The Genetics of Long-Distance Flying

Every year, some 50 billion birds take to the air for their seasonal migrations. They may go 500 kilometers in a day and a few even travel from pole to pole. But how do they know when, where, and how far to fly? Although some of the answer lies in their DNA, nobody knew which genes or how they worked. Now ornithologists have pinned down one of those genes, and strange as it may sound, the length of that gene influences the length of the flights.

“If we understand the genetics underlying migratory behavior, we can understand more about how and why migration evolves,” says Chris Guglielmo, who studies bird migration at the University of Western Ontario in Canada. “We may also be better able to understand how quickly migration can disappear in response to climate change.”

As the moment for migration approaches, birds bulk up, adding muscle and fat. They hop and flap restlessly at night, shifting their internal clocks in anticipation of nighttime flights. Breeding experiments have shown that these shifts have a genetic basis, as do the timing, amount, and intensity of flights.

Since the 1970s, ornithologists at the Max Planck Institute for Ornithology in Starnberg, Germany, have studied European blackcaps (Sylvia atricapilla), a common warbler in Europe, which typically head to the Mediterranean for the winter. Some blackcaps had established a new wintering area in the past few decades. The researchers wanted to know the genetic basis for the change.

To hunt down a migration gene, Jakob Mueller and Bart Kempenaers of Max Planck, along with Francisco Pulido, now at the Complutense University of Madrid in Spain, selected six genes to evaluate. They picked ones known to influence how active a bird is at night or how much it tends to hop from branch to branch as it explores its environment.

The researchers evaluated 14 populations of blackcaps ranging from western Russia, through Europe, south to Africa. These populations varied in their inclinations to migrate. Blackcaps in Cape Verde, for example, never leave home, whereas those in Russia travel more than 3500 kilometers. Others fly shorter distances seasonally. The Max Planck team had previously captured these birds and taken blood samples, so studying their DNA was a snap.

When Mueller, Kempenaers, and Pulido compared the genes with the behavior, they found a link in just one gene, called ADCYAP1, as they report online today in the Proceedings of the Royal Society B. Different versions of the gene have different numbers of extra copies of a bit of DNA—called a two-base repeat—stuck on the gene’s far end. The researchers found that the length of the gene was correlated with how much the birds hopped and flapped around their cages at night.

Such nighttime restlessness shows how eager a bird is to migrate, says Mueller. The more fidgety birds had more copies of the two-base repeat than calmer birds. Looking at the populations as a whole, the researchers found that groups that stayed put tended to have shorter version of the gene, whereas long-distant migrants tended to have longer versions. “We found a continuous relationship between gene [version] length and behavior,” says Mueller. This gene specifies a peptide in the brain. Among other functions, the peptide influences daily rhythms and affects energy use—increasing body temperature, metabolic rate, and fat usage. These sorts of changes occur as a bird gets ready to migrate, Mueller points out.

Staffan Bensch, an ornithologist at Lund University in Sweden, is not convinced that this gene, not another nearby, is what’s causing the variation in migratory behavior. But Guglielmo says the finding is significant. “It is the first demonstration,” he says, “of a specific gene that is important for the expression of migratory behavior in birds.”

It won’t be the only one, says Mueller. The particular version of ADCYAP1 determines only about 3% of the migratory behavior. Dozens or even hundreds of gene variants might also be involved. And genes don’t tell the whole story; the environment also influences migration. The study of the genetics of migration, clearly, is just getting off the ground.

source: science now

Monkey Behavior May Provide Clues to Autism

A chance discovery of a macaque behavior could lead to new insights into autism. Among adult rhesus macaques, eye contact is a good way to get into a fight. But for newborns, time spent looking directly at the mother and, subsequently, imitating her facial gestures may be key to a well-adjusted adulthood. Individuals who don’t get this face-time tend to develop autistic-like behavior, rocking back and forth and failing to maintain good social connections, Stephen Suomi reported here yesterday .

Suomi studies macaques at the National Institute of Child Health and Human Development, and has a large program in which he raises some newborns separated from their mothers to assess the effects of early development on adult behavior. In 2006, while filming macaque behavior, he and his colleagues discovered that mother macaques spend their newborn’s first week encouraging infants to look directly at them, a behavior thought to occur only in humans (see video). This contact and the imitative behavior that ensues—the infants will smack their lips in response to the mother doing the same, for example—helps bond the infant to the mother. Within a month, however, these face-to-face encounters cease; newborns stop imitating their mothers after just a week.

About half of the infants separated from their mothers, fed briefly by humans, and then raised among peers don’t respond to human efforts to get them to imitate. They quickly start lagging behind in their ability to reach out and grab objects, play half as much, and some later seem autistic.

In making the link between these abnormal behaviors and imitation, “we may have stumbled on a very early screening test for the risk of autism,” says Suomi. It could be that autistic children don’t imitate as young infants, though that has not been investigated. At the meeting Suomi described differences in the brain wave patterns between these individuals and those that do imitate when young, indicating that the face-to-face contact can lead to long-lasting physical effects in the brain.

“Neural development is retarded because of [a] lack of maternal-infant stimulation,” says Bruce McEwen, a neuroscientist at Rockefeller University in New York City. In the macaques, “the reciprocal interaction between mother and infant is critical for normal brain-behavior development and socialization.”

Suomi’s group plans to provide extra stimulation—and more face time either with humans or with 3D computer-animated macaques —for infant macaques raised without their mothers to see if their behavior later in life improves. The intervention may need to occur very early, as differences in imitative ability show up quite fast. “By day three, we already have a major rearing condition effect,” he points out.

source: science now

Detecting undiagnosed diabetes using glycated haemoglobin

To assess the utility of glycated haemoglobin (HbA1c) level as an automated screening test for undiagnosed diabetes among hospitalised patients and to estimate the prevalence of undiagnosed diabetes among hospitalised patients.

A 3-month prospective study of all adult patients admitted to a tertiary hospital. An HbA1c test was automatically undertaken on admission for all patients with a random plasma glucose (RPG) level ≥ 5.5 mmol/L. Demographic, admission and biochemical data were obtained from hospital databases. A subset of patients was recruited for an oral glucose tolerance test (OGTT) after discharge.

Prevalence of undiagnosed diabetes (defined as HbA1c ≥ 6.5% in accordance with International Expert Committee and American Diabetes Association recommendations) and utility of automated HbA1c testing.

The prevalence of undiagnosed diabetes was 11% (95% CI, 9.8%–12.4%) (262/2360) during the study period. A further 312 patients with known diabetes were admitted. The prevalence of undiagnosed diabetes was highest in the 65–74-years age group. The HbA1c test cost was $152 per new diagnosis of diabetes. Conservatively assuming an annual incidence of undiagnosed diabetes of 0.8%, the ongoing cost of testing hospitalised patients would be $2100 per new diagnosis of diabetes. RPG testing was not sensitive or specific in diagnosing diabetes. Patients were poorly compliant with the post-discharge OGTT (27% completion rate).

HbA1c is a simple, inexpensive screening test that can be automated using existing clinical blood samples. Hospital screening for diabetes needs to be coupled with resources for management in the community.

source: medical journal of australia