How do we decide who to protect? (photo credit: Rupert Ganzer via Flickr)
You don’t have to look far to find stories of species or ecosystems under threat. Whether it’s the critically endangered black rhinoceros in Africa, or the local wetlands under threat from urban sprawl, our collective failure to protect the world’s natural heritage can seem exasperating.
But in a world where resources to put toward protection are limited, making decisions about where to direct our efforts, or how to prioritise our donations, can be equally as frustrating. And it’s not just individuals who struggle with these choices — governments too are often faced with difficult decisions.
So how do we go about placing a value on our natural heritage? Should we even try to weigh the relative merits of saving one species or one ecosystem over another? And how can government policies help to guide us through the murky waters of environmental decision making?
To answers some of these questions, I was joined on Up Close recently by Brendan Wintle, a conservation ecologist who has been working with economists and policy makers to improve environmental decision making. Brendan is based at the School of Botany, at the University of Melbourne, and he’s also Deputy Director of the National Environmental Research Program Environmental Decisions Hub.
3D-printed model of a ribosome (photo credit: Steve Jurvetson via Flickr)
If I were to say the word ‘protein’, you’d probably think of a juicy steak, or perhaps a muscle-building protein shake. But in our bodies, proteins give us far more than just muscular bulk. They’re the enzymes that carry out cellular reactions — the microscopic sensors that allow us to detect the smell of a rose, or the pain of a burn. They’re the cement that connects our cells together, give our nose cartilage its rigidity and our skin its elasticity. And they serve all of these incredible functions in organisms from the lowly bacterium, to the majestic sequoia, and everything in between.
But proteins, in their myriad forms, could not exist without a complex piece of cellular machinery known as the ribosome. As important as it is, the ribosome — unlike the proteins it makes — is hardly a household name.
A few weeks ago on Up Close, I spoke to Ada Yonath, who won the Nobel Prize in Chemistry in 2009 for her pioneering work on the structure of the ribosome. She is now the Director of the Helen and Milton A. Kimmelman Center for Biomolecular Structure and Assembly at the Weizmann Institute of Science in Israel.
Tortoiseshell cats get their dappled colouration from X inactivation (photo credit: Tony Hammond via Flickr)
Our genetic make-up determines a lot about who we are – it determines whether we have blue eyes or brown, what blood group we have, or whether we’re predisposed to cystic fibrosis or sickle cell anaemia. But we’re beginning to learn that we’re far more than the sum of our genetic parts. Our genes only tell part of the story of who we are.
Just as important as what genes we’ve inherited from our parents, is how those genes are switched on and off throughout our lifetime. This complex system of genetic regulation has been the focus of the burgeoning field of epigenetics.
I was joined on Up Close recently by geneticist Marnie Blewitt. We chatted about epigenetics and her work on one of the coolest areas of epigenetics – X inactivation. Marnie heads a lab that studies epigenetics at the Walter and Eliza Hall Institute of Medical Research.
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.