Leaping eels lend credence to Humboldt’s legend
Eel ascends a prosthetic predator.
In March 1800, the German naturalist Alexander von Humboldt witnessed an encounter between electric eels trapped during the dry season in a turbid pool in Venezuela and horses herded into the pool by fishermen to lure the eels. The eels repeatedly stunned the horses, and the offensive attack ostensibly drained the eels’ zest and enabled their capture. In a study that lends support to the veracity of the account, Kenneth Catania (pp. 6979–6984) observed the reaction of electric eels housed in an aquarium to a partially submerged conductive rod and plate. Eels ascended and electrocuted the approaching rod and plate, and the current magnitude rose with the eels’ ascent. Slow-motion videos revealed that the eels bent their necks to maintain contact between their electric organs and the conductors, suggesting the use of targeted high-voltage volleys rather than random electric discharges. LED lights that were connected in series on the surface of a prosthetic predator using strips of conductive tape revealed that the offensive lunge allows eels to progressively electrify the bodies of moving and grounded targets. Because eels are often entrapped in pools during the dry season, such directed attacks on predators may prove advantageous over passive defense by electrification of the surrounding water, where current can be quickly dissipated. According to the author, the study lends verisimilitude to Humboldt’s centuries-old report. — P.N.
Trace fossil record of early evolutionary radiations
Sandstone bed in northwest Argentina covered by trilobite trace fossil.
Two major evolutionary events, the Cambrian Explosion (CE) and the Great Ordovician Biodiversification Event (GOBE), shaped marine biodiversity. Body fossil evidence indicates that most body plans appeared during the CE, whereas diversity at lower taxonomic levels increased during GOBE. Luis Buatois et al. (pp. 6945–6948) surveyed trace fossils, which are records of organisms’ activities rather than the organisms themselves, from the Ediacaran Period to the Ordovician Period to further illuminate the contrasting natures of these two events. The authors report a 300% increase in the diversity of trace fossils in soft substrates, such as sediments, at the beginning of the Cambrian period approximately 540 million years ago, coincident with the CE, and earlier than the rapid diversification indicated by shell-containing fossils. This increase in diversity was accompanied by an increase in the disparity of trace fossil architectural designs. The diversity and architectural disparity of trace fossils in hard substrates remained low throughout the Cambrian Period, with rapid increases occurring during the GOBE, approximately 80 million years after the diversification of soft substrate fossils. According to the authors, the results suggest decoupled evolution between hard and soft substrate communities, possibly due to an increase in hard substrates or predation during the Ordovician, or to higher energetic requirements for boring in hard substrates than soft substrates. — B.D.
Ancestry of early European farmers
Human burials from the Early Neolithic site of Revenia, northern Greece. Image courtesy of Fotini Adaktylou and the Ephorate of Antiquities of Pieria.
Farming was introduced to Europe from Anatolia in modern-day Turkey. The extent to which this process was mediated by the migration of Anatolian farmers versus cultural diffusion has been a subject of debate. Zuzana Hofmanová et al. (pp. 6886–6891) obtained DNA sequences from five individuals from early agricultural sites in northwestern Turkey and northern Greece. These sites date from the time of initial spread of farming to Europe and lie along the proposed route of this spread. The authors observed similarity between the genomes of the samples and those of individuals from early farming societies in central and southern Europe. By modeling ancient and modern genomes as mixtures of DNA from other ancient genomes, the authors traced the majority of the ancestry of individuals from ancient farming societies in Germany and Hungary to the ancient Anatolian and Greek genomes. Ancient Greek and Anatolian genomes contributed to all modern-day European populations, and are particularly similar to modern Mediterranean populations as well as to Ötzi, the ice mummy from the Alps. According to the authors, the results suggest a continuous chain of ancestry from Europe to Greece and Anatolia, indicative of the route of migration. — B.D.
Childbirth, childcare, and evolution of intelligence
Why human cognition differs drastically from that of our closest evolutionary relatives remains an unresolved question. Steven Piantadosi and Celeste Kidd (pp. 6874–6879) developed a model in which the evolution of intelligence is driven by childbirth and childrearing. According to the model, children are unlikely to survive birth if their head size at birth exceeds a critical threshold. Thus, selective pressure favors the birth of children early in development, when the head is small. The probability of immature children surviving to adulthood increases with parents’ intelligence, which is linked to brain and head size. Therefore, the selective pressures for large brains and early birth ages could become self-reinforcing, leading to the runaway evolution of high intelligence and immature offspring in the absence of other selective pressures. In support of this model, the authors observed a significant correlation between time to weaning, which is a proxy for the immaturity of offspring, and a measure of general intelligence across 23 primate genera. According to the authors, the runaway evolution of intelligence observed in the model requires both live birth and large brains, suggesting why human-level intelligence evolved in mammals and not in other animal classes. — B.D.
How light causes eye damage in macular degeneration
Macular degeneration is a leading cause of vision loss in older adults. The disease is characterized by the build-up of harmful compounds in specialized cells of the retina, leading to photoreceptor death and impaired central vision. Keiko Ueda et al. (pp. 6904–6909) found that retinal damage in macular degeneration arises from ongoing light-driven processes called photooxidation and photodegradation, which break down molecules called bisretinoids to generate damaging molecular fragments. To examine the effects of light exposure on bisretinoid levels, the authors exposed mice with a mutation in the Abca4 gene, implicated in macular degeneration, to cyclic light or constant darkness. Light exposure reduced bisretinoid levels in the eyes and damaged photoreceptor cells. However, treatment with the antioxidant vitamin E mitigated the effects of light exposure, preserving bisretinoid levels and reducing photoreceptor damage in Abca4-mutant mice. Together, the findings demonstrate that light-induced degradation and oxidative processes interact to control bisretinoid levels and retinal damage in macular degeneration. Moreover, the results suggest that bisretinoid photodegradation could explain why sunlight exposure may increase the risk of macular degeneration, while antioxidant treatment could reduce disease progression by decreasing bisretinoid oxidation. According to the authors, the study provides support for bisretinoid-targeted therapies. — J.W.
How disease-causing parasites defeat insect gut defenses
Insects transmit a wide range of fatal human diseases, causing more than 1 million deaths worldwide each year. Current treatment approaches are limited by the lack of effective vaccines and the emergence of drug resistance. Emre Aksoy et al. (pp. 6961–6966) investigated the molecular mechanisms by which parasites colonize the insect gut early in the infection process. The authors provided tsetse flies with either normal blood as a control or blood infected with the protozoan parasites African trypanosomes, which cause a fatal disease known as sleeping sickness. The authors used high-throughput RNA sequencing to monitor gene expression in the tsetse gut. Upon entering the gut, the mammalian trypanosomes shed their cell-surface molecules, called variant surface glycoproteins (VSG), which decreased the expression of the tsetse microRNA mir-275, and interfered with the Wnt-signaling pathway and the Iroquois/IRX transcription factor family. The interference reduced the function of the fly’s gut barrier, known as the peritrophic matrix, resulting in the parasite’s successful colonization of the gut. Taken together, the findings reveal a key role for the VSG coat in promoting parasite colonization of the tsetse gut. According to the authors, the findings could lead to the development of alternative strategies that block parasite development in insect vectors to prevent disease transmission. — J.W.
Therapeutic insights into liver-stage malaria
Malaria remains one of the world’s deadliest diseases, causing nearly 600,000 deaths worldwide each year. Of the handful of malaria-causing parasitic species, Plasmodium vivax has the most widespread distribution, most likely due to its long-lasting dormancy in the liver. Rachasak Boonhok et al. (pp. E3519–E3528) identified a molecular mechanism by which the immune molecule IFN-γ eliminates the liver-stage parasites. The authors found that treatment of human liver cells with IFN-γ induced an immune defense mechanism called autophagy, a cellular process in which pathogens are delivered to organelles called lysosomes for destruction. This process depends on the autophagy-related proteins Beclin 1, PI3K, and ATG5, but not on the autophagy-initiating protein ULK1. The results suggest that protection against liver-stage P. vivax relies on a noncanonical autophagy pathway resembling a form of phagocytosis, previously shown to control other types of pathogens implicated in foodborne illnesses and other diseases. The findings could lead to the identification of treatment strategies for P. vivax infection, which has recently shown an alarming increase in resistance to existing drugs. By targeting the liver stage of the parasites, the incidence and severity of malaria worldwide might be lowered, according to the authors. — J.W.
Genomics of ancient Aboriginal Australians
Original excavation of Mungo Man. Image courtesy of Wilfred Shawcross (photographer).
A 2001 study that reported mitochondrial (mt) DNA sequences from ancient Aboriginal Australian remains suggested that some of these remains were not part of the same lineage as contemporary humans. The study challenged the notion of an African origin for all modern humans, including most Aboriginal Australians, and raised questions about whether Aboriginal Australians were indeed the first people of Australia. Tim Heupink et al. (pp. 6892–6897) analyzed mtDNA from five of the same sets of remains examined in the 2001 study. The authors used second generation sequencing methods to replicate the earlier study’s findings. Three samples had no recoverable DNA. From another set of ancient remains that belonged to Mungo Man, the oldest known Australian, five sequences were recovered, all of which were modern European contaminants. From a fifth specimen, the authors assembled two complete mitochondrial genomes, one belonging to an Australian lineage, and the other to a European lineage. All but one of the recovered sequences differed from those from the original study. The results challenge the findings of the earlier study, but also suggest that meaningful genetic information can be recovered from ancient Aboriginal Australian remains through advanced sequencing technologies. — B.D.
Cell transplantation in glaucoma
Glaucoma is one of the most common causes of irreversible vision loss and blindness worldwide. Vision loss is caused by the death of retinal ganglion cells due to elevated intraocular pressure, which is regulated by trabecular meshwork (TM) cells. Wei Zhu et al. (pp. E3492–E3500) found that transplanting stem cell-derived TM cells lowers intraocular pressure and prevents the death of retinal ganglion cells in mice with glaucoma. The authors genetically reprogrammed skin cells from mice into induced pluripotent stem cells (iPSCs), which were then converted into TM cells. Next, the authors injected either iPSC-TM cells, or an equal volume of saline as a control, into the eyes of mice with a genetic mutation that causes glaucoma in humans. Unlike saline injection, the cell replacement therapy prevented the development of elevated intraocular pressure for at least 9 weeks and preserved the number of both TM and retinal ganglion cells. Additional evidence suggested that direct contact with transplanted iPSC-TM cells may stimulate the proliferation of preexisting TM cells in the eye. By preventing elevated intraocular pressure and neuronal loss, cell replacement therapy could potentially preserve vision and increase the quality of life of patients with glaucoma, according to the authors. — J.W.