When Francis Crick was 31, he decided he needed to change his luck. As a graduate student in physics during World War II, his research hadn’t gone so well; his experiment was demolished by a bomb. To beat the war, he joined it, working on naval warfare mines for the British Admiralty.

After the war, he sought a new direction.

“There are lots of ways of being unlucky,” Crick told me in an interview in 1998. “One is sticking to things too long. Another is not adventuring at all.”

He decided to adventure.

Molecular biologists everywhere will celebrate that decision on June 8, the centennial of Crick’s birth, in Weston Favell, Northampton, England, in 1916.

“Crick was one of the central figures, one might say the central figure, in the molecular revolution that swept through biology in the latter half of the 20th century,” science historian Robert Olby wrote in a biographical sketch.

In 1953, at the University of Cambridge, Crick and his collaborator James Watson figured out how life’s most important molecule, deoxyribonucleic acid, was put together. DNA, the stuff that genes are made of, became the most famous of biological molecules. Today the image of its double helix structure symbolizes biology itself. It would be easy to make the case that discovering DNA’s structure was the single greatest event in the history of biology — and always will be. In 1962, Watson and Crick won the Nobel Prize for their work (which was, of course, greatly aided by X-ray diffraction imagery from Rosalind Franklin, who unfortunately died before the Nobel was awarded).

Crick’s DNA adventure began at a time when molecular biology was ripe for revolution. But Crick didn’t know that. His choice was lucky.
“I had no idea when I started that molecular biology would advance so fast,” he said. “No idea at all.”

In fact, Crick very nearly chose a different path. His interest in genes was equaled by his curiosity about the brain. Both were topics that he liked to gossip about.

“But I didn’t know enough about either subject,” he said. He just knew a little bit more about biochemistry.

“I thought ‘Well look, I have a training in physics and I know a bit of chemistry, I don’t know anything about the brain.’” So he decided it would be more sensible to start with genes.

“I thought that problem of what genes were and how they replicate and what they did would last me the rest of my life,” he said.

As it happened, genes did occupy him for a couple of decades. Crick made major contributions to elucidating the genetic code during that time. But he never forgot his interest in the brain, and more specifically, consciousness. In the 1970s, he moved from England to California, where he began consciousness research in San Diego at the Salk Institute for Biological Studies.

Consciousness turned out to be a much tougher problem than understanding genes. In retrospect, Crick could see why.

With genetics, “what really made the thing was the simplicity of the double helix. It wrote the whole research program,” he said. “It probably goes back to near the origin of life, when things had to be simple.” Consciousness appeared on the scene only much later, after the evolution of the brain’s vast complexity.

Nevertheless, Crick perceived parallels between genetics and consciousness as subjects for scientific inquiry. As the 20th century came to an end, he mused that consciousness as a concept remained vague — researchers did not all agree about what the word meant. The situation with genes had at one time been similar.

“In a sense people were just as vague about what genes were in the 1920s as they are now about consciousness,” Crick said. “It was exactly the same. The more professional people in the field, which was biochemistry at that time, thought that it was a problem that was too early to tackle. And I think they were right in the ’20s.”

At the end of the 20th century, research on consciousness found itself in much the same state.

“Everybody agrees that it’s an interesting question,” Crick said, “but there are two points of view among scientists: One is that it isn’t a scientific question and is best left to philosophers. And the other one is that, even if it’s a scientific question, it’s too early to tackle it now.”

Crick tackled it anyway. Until his death in 2004, he worked vigorously on the subject with his collaborator Christof Koch, making substantial inroads into identifying the brain activity associated with conscious awareness. Crick was not lucky enough to solve the problem of consciousness, but he perhaps brought the arrival of that solution a little closer.

When plankton on the high seas catch a cold, the whole ocean may sneeze. Viruses hijacking these microbes could be an important overlooked factor in tracing how living things trap — or in this case, fail to trap — the climate-warming gas carbon dioxide.

Plants and other organisms that photosynthesize use energy from the sun to capture CO2 for food. The most abundant of these photosynthesizers on the planet are marine cyanobacteria with hardly any name recognition: Synechococcus and Prochlorococcus.
Now, for the first time, a study looks in detail at what happens when some of the abundant viruses found in the sea infect these microbes. Two viruses tested in the lab hijacked cell metabolism, allowing photosynthesis to continue but shunting the captured energy to virus reproduction. The normal use of that energy, capturing CO2, largely shuts down, David Scanlan of the University of Warwick in England and colleagues report online June 9 in Current Biology. As a result, people could be overestimating by 10 percent the amount of CO2 that photosynthesis in the oceans captures.

On any given day, 1 to 60 percent of these plankton may have picked up a viral infection, researchers have estimated. That means that between 0.02 and 5.39 petagrams of carbon — up to 5.39 billion metric tons — may not be captured by marine organisms a year. The high end of that scenario is equivalent to 2.8 times the CO2 routinely captured annually by all the planet’s salt marshes, coral reefs, estuaries, sea grass meadows and seaweeds put together.

Synechococcus and Prochlorococcus plankton “are organisms that you’ve never heard of but you really should have,” says Adam Martiny of the University of California, Irvine. He studies the same kinds of plankton but wasn’t involved in the new virus research, and what he appreciates about it is the intriguing biology of viral manipulation the new work has uncovered.

Until now, Scanlan says, the prevailing view was that while infected plankton were still alive, they were probably carrying on normal photosynthesis. As early as 2003, researchers had clues that the viruses attacking these tiny marine organisms might manipulate photosynthesis in some way, perhaps keeping the process running in an infected cell. These viruses have genes for proteins used in photosynthesis, even though a virus doesn’t even have its own cell much less a way to photosynthesize.

What the viruses are doing, Scanlan and his colleagues have now shown, is subverting their victim’s photosynthesis. Energy capture, the part of photosynthesis directly involved with light, goes on as usual; the cells carry out the routine electron transport for catching energy. But instead of using those sizzling electrons to capture CO2 and turn it into carbohydrates for basic cell metabolism, the viruses shut down this process (called carbon fixation). The light reactions are the ones that researchers normally measure to estimate how much carbon photosynthesis captures in the oceans, but the covert viral shunting means that estimate could be too high.

Scanlan cautions that this is just the beginning of working out the numbers and possible climate effects of virus diseases for these organisms. Whatever the current effects of this takeover turn out to be outside the lab, they may intensify as the climate changes. Synechococcus and Prochlorococcus are “projected to be winners in the new, warmer oceans” and may become even more numerous, Martiny says. And what’s good for them may also increase the abundance of the viral pirates that hijack them.

Since 1973, eight spacecraft have flown past or orbited Jupiter. On July 4, NASA’s Juno probe will become the planet’s ninth visitor.

Juno’s trajectory is different than all others, as seen in the plot above and in the video. For 20 months, Juno will repeatedly skim the cloud tops, looping over the poles on orbits that are almost perpendicular to Jupiter’s equator.

Most other spacecraft zipped by, using the planet’s gravity to speed them along to other destinations. Only Galileo, which arrived in 1995, stuck around; it spent nearly eight years circling Jupiter’s equator, repeatedly buzzing the four largest moons.

Young zebra finches (Taeniopygia guttata) learn to sing from a teacher, usually dad. Remembering dad’s tunes may even be hardwired into the birds’ brains.

Researchers at the Okinawa Institute of Science and Technology in Japan measured activity in the brains of male juvenile birds listening to recordings of singing adult males, including their fathers. The team focused its efforts on neurons in a part of the brain called the caudomedial nidopallium that’s thought to influence song learning and memory.

A subset of neurons in the caudomedial nidopallium lit up in response to songs performed by dad but not those of strangers, the team reports June 21 in Nature Communications. The more baby birds heard songs, the more their neurons responded and the clearer their own songs became. Sleep and a neurotransmitter called GABA influenced this selectivity.

The researchers suggest that this particular region of the brain stores song memories as finches learn to sing, and GABA may drive the storage of dad’s songs over others.
Researchers played a variety of sounds for young zebra finches: their own song, dad’s song and songs and calls from other adult finches. Over time, their songs became more and more similar to that of their father.