Tiny molecules drove the evolution of the vertebrates

Blogging on Peer-Reviewed ResearchThe spinal column that runs down your back is an identity badge that signifies your membership among the vertebrates – animals with backbones. Vertebrates have arguably the most complex bodies and genomes of any animal group and certainly, our lineage has come a long way from its last common ancestor.

TigerThe closest evolutionary cousins of the vertebrates are simple aquatic creatures such as the jawless lancelets and the sac-like, immobile sea squirts. How did these simple body plans diversify into the vast array of sophisticated forms wielded by today’s fish, amphibians, reptiles and mammals?

Gene number

Many scientists have suggested that the answer lies in the number of our genes. At three different points, the vertebrate genome (its full suite of genes) experienced a massive jump in size as huge chunks of genes – possibly the entire lot – were duplicated. The first of these coincided with the origins of the group itself and the second happened alongside the rise of the first jawed fish, setting them and their descendants aside from more ancient jawless forms like the lampreys.

So far, there seems to be a tidy connection between gene number and complexity, but the third round of duplication is a bit of a stumbling block. It happened at some point during the evolution of the bony fishes and while this group proceeded to radiate into a multitude of different shapes, their basic body plan stayed essentially the same. No big jump in complexity there.

Indeed, as the full genome sequences of more and more species are revealed, it’s becoming clear that the basic genetic toolkit that controls the development of animal bodies is remarkably consistent across the kingdom. Even the genome of a sea anemone, one of the simplest and most ancient animals on Earth, is strikingly similar to that of vertebrates.

In this light, it’s looking increasingly unlikely that the advent of new genes can account for the large rise in vertebrate complexity. Now, Alysha Heimberg and colleagues from Dartmouth College have proposed a new theory, centred around tiny molecules called microRNAs.

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Third cousin couples have the most children and grandchildren

Blogging on Peer-Reviewed ResearchMarriage between closely related cousins is a heavy taboo in many cultures and its critics often cite the higher risk of genetic diseases associated with inbreeding. That risk is certainly apparent for very close relatives, but a new study from Iceland shows that very distant relatives don’t have it easy either. In the long run, they have just as few children and grandchildren as closely related ones.

Shuffling the genetic deck

Indian marriageSex chromosomes aside, every person has two copies of each gene, one inherited from their father and one by their mother. Not every gene will be in correct working order, but there’s a good chance that a faulty copy will be offset by a functional one from the other parent.

However, if two parents are closely related, there’s a higher-than-average chance that they will already share some of the same genes and a similarly increased chance that their child will receive two defective copies. That can be very bad news indeed and in cases where important genes are affected, the results can include miscarriage, birth defects or early death.

Sex, then, is a shuffling of their genetic deck and theoretically the more closely related the partners are, the greater the chance that their child will be dealt a dud hand. And yet, some studies have found that some closely related couples actually do better than distant relatives in terms of the number of children they manage to raise. This trend is certainly unexpected and the big question is whether it is the result of biology or money.

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Editing Ebola – how to tame one of the world’s deadliest viruses

Blogging on Peer-Reviewed ResearchIn a list of the most dangerous jobs in the world, ‘Ebola researcher’ must surely rank near the top. But if new research is anything to go by, it may soon fall several places. An international team of scientists have recently found a way to neuter the virus, making it easy to study without risking your life. The altered virus looks like Ebola and behaves like Ebola, but it can’t kill like Ebola. It should make studying the virus easier and most importantly, safer.

Ebola virusThe Ebolaviruses and their cousins, the closely related Marburg family, have a chilling and deserved reputation. In some outbreaks, 90% of those infected die from massive blood loss. There is no approved antiviral treatment. There is no vaccine. And given that it’s almost a rite du passage for infectious disease scientists to contract the contagion they study, working with Ebola is a delicate affair.

Maximum protection

Ebola research requires the highest level of safety possible – the “Biosafety Level-4” laboratory. The stand-alone facilities are designed to be easily sealed and impervious to animals and insects. All routes in and out, including all pipes and ventilation, are peppered with multiple airlocks, showers and rooms designed to prevent any chance of escaping viruses.

There are very few people who are qualified to work in such a prohibitive environment and those that do have to wear a Hazmat suit at all times and breathe from a self-contained oxygen supply. No wonder then that the majority of Ebola research doesn’t actually use live, infectious viruses.

Scientists must instead settle with isolated proteins, proteins shoved into other, less harmful viruses or even “virus-like particles”. But these artificial systems are different to the virus proper, and using them is like staring at a complex machine through a cobweb-covered keyhole. Peter Halfmann from the University of Wisconsin has found a way around this, opening the door for scientists to get a proper look at the virus.

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Cross-breeding restores sight to blind cavefish

Blogging on Peer-Reviewed ResearchIn the caves of Mexico lives a fish which proves that a million years of evolution can be undone with a bit of clever breeding.

Blind cavefishThe blind cavefish (Astyanax mexicanus) is a sightless version of a popular aquarium species, the Mexican tetra. They live in 29 deep caves scattered throughout Mexico, which their sighted ancestors colonised in the middle of the Pleistocene era. In this environment of perpetual darkness, the eyes of these forerunners were of little use and as generations passed, they disappeared entirely. They now navigate through the pitch-blackness by using their lateral lines to sense changes in water pressure.

But there is a deceptively simple way of restoring both the eyes and sight that evolution has taken, and Richard Borowsky from New York University’s Cave Biology Research Group has found it. You merely cross-bred fish from different caves.

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Songbirds need so-called “human language gene” to learn new tunes

Blogging on Peer-Reviewed ResearchThe nasal screech of Chris Tucker sound worlds apart from the song of a nightingale but both human speech and birdsong actually have a lot in common. Both infants and chicks learn their respective tongues by imitating others. They pick up new material most easily during specific periods of time as they grow up, they need practice to improve and they pick up local dialects. And as infants unite words to form sentences, so do songbirds learn to combine separate riffs into a full song. Songbirds need so-called “human language gene” to learn new tunes

Because of these similarities, songbirds make a good model for inquisitive neuroscientists looking to understand the intricacies of human speech. Zebra finches are a particularly enlightening species and they have just shown Sebastian Haesler that the so-called human ‘language gene’ FOXP2 also controls an songbird’s ability to pick up new material.

FOXP2 has a long and sordid history of fascinating science and shoddy science writing. It has been consistently mislabelled as “the language gene” and after the discovery that the human and chimp versions differed by just two small changes, it was also held responsible for the evolution of human language. Even though these claims are far-fetched (for reasons I’ll delve into later), there is no doubt that faults in FOXP2 can spell disaster for a person’s ability to speak.

Mutated versions cause a speech impairment called developmental verbal dyspraxia (DVD), where people are unable to coordinate the positions of their jaws, lips, tongues and faces, even though their minds and relevant muscles are in reasonable working order. They’re like an orchestra that plays a cacophony despite having a decent conductor and tuned instruments.

Brain scans of people with DVD have revealed abnormalities in the basal ganglia, an group of neurons at the heart of the brain with several connections to other areas. Normal people show strong activation of FOXP2 here and fascinatingly, so do songbirds. Haesler reasoned that studying the role of this gene in birds could tell him more about its human counterpart.

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Human skin cells reprogrammed into stem cells

Blogging on Peer-Reviewed ResearchPotential is a sad thing to lose. Have you ever thought that it would be great to return to your childhood, when your options seemed limitless and life hadn’t taken you down increasingly narrow corridors of possibility? Wouldn’t it be great to rewind the clock and have the choice to start over?

Human skin cells are reprogrammed into stem cellsWhile that’s still the stuff of science-fiction, for some cells in your body it may soon be science fact. In one of the most exciting scientific breakthroughs of the year, two groups of scientists have found a way of turning adult human cells back into the stem cells of embryos.

Creating embryonic stem cells

Embryonic stem cells are the embodiment of potential. Armed with a trait called ‘pluripotency‘, they can give rise to every single type of cell and tissue in the body, renewing themselves indefinitely while their daughters take up the mantle of nerves, muscles, blood and more.

For years, stem cells have been touted as the Holy Grail of modern medicine. Within their membranes lies the potential to understand how we develop, test new drugs and most importantly, provide replacement cells to treat Alzheimer’s, Parkinson’s, spinal cord injuries, diabetes, stroke and more.

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Metabolic gene and breastfeeding unite to boost a child’s IQ

Blogging on Peer-Reviewed ResearchBreastfed babies have higher IQs if they have the ‘C’ version of the FADS2 gene.The nature-nurture debate is one of the most famous in biology, but its own nature has shifted substantially in recent years. We now know that genes and environment are not opposing agents that shape our lives separately, but partners walking hand-in-hand. More often than not, genes affect our bodies and behaviour by altering the ways in which we react to our environment.

Now, an international team of researchers have discovered a stark example of this gene-environment partnership. They found that breastfed children have higher IQ scores, but only if they have a certain version of a gene called FADS2.

The concept of IQ has been central to the nature-nurture debate for years, ever since studies in twins suggested that a large part of the variation in IQ scores could be explained through inherited genetic factors. Avshalom Caspi and Terrie Moffitt from King’s College London wanted to kill this tiresome debate finding a gene that affected IQ via the environment.

They chose to look at breastfeeding, as studies have mostly found that babies who drink their mothers’ milk have higher IQ scores, among other benefits. These higher scores persist into adulthood and across social classes. We also have a reasonable idea of how breastfeeding could affect brain development at a molecular level, and it involves fatty acids.

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