Mass whale strandings aren’t all in the family

Each year, more than a thousand marine mammals die during mass strandings, which are grisly events in which large numbers of whales or dolphins become beached on the shore together. But scientists still don’t know exactly why these strandings occur. Climatic events, unfamiliar underwater topography, and noise from seismic surveys and naval exercises have all been suggested to play a role. In another theory based on family ties, one or a few whales, driven by disease or starvation, veer off in the wrong direction and draw well-meaning family members into shallow, dangerous waters as they try to help.

However, a paper in this week’s Journal of Heredity suggests that the role of relatives in mass strandings may not be quite so straightforward.

The researchers collected skin samples and information about the spatial distribution of 490 long-finned pilot whales stranded in 12 events across New Zealand and Tanzania. By studying the whales’ mitochondrial DNA (a type of genetic information passed on from mother to offspring), the researchers could determine how closely-related the stranded animals were.

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Wetware advances: Biological logic gate built by splitting viral gene

MIT

In recent years, researchers in the messy world of biology have been able to build systems that function like the clean, binary switches on computer chips—and we've covered a number of reports in this area. Unfortunately, most of these share a significant limitation: they rely on proteins from bacteria that act as switches to turn genes on and off under specific conditions. We know about only a limited number of these genetic switches, which may set a severe limit on the number of logical operations we can string together inside a cell.

A paper in this week's PNAS describes a system that may allow us to get around this limitation. The new method takes a protein from a virus that infects bacteria and cuts it in two, making a pair of genes (A and B) that each produce part of the mature protein. The two parts then act as a biological version of an AND logic gate, with output (in the form of protein activity) present only when both A and B interact. When either or both A and B are missing, the output is off.

In biological terms, the inputs usually involve a simple molecule that can be sensed by proteins inside a bacteria. This paper, for example, used two kinds of sugars (arabinose and lactose). When the sugars are present, they attach to proteins inside the cell, activating genes that are controlled by those proteins. To make an AND gate, you need to design a bit of biology that can respond to both of these signals—it should be active only when both a gene regulated by arabinose and a gene regulated by lactose are each active.

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Polynesians reached South America, picked up sweet potatoes, went home

An artist's depiction of the canoes used by the Polynesians of the Hawaiian islands.

Hawaii.edu

The sweet potato was one of a number of crops domesticated in the Andes and, like many of the rest, it became a global crop in the colonial era. But there were some hints that the sweet potato may have already started its global sweep before the Europeans ever took a bite out of one. Some of the early European explorers, including Captain Cook, reported finding it in places like Hawaii. All of which implies that the Polynesians, who managed to spread widely across the Pacific, had made it all the way to South America.

But it was difficult to be sure, given that European travelers later enhanced its spread within the Pacific and elsewhere. This has also created a complex genetic legacy that obscures its origins. Now, researchers have gone back and obtained DNA from museum samples, including some collected by Cook's crew, and find that the DNA indicates that Polynesians made it as far as South America.

Archeological remains appear to place sweet potato cultivation in the core of Polynesia by the year 1200, and it spread with further migrations to places like New Zealand and Hawaii. It's possible that the plant had naturally spread as seeds across the ocean and the Polynesians learned to cultivate it independently. One of the arguments against this is the fact that the Polynesian terms for the crop appear to be closely related to its name in Quechua, the language of the Peruvian Andes. ("Kuumala" and derivatives vs. "kumara" and relatives.)

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Fire ant “supergene” controls social behavior

A fire ant shows off one of the reasons for its low popularity.

UCSD

When invasive fire ants (Solenopsis invicta) were first discovered in the United States, scientists observed that their colonies each had a single queen, and that the ants were extremely aggressive toward individuals that immigrated from other colonies. However, they soon found that certain S. invicta colonies have multiple queens and even tend to adopt queens from other colonies. It turned out that different forms of a single gene, called Gp-9, determine a particular colony’s social system.

Now, scientists studying this gene have found that Gp-9 is part of a “supergene” that controls a large suite of traits related to sociality, and the chromosomes carrying this supergene behave a lot like sex chromosomes. Their research was published this week in Nature.

The Gp-9 gene determines whether S. invicta colonies will accept one queen or more; colonies composed of ants that are homozygous for one form of this gene will tolerate only one queen, while colonies that include heterozygous ants will tolerate multiple matriarchs. Gp-9 codes for an oderant-binding protein; these proteins specialize in helping pheromones and other odor molecules get from the environment to an animal’s olfactory receptors. It is likely, therefore, that chemical communication regulates the number of queens that are accepted into a colony.

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Bacterial “immune system” used to engineer human DNA in human cells

Artist's conception of the CRISPR system in action, with the guide RNA (red) leading a protein to a specific site in the genomic DNA (blue) where it makes a cut.

Stephen Dixon and Feng Zhang

Precisely engineering the genome of human cells remains largely in the realm of science fiction. It's possible, with the right virus, to get new or modified genes into cells. But the regular collection of the genes in the cell are still there—we can't typically eliminate a gene that has gone bad or replace a broken copy with a working one. Although some progress has been made in creating proteins that target specific spots in the genome, it's tough to make these proteins both specific enough to only target a single sequence yet flexible enough to work on lots of targets.

Now, it turns out we don't have to make proteins after all. Bacteria have a system that targets the DNA of viral invaders, acting a bit like an immune system. And two teams of researchers have shown it's possible to direct that system so it targets specific locations in a mammalian genome. Once targeted, the cell's normal DNA repair system can replace the sequence with an engineered one of the researchers' choosing.

The efficiency is under 10 percent, so don't start thinking we're going to edit every cell of the human body. But that rate still makes it practical for a variety of purposes—and potentially even therapies.

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What we know—and don’t know—about the biology of homosexuality

The media was abuzz this week after an international group of researchers proposed that scientists may have been looking for the biological underpinnings of homosexuality in the wrong place. Although scientists have spent the last few decades scouring our genome for a “gay gene,” William Rice, Urban Friberg, and Sergey Gavrilets suggest in The Quarterly Review of Biology that homosexuality may have its roots in epigenetics, rather than in genetics.

According to the authors, much of we know about homosexuality suggests that it is not simply a result of direct genetic inheritance. First, despite thorough genome-wide research, no study has been able to find a gene or genetic marker that is consistently associated with homosexuality. Second, although twenty to fifty percent of the variation in sexual orientation appears to be inherited in some way, identical twins don’t necessarily share a sexual orientation; if one twin is gay, there’s only a twenty percent probability that the other twin is, too. This low probability (or “concordance”) suggests that simple genetic inheritance might not drive sexual orientation. Finally, the authors argue that any purely genetic “fitness-reducing phenotypes” like homosexuality would be selected against and weeded out of the gene pool.

Instead, the researchers suggest, epigenetic inheritance via “epi-marks” might be responsible for sexual orientation. Epi-marks are physical changes in our genetic material (such as chemical modification or changes in DNA packaging proteins) that regulate gene activity without actually changing the sequence of bases.

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Are genes our puppet masters, or just a single link in a complex chain?

In addition to DNA sequences, the structures that compact DNA can be passed on as cells divide. This is called epigenetic inheritance.

Penn State

The afternoon sessions at the Nobel Week Dialogue covered a lot of ground, which was inevitable if you put six extremely smart people on the stage, give them a topic, and set them loose. Although there's no way to summarize the full conversation, it's possible to pull out some important themes that the speakers returned to. I'll attempt to do that for the discussion on genetics and the environment.

One of the things that became clear at this panel (and more generally through the day) is that we may have become a bit sloppy in our thinking about heritable and environmental influences on human health and behavior. If we don't attempt to form clear hypotheses and demand evidence to support them, there's a chance that we'll end up accepting things that appeal to our personal biases.

That may sound a bit dry, but it played out in dramatic fashion across the course of the panel, in part because of the prickly presence of James Watson.

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Where did dogs come from? It turns out we don’t really know

These happy Samoyeds look ancient (genetically), but probably aren't.

Flickr user jurvetson

Dogs were the very first creatures that humans domesticated, and their remains have been found along with those of humans from before we even had basic things like agriculture. And, with the advent of molecular tools, researchers were able to identify the animal that was domesticated (the gray wolf), as well as a handful of breeds that appear to be "ancient," and split off close to the source of domestication.

It was a nice picture, but apparently it was probably wrong. That's the conclusion of a study that appeared in this week's PNAS, which uses a combination of genetic, archeological, and historic evidence to argue that the history of domestic dogs is such a mess that we're not going to be able to unravel it without resorting to large-scale genome sequencing efforts.

The challenges of sorting out what happened from archeological remains is significant. The source of domesticated dogs, the gray wolf, historically ranged across all of North America, Europe, and Asia. The earliest domesticated dogs, which appeared about 15,000 years ago, looked a whole lot like the wolves they were descended from, making unambiguous identification of domestic vs. wild animals a challenge. And once things that were clearly dogs started appearing, they appeared over a huge geographic range. The earliest remains appear in Europe, the Middle East, and Kamchatka (on Russia's Pacific coast) all within 1,500 years of each other. Within another thousand years after that, domestic dogs were present in North America, as well.

We’re all mutants now

Enlarge / We might all be mutants now, but don't break out the spandex just yet.

Image courtesy of Marvel's classic comic, Giant-Size X-Men

The field of study called population genetics played a critical role in the development of modern biology, helping unite Mendelian genetics and Darwinian evolution into one coherent framework. In most genetics classes, though, it typically gets plowed through in a simplified form in a single lecture. I suspect this is because it involves a lot of math, and most biologists like being in the field precisely because it's generally possible to avoid all but the simplest math.

Nevertheless, population genetics has some critical insights to offer in the area of modern genomics, as evidenced by a paper that appeared in this week's edition of Science. Some population geneticists have looked into the results of the search for mutations in genome data. Their conclusion: the human population explosion has led to the appearance of many new, rare mutations in the human population, and it's throwing all the math off, which has some serious implications for medical research.

At the simplest level, population genetics can help us predict how often a mutation should be present in a specific population. Feed its equations things like the population size, how harmful or beneficial the mutation is, the typical mutation rate, and so forth, and it will spit out a nice prediction of what the final frequency of the mutation should be. It nicely demonstrates why even harmful mutations stick around at low levels in a population, even as evolution is doing its best to get rid of them.

We’re all mutants now

Enlarge / We might all be mutants now, but don't break out the spandex just yet.

Image courtesy of Marvel's classic comic, Giant-Size X-Men

The field of study called population genetics has played a critical role in the development of modern biology, helping unite Mendelian genetics and Darwinian evolution into one coherent framework. In most genetics classes, though, it typically gets plowed through in a simplified form in a single lecture. I suspect this is because it involves a lot of math, and most biologists like being in the field precisely because it's generally possible to avoid all but the simplest math.