#not equine

[equine-science]

[E]volution is not a flawless engine, continually driving living things onwards to make better and better versions of themselves in the generations that come after. This misconception comes about as a result of the way that evolution is often described, especially in school. We’re taught that a DNA sequence gets altered, creating some kind of change in the resulting organism. If this is advantageous, then these genetic changes get to stay in the population. If they’re not, they get ditched. Over time the useful variation might even become the only version of that part of the genome in the whole species, like the missing control switch in the hipless lake-dwelling sticklebacks from Chapter 7. Evolutionary biologists refer to this as ‘fixing’ a trait. This process is natural selection at its finest – survival of the fittest and all that. And while this is certainly one way that genes shift and change over time, it’s not the only one. Things aren’t as clear cut as a school biology class might make them out to be. That’s because evolution doesn’t really care whether you’re the bestest, fittest organism you can possibly be. All it cares about is that you get laid and pass your genes on. You could have a genetic variation that makes you 10 times smarter than everyone else, but if you spend all of your time in the library instead of trying to meet someone of the opposite sex and make babies with them, your brilliant genes will die with you. All the time, random changes are happening in our genomes that get passed on to the next generation. Some of them are handy, some of them are positively damaging, while most are just neutral – the genetic equivalent of a Gallic shrug. Bof. Whatever. Due to the vagaries of life and love, the proportion of some of these neutral variations will increase in the population, despite not being actively advantageous, while others fade away. This is known as genetic drift, conjuring up a nice image of a random tide of DNA variations ebbing and flowing through time, with as little purpose or direction as the sea splashing on the shore. This vision of genetics is a stark contrast to the analogies that started to come forward in the 1970s in the wake of the twin revolutions in molecular biology and electronics. Everyone was buzzing with the idea of DNA as a form of computer code or blueprint, with genes forming neat regulatory circuits that could be pulled apart and put back together again. Although this view of genetics-as-electronics was helpful in some ways, time has shown that it was deeply flawed in many others. Real life is a long way from mimicking the tidy precision of a pre-printed circuit board. Our genome was not designed by an engineer, plotting out the most sensible way to make protein X or respond to signal Y. It was bodged and pasted together, not needing to be great, but just good enough to make a human that can pass it on. Probably the thing that has struck me the most is how consistently this process works, despite the fact that it’s driven by essentially stochastic (i.e. chaotic) chemical interactions. As I learned from people like Wendy Bickmore with her baubles and Ben Lehner with his wobbly worms, when you get right down to the level of the writhing DNA and blobby proteins inside a single cell’s nucleus, physics takes over from biology. The interactions between control switches and transcription factors are flaky, and it’s a matter of chance that the right things will come together at the right time. Obviously things have evolved so there’s a pretty good chance that it’ll happen, otherwise we wouldn’t be here, but it’s still a statistical event rather than a guaranteed one. Engineers, mathematicians and religious believers hate this idea, maintaining that a better understanding of the complexities of DNA will explain exactly how it all works (or that we’ll give up and just accept that God did it). But it won’t, in my view. Not completely. We live in a world driven by probabilities, not certainties.2 All too often genetics is sold to the public as solid fact: this gene does this, that gene does that. Yet as I’ve spoken to scientists in the course of my travels, it’s become increasingly clear to me that there’s a huge amount we don’t know about how our genes work. There may well be things we can never know. But the pace of change is accelerating rapidly, and there’s talk of entering a ‘golden age’ of genomics where high-speed, cut-price gene sequencing will finally lay open more of the mysteries in our DNA.

Herding Hemingway's Cats: Understanding How Our Genes Work by Kat Arney

[equine-science]

It’s not just fish hips and cat thumbs that are the result of small changes in genetic control switches. David Kingsley has also discovered a few human traits that work in the same way, with the most immediately obvious being skin and hair colour. A few years back, he and his team discovered that the DNA around a gene called Kitlg, found in many animals including both sticklebacks and humans, seemed to be chock-full of control switches. The protein encoded by Kitlg (known as Kit ligand) is a biological multi-tasker, helping to make blood, sperm and cells packed full of the dark pigment melanin. It’s this molecule that determines your coloration. More melanin and you’ll be darker, less and you’ll be lighter. Kingsley and his team discovered that playing with these switches in sticklebacks changed their coloration, making them darker or lighter depending on which ones were missing. So they took the same DNA region from humans and broke it down into pieces, testing each one to find out when and where it was active. Sure enough, they tracked down one specific control switch that could turn on the gene only in skin and hair. Then when they looked at the DNA sequence of this switch in West Africans and white Europeans, they noticed a consistent difference in a region more than 300,000 letters (300 kilobases) away from Kitlg. Not as far as the distance between Sonic Hedgehog and its limb control switch, but still a long way off. One single letter was switched: an A in the Africans, a G in Europeans. Just one. Next, they tested whether this change affected how well the switch could turn on Kitlg, by looking at the two different versions in skin cells grown in the lab. They discovered that it wasn’t as simple as an on/off (or rather, black/white) switch. Instead, the version in Europeans wasn’t quite as effective at activating the gene as the African version was. A quick calculation in their paper suggests that having two copies of Kitlg with the European switch makes a person’s skin around six or seven shades lighter than someone with two West African versions. Because you have two copies of every gene – one from Mum and one from Dad – the effects of the switches will be more apparent if they are both the same, while having one of each will give a colour somewhere in the middle. However, there are around 30 shades between a typical Nigerian’s dark skin and a pale European complexion, so the difference in the Kitlg switch only explains part of our skin colour, rather than the whole thing. David suspects that there are probably other similar genes and switches out there that add up to give each person their particular hue. But even so, just a single letter can make a big difference to what you look like. This is true of hair colour as well as skin. In 2014 Kingsley and his team published another paper showing that European blondes have a single letter difference in a control switch around 350,000 DNA letters (350 kilobases) away from the Kitlg gene, compared to dark-haired people. Again, it’s a tiny change miles away from the gene, but it has a big impact. This subtle alteration in blondes means that a transcription factor protein called Lef can’t stick quite as well to the DNA of the control switch, so it’s not as effective at turning on Kitlg activity. It’s not on/off, but it’s enough to significantly cut down the melanin production in hair cells, and make them fair. Growing up in the 1980s, I would often hear jokes about blondes being stupid – and as a brunette (to my shame) I would often repeat them. I now know better, but many people apparently don’t. In a news article about his hair colour research, Kingsley attacked this long-held stereotype, saying, ‘It’s clear that this hair colour change is occurring through a regulatory mechanism that operates only in the hair. This isn’t something that also affects other traits, like intelligence or personality. The change that causes blonde hair is, literally, only skin deep.’ Blonde jokes aside, his work on coloration has more profound implications. As I’m writing this chapter, the United States is fracturing under the stress of racial tension following several high-profile incidents of white police officers killing unarmed black people, and a horrific racist shooting in a church. Countless numbers have been unfairly judged, oppressed or killed throughout history because of the colour of their skin, yet it boils down to little more than a handful of DNA letters in a few genetic switches. For a species named after our intelligence – Homo sapiens translates as ‘man who knows’ – we really are very stupid at times."

Herding Hemingway's Cats: Understanding How Our Genes Work by Kat Arney

[equine-science]

'Then there’s the evolutionary problem,’ Mark tells me. ‘We have roughly the same number and essentially the same genes, let’s say, as a chimpanzee. And the difference between our actual protein-coding genes and any other mammal’s is extremely small. Contrary to what people assumed, a large part of evolution has nothing to do with changing what the genes encode, or the nature of the protein they make. It has to do with changing how they’re regulated.... So, now we look inside the genome and we see these areas of DNA that encode proteins and we call them genes. Then lying between the genes in the so-called dark matter are these things that we could roughly call the genetic switches. And they determine whether the gene is on or off. But they do so by virtue of what proteins bind to them at any given time.’ It’s these proteins, the transcription factors, that create an enticing platform to attract the gene-reading RNA polymerase. Once the polymerase is there, it starts copying out the gene into RNA – et voilà (as Jacob and Monod might have put it), the gene is switched on and active. ‘The astounding thing is that the basic mechanism by which you turn a gene on is so simple – it’s just combinations of proteins binding to these switches. For years and years scientists have been, like “Oh, we always knew that that!”, but they didn’t.’ [...] 'This kind of set-up makes it plausible that evolution can change species over time – something we’ll come back to later – creating the incredible diversity of life we see today. ‘You’re taking the same genes, but just by moving these sites – the switches – from one gene to another you change when it’s active. All the proteins do is bind to the switches and recruit the RNA reading machine to the gene. In higher organisms you can have a whole bunch of these switches. And one will work, and another will work, and so on, and you can mix them up.... So what you do is produce complexity by combinatorial use of these bits. You change the specificity, change the order of the pieces, and you get new kinds of organisms.'

Herding Hemingway's Cats: Understanding How Our Genes Work by Kat Arney

[hoofstomper]

y'ever feel like a deer but not a deer but you're a ram but you're not and you don't think you have split hooves but you also feel like you have the sheep head but you don't but you do but. what

[takebacktheyuri]

Matagi taur girls anyone ?

[equine-science]

Part of the reason for my semi-hiatus is that I have been working a lot with shelter dogs (and sometimes cats and birds and, on one notable occasion, ferrets), and recently adopted a second dog. I may also be getting a job in a small animal shelter, so I’m reading up. Also, for the first time in 20+ years, I haven’t been able to afford regular riding in almost a year. So unfortunately, equine stuff has taken a back seat.

If anyone is interested, I’ve started a dog blog.

http://poofandnub.tumblr.com/

To include pictures/videos of my dogs, pictures/videos of shelter dogs, quotes from dog books I read, and dog articles. And probably other stuff.

- Q

[equine-science]

An entomologist named Alan A. Berryman addressed it some years ago in a paper titled "The Theory and Classification of Outbreaks." He began with basics: "From the ecological point of view an outbreak can be defined as an explosive increase in the abundance of a particular species that occurs over a relatively short period of time." Then, in the same bland tone, he noted: "From this perspective, the most serious outbreak on the planet earth is that of the species Homo sapiens." Berryman was alluding, of course, to the rate and the magnitude of human population growth, especially with the last couple centuries. He knew he was being provocative. But the numbers support him. At the time Berryman wrote, in 1987, the world's human population stood at 5 billion. We had multiplied by a factor of about 333 since the invention of agriculture. We had increased by a factor of 14 since just after the Black Death, by a factor of 5 since the birth of Charles Darwin, and by doubling within the lifetime of Alan Berryman himself. That growth curve, on a coordinate graph, looks like the southwest face of El Capitan. Another way to comprehend it is this: From the time of our beginning as a species (about 200,000 years ago) until the year 1804, human population rose to a billion; between 1804 and 1927, it rose by another billion; we reached 3 billion in 1960; and each net addition of a billion people, since then, has taken only about thirteen years. In October 2011, we came to the 7-billion mark and flashed past like it was a "Welcome to Kansas" sign on the highway. That amounts to a lot of people, and certainly qualified as an "explosive" increase withing Berryman's "relatively short period of time." The rate of growth has declined within recent decades, true, but it's still above 1 percent, meaning we're adding about 70 million people yearly. ... And here's the thing about outbreaks: They end. In some cases they end after many years, in other cases they end rather soon. In some cases they end gradually, in other cases they end with a crash. In certain cases, even, they end and recur and end again, as though following a regular schedule. Populations of tent caterpillars and several other kinds of forest lepidopterans seem to rise steeply and fall sharply on a cycle of anywhere from five to eleven years. A population of tent caterpillars in British Columbia, for instance, has shown a cycle like that dating back to 1936. The crash endings are especially dramatic and for a long while they seemed mysterious. What could account for such sudden and recurrent collapses? One possible factor is infectious disease.  ... The Next Big One [pandemic] could very well be flu. Greg Dwyer knew this, which is why he mentioned it. I'm sure you don't need reminding that the 1918-1919 flu killed about 50 million people; and there's still no magical defense, no universal vaccine, no foolproof and widely available treatment, to guarantee that such death and misery don't occur again. Even during an average year, seasonal flu causes at least 3 million cases and more than 250,000 fatalities worldwide. So influenza is hugely dangerous, at best. At worst, it would be apocalyptic. ... None of them [disease scientists] has disputed the premise, by the way, that if there IS a Next Big One it will be zoonotic. ... These scientists are on alert. They are our sentries. They watch the boundaries across which pathogens spill. And they are productively interconnected with one another. When the next novel virus makes its way from a chimpanzee, a bat, a mouse, a duck, or a macaque into a human, and maybe from that human into another human, and thereupon begins causing a small cluster of lethal illnesses, they will see it--we hope they will, anyway--and raise the alarm. Whatever happens after that will depend on science, politics, social mores, public opinion, public will, and other forms of human behavior. It will depend on how we citizens respond. So before we respond, either calmly or hysterically, either intelligently or doltishly, we should understand in some measure the basic outlines and dynamics of the situation. We should appreciate that these recent outbreaks of new zoonotic diseases, as well as the recurrence and spread of old ones, are part of a larger pattern, and that humanity is responsible for generating that pattern. We should recognize that they reflect things that we're DOING, not just things that are HAPPENING to us. We should understand that, although some of the human-caused factors may seem virtually inexorable, others are within our control.

Spillover: Animal Infections and the Next Human Pandemic by David Quammen