In This Issue

doi:10.1073/iti3908105

ANTHROPOLOGY

Aboriginal fires produce local biodiversity

Indigenous peoples have often relied on burning small areas of land to increase the bounty of their hunts, setting fires that may subsequently play a role in enhancing biodiversity. Rebecca Bliege Bird et al. studied the patterns of biodiversity created by the Martu people, a group indigenous to Australia's Western Desert, and found that the anthropogenic fires are indeed a valuable resource management strategy, producing greater habitat diversity in the hunters' range and increasing foraging returns for the hunters. The authors combined ethnographic observations of Aboriginal hunting and burning with satellite image analysis to document the origins and consequences of mosaic burning practices. Linking alterations in landscape and biodiversity to foraging activity, Bliege Bird et al. found that burning off the spinifex grass that covers much of the region allowed the hunters to increase their encounter rate and capture success for game such as monitor lizards. The authors also observed that, over time, this approach created a different landscape than that produced by lightning or natural fires; the habitat rearranged into smaller patches, and the animal and plant populations diversified. These results have implications beyond contemporary questions of biodiversity and suggest that anthropogenic influences are more likely to alter local habitats only in conjunction with broad-spectrum foraging economies, according to the authors. — F.A.

A Martu woman setting a fire line in preparation for a hunt.

“The ‘fire stick farming’ hypothesis: Australian Aboriginal foraging strategies, biodiversity, and anthropogenic fire mosaics” by R. Bliege Bird, D. W. Bird, B. F. Codding, C. H. Parker, and J. H. Jones (see pages 14796–14801)

AGRICULTURAL SCIENCES

Plant-parasitic nematode genome

The genome of Meloidogyne hapla, a plant-parasitic nematode, is now complete. At 54 Mbp, it is not only the smallest nematode genome, but also the smallest metazoan genome to date, containing significantly fewer base proteins than the Caenorhabditis elegans genome. Charles Opperman et al. suggest that the fewer genes reflect functions the parasite may be able to derive from the host, thus allowing the nematode to shed excess genetic “baggage.” The authors also report that M. hapla has acquired genes from other species by horizontal gene transfer that may enable it to exploit its plant hosts. Although little apparent macrosynteny was seen between the C. elegans and M. hapla genomes, small pockets of microsynteny between the two suggest that these regions contain essential biological functions. The authors say the M. hapla genome will provide a window into the roots and evolution of parasitism and pathogenicity. — B.P.T.

Four multinucleate giant cells around the head of the feeding M. hapla.

“Sequence and genetic map of Meloidogyne hapla: A compact nematode genome for plant parasitism” by Charles H. Opperman, David M. Bird, Valerie M. Williamson, Dan S. Rokhsar, Mark Burke, Jonathan Cohn, John Cromer, Steve Diener, Jim Gajan, Steve Graham, T. D. Houfek, Qingli Liu, Therese Mitros, Jennifer Schaff, Reenah Schaffer, Elizabeth Scholl, Bryon R. Sosinski, Varghese P. Thomas, and Eric Windham (see pages 14802–14807)

EVOLUTION

Synergistic drug combinations encourage antibiotic resistance

Antimicrobial treatments frequently rely on synergistic combinations of several drugs to wipe out pathogens and reduce the emergence of resistant forms of bacteria. However, a theoretical–experimental study by Jean-Baptiste Michel et al. suggests that this combination approach may have the opposite effect. The authors tested the impact of various drug combinations on the emergence of antibiotic resistance in the medically important pathogen Staphylococcus aureus and found that when two drugs act synergistically, there is a greater probability that drug-resistant forms of S. aureus will arise. Conversely, the authors predict that drugs that function antagonistically will reduce the emergence of resistance. These findings have relevance to clinical medicine, the authors say, where synergistic drug combinations are favored for their enhanced killing ability, but where the tradeoff may be the evolution of more virulent, multidrug-resistant bacterial strains that will make fighting infections even more difficult. — B.P.T.

Drug-resistant bacterial colonies with 10³ (Upper) and 10^1.5 (Lower) cells after 5 days.

“Drug interactions modulate the potential for evolution of resistance” by Jean-Baptiste Michel, Pamela J. Yeh, Remy Chait, Robert C. Moellering, Jr., and Roy Kishony (see pages 14918–14923)

NEUROSCIENCE

How a healthy brain mellows with age

The giddy expectation of unwrapping a present is best enjoyed by the young, highlighting a fundamental neurochemical reward mechanism that mellows with age. Dopamine—believed to be the currency of the brain's reward-processing circuitry—declines naturally as part of healthy aging, but the consequences of this cerebrovascular decline have remained elusive. Jean-Claude Dreher et al. used a video slot machine and a combination of brain imaging techniques to determine which parts of the brain are stimulated when rewards, or the promise of rewards, are presented to both younger and older adults. Functional MRI showed that activation of dopamine-triggered brain regions during the anticipation and receiving of a reward was more profound in younger subjects (average age 25 years) than in their older counterparts (average age 65 years), although PET scans revealed no difference in the production of dopamine in the subjects' brains. Based on these findings, the authors describe a link between dopamine synthesis and reward-related brain activity in humans and identify changes in this regulatory circuit that accompany healthy aging. — C.E.

Correlation maps for older and younger subjects at the time of reward delivery.

“Age-related changes in midbrain dopaminergic regulation of the human reward system” by Jean-Claude Dreher, Andreas Meyer-Lindenberg, Philip Kohn, and Karen Faith Berman (see pages 15106–15111)

NEUROSCIENCE

Gene therapy restores human sight

The retinoid cycle is critical for normal vision in mammals. The cycle regenerates vitamin A needed to convert light into neural signals in the retina. Mutations in a key enzyme, RPE65 isomerase, block the functioning of this cycle and cause a severe form of inherited blindness called Leber congenital amaurosis (LCA). Adeno-associated virus (AAV)-based gene therapy can be used in cases where normal levels of RPE65 are not present, and this treatment strategy restores vision in animals with the genetic deficiency. Artur Cideciyan et al. used an AAV vector to deliver RPE65 to one eye of each of three young-adult human patients with LCA, whose visual sensitivity increased significantly within 1 month and was localized to retinal regions exposed to the gene therapy vector. The authors detected up to 50-fold improvement in cone vision, and a dramatic increase in rod vision—up to 63,000-fold—allowed the patients to overcome the impaired light sensitivity resulting from the biochemical blockade. Unexpectedly, the reconstituted retinoid cycle had abnormally slow kinetics. The authors suggest that gene therapy, although imperfect, may offer dramatic improvement in night and day vision in victims of this human eye disease. — M.M.

Eye with retinal degeneration caused by mutations in the RPE65 gene.

“Human gene therapy for RPE65 isomerase deficiency activates the retinoid cycle of vision but with slow rod kinetics” by Artur V. Cideciyan, Tomas S. Aleman, Sanford L. Boye, Sharon B. Schwartz, Shalesh Kaushal, Alejandro J. Roman, Ji-jing Pang, Alexander Sumaroka, Elizabeth A. M. Windsor, James M. Wilson, Terence R. Flotte, Gerald A. Fishman, Elise Heon, Edwin M. Stone, Barry J. Byrne, Samuel G. Jacobson, and William W. Hauswirth (see pages 15112–15117)