still debating exactly how this occurred.
The Novosibirsk experiment is noteworthy not only because it revealed that tameness could indeed be bred into a line of wild animals after only a few generations. Nor because the landmark experiment is still running, sixty years on. It is noteworthy because it has demonstrated another aspect of domestication that biologists since Charles Darwin have puzzled over — that domesticated animals aren’t just tame, but they are cute to boot. Many have floppy ears, baby faces and endearing patches of white fur that could well spell death for an animal in the wild. In the Novosibirsk experiment, foxes started looking more like pets over the generations, even though the sole criterion for selection was tameness.
A threesome of academics has now come up with a hypothesis that could explain why selecting for a docile behaviour bring with it the suite of physical characteristics known as ‘domestication syndrome.’ According to the hypothesis, it could all come down to a group of stem cells called neural crest cells. These cells form near the spinal cord and then march across the developing vertebrate embryo to form pigment-producing melanocytes; bone, cartilage and teeth in the skull; and portions of the adrenal gland and brain.
The question that this hypothesis raises is: could small changes to neural crest cell gene expression be at the centre of domestication syndrome’s disparate features? Experimental evidence will need to sort the answer out to that, but it’s an intriguing idea nonetheless.
I wrote a brief article on the paper for Cosmos — check it out here.
Vaccinating against polio (Image credit: Sanofi Pasteur via Flickr)
For most places in the world, the sight of children in leg calipers has been relegated to the pages of history. The paralysing effects of the poliovirus have become a thing of the past. The advent of the polio vaccine in the 1960s has seen polio progressively extinguished in well-off regions like North America, Australia and Europe, as well as in poorer parts of the world. Gradually — and with the dogged determination of coordinated vaccination teams — efforts to eradicate the disease have restricted its occurrence to just a handful of war-torn nations.
But as we await that final declaration that polio is no more, it’s perhaps a good time to reflect on how well we actually understand this mortal enemy. How does poliovirus infect? Why is it so debilitating? And will we, in fact, ever be able to rid the world forever of polio?
In the latest episode of Up Close I interviewed Vincent Racaniello, a virologist who’s investigated the intricacies of poliovirus infection. Vincent is Professor of Microbiology at Columbia University Medical Center and he’s also the creator of a number of science podcasts worth checking out including This Week in Virology, This Week in Microbiology and This Week in Parasitism.
Eastern Quoll (Photo credit: David Jenkins via Flickr)
Globally, fourteen percent of land is tied up in protected areas — national parks, nature reserves and the like — ostensibly to protect the world’s dwindling biodiversity. But how effective are these areas at actually preventing extinctions? Not very, according to a landmark study a decade ago that showed only a paltry 11% of threatened birds, mammals and amphibians were adequately protected. One fifth of the species weren’t found anywhere in network.
A decade on, protected areas have expanded, but a new study shows that the situation for the world’s most vulnerable species remains poor — many are still missing out.
So, what can we do? The new analysis suggests a way forward. By calculating the value of setting aside different packets of land, they found that instead of setting aside the cheapest land available — as mostly happens now — a slightly larger investment could improve the protected area network drastically.
I wrote about this study for Cosmos Magazine, so check out the full article here.
Our understanding of biological systems — including our own body — is largely based on laboratory studies. By looking at cells grown in petri dishes, or conducting experiments on animals, we can pick apart how biology works.
But how well do our lab techniques actually represent real life? In many cases, when candidate drugs make it to clinical trials we discover that promising outcomes in animals don’t always translate into the same in humans. Is there a better way — a more accurate way — of investigating human physiology in the lab that might also reduce our need for animal experimentation? This is the exciting promise of organs-on-a-chip.
To learn more about the exciting field of organ-on-chip technologies, I was joined on Up Close by Prof Donald Ingber, Founding Director of the Wyss Institute for Biologically Inspired Engineering at Harvard University. Don is also the Judah Folkman Professor of Vascular Biology at Harvard Medical School & Boston Children’s Hospital and Professor of Bioengineering at the Harvard School of Engineering & Applied Sciences.
Check out the interview as a podcast or transcript here.
Picasso’s ‘Girl before a mirror’ (Photo credit: Nathan Laurell via Flickr)
What is beauty? Is there an objective way of defining what it is that makes something beautiful, or is beauty — as the old cliché goes — in the eye of the beholder? These questions were, for centuries, the domain of philosophers and artists. Evolutionary biologists since Darwin have also speculated on the question of whether there are universal features of beauty that hold true for different species.
But it’s only been very recently that neurobiologists have stepped into the fray. With developments in brain imaging techniques, we can now start to ask, not only what do you find beautiful, but also, what’s actually going on in your brain when you lay eyes on a beautiful person, or a stunning landscape painting, or when you hear a spine-tingling piece of music?
I was joined on Up Close recently by a pioneer in the field of neuroesthetics, Professor Semir Zeki, Professor of neuroesthetics in the Department of Cell and Developmental Biology at University College London. Check out the interview here.
There’s an old video clip that many Australians are familiar with. In black and white, the last known thylacine – or Tasmanian tiger – quietly paces about its caged enclosure, reclines in the sun, yawns at the camera.The footage was recorded in 1933 at the Beaumaris Zoo in Hobart, and serves as an eerie reminder of just how final extinction is.
In her latest book, The Sixth Extinction: An Unnatural History, American journalist Elizabeth Kolbert takes us on a global tour of extinction, in all its finality, as well as while it is happening before our eyes. The focus of the book is the latest, human-induced wave of destruction creeping around the globe, but Kolbert has widened her investigative lens to enlighten us about the processes behind extinction, as much as its victims. Disparate tales of species collapse are united by an unflinching exploration of the science – and the scientists – dedicated to understanding their demise. Continue reading
(3 billion letter in the human genome – what are they all doing? Image: Adam Nieman via Flickr)
I’ve been really slow off the mark with this one. A couple of months ago, I wrote a feature for COSMOS magazine on junk DNA.
There’s still a lot of debate about what goes on in the vast stretches of our genome that doesn’t code for proteins. Evidence is mounting that there’s far more to our genome than protein coding genes, but how much of our genomic ‘dark matter’ is functional is unknown. While some people think that it’s just a matter of time before we assign function to the majority of our genetic sequences, others maintain that it just doesn’t make evolutionary sense for all of our genome to be useful. You can check out the full article (or even listen to it) here.