Asymptotic prey profitability drives star-nosed moles to the foraging speed limit

Foraging theory provides models for predicting predator diet choices assuming natural selection has favoured predators that maximize their rate of energy intake during foraging. Prey profitability (energy gained divided by prey handling time) is an essential variable for estimating the optimal diet. Time constraints of capturing and consuming prey generally result in handling times ranging from minutes to seconds, yet profitability increases dramatically as handling time approaches zero, providing the potential for strong directional selection for increasing predator speed at high encounter rates (tiny increments in speed increase profitability markedly, allowing expanded diets of smaller prey). We provide evidence that the unusual anatomical and behavioural specializations characterizing star-nosed moles resulted from progressively stronger selection for speed, allowing the progressive addition of small prey to their diet. Here we report handling times as short as 120 ms (mean 227 ms) for moles identifying and eating prey. 'Double takes' during prey identification suggest that star-nosed moles have reached the speed limit for processing tactile information. The exceptional speed of star-nosed moles, coupled with unusual specializations for finding and eating tiny prey, provide new support for optimal foraging theory.     

Plasma formation and temperature measurement during single-bubble cavitation

Single-bubble sonoluminescence (SBSL) results from the extreme temperatures and pressures achieved during bubble compression; calculations have predicted the existence of a hot, optically opaque plasma core with consequent bremsstrahlung radiation. Recent controversial reports claim the observation of neutrons from deuterium-deuterium fusion during acoustic cavitation. However, there has been previously no strong experimental evidence for the existence of a plasma during single- or multi-bubble sonoluminescence. SBSL typically produces featureless emission spectra that reveal little about the intra-cavity physical conditions or chemical processes. Here we report observations of atomic (Ar) emission and extensive molecular (SO) and ionic (O2+) progressions in SBSL spectra from concentrated aqueous H2SO4 solutions. Both the Ar and SO emission permit spectroscopic temperature determinations, as accomplished for multi-bubble sonoluminescence with other emitters. The emissive excited states observed from both Ar and O2+ are inconsistent with any thermal process. The Ar excited states involved are extremely high in energy (>13 eV) and cannot be thermally populated at the measured Ar emission temperatures (4,000-15,000 K); the ionization energy of O2 is more than twice its bond dissociation energy, so O2+ likewise cannot be thermally produced. We therefore conclude that these emitting species must originate from collisions with high-energy electrons, ions or particles from a hot plasma core.     

FAS and NF-κB signalling modulate dependence of lung cancers on mutant EGFR

Human lung adenocarcinomas with activating mutations in EGFR (epidermal growth factor receptor) often respond to treatment with EGFR tyrosine kinase inhibitors (TKIs), but the magnitude of tumour regression is variable and transient. This heterogeneity in treatment response could result from genetic modifiers that regulate the degree to which tumour cells are dependent on mutant EGFR. Through a pooled RNA interference screen, we show that knockdown of FAS and several components of the NF-κB pathway specifically enhanced cell death induced by the EGFR TKI erlotinib in EGFR-mutant lung cancer cells. Activation of NF-κB through overexpression of c-FLIP or IKK (also known as CFLAR and IKBKB, respectively), or silencing of IκB (also known as NFKBIA), rescued EGFR-mutant lung cancer cells from EGFR TKI treatment. Genetic or pharmacologic inhibition of NF-κB enhanced erlotinib-induced apoptosis in erlotinib-sensitive and erlotinib-resistant EGFR-mutant lung cancer models. Increased expression of the NF-κB inhibitor IκB predicted for improved response and survival in EGFR-mutant lung cancer patients treated with EGFR TKI. These data identify NF-κB as a potential companion drug target, together with EGFR, in EGFR-mutant lung cancers and provide insight into the mechanisms by which tumour cells escape from oncogene dependence.     

The cost of inbreeding in Arabidopsis

Population geneticists have long sought to estimate the distribution of selection intensities among genes of diverse function across the genome. Only recently have DNA sequencing and analytical techniques converged to make this possible. Important advances have come from comparing genetic variation within species (polymorphism) with fixed differences between species (divergence). These approaches have been used to examine individual genes for evidence of selection. Here we use the fact that the time since species divergence allows combination of data across genes. In a comparison of amino-acid replacements among species of the mustard weed Arabidopsis with those among species of the fruitfly Drosophila, we find evidence for predominantly beneficial gene substitutions in Drosophila but predominantly detrimental substitutions in Arabidopsis. We attribute this difference to the Arabidopsis mating system of partial self-fertilization, which corroborates a prediction of population genetics theory that species with a high frequency of inbreeding are less efficient in eliminating deleterious mutations owing to their reduced effective population size.     

A Mott insulator of fermionic atoms in an optical lattice

Strong interactions between electrons in a solid material can lead to surprising properties. A prime example is the Mott insulator, in which suppression of conductivity occurs as a result of interactions rather than a filled Bloch band. Proximity to the Mott insulating phase in fermionic systems is the origin of many intriguing phenomena in condensed matter physics, most notably high-temperature superconductivity. The Hubbard model, which encompasses the essential physics of the Mott insulator, also applies to quantum gases trapped in an optical lattice. It is therefore now possible to access this regime with tools developed in atomic physics. However, an atomic Mott insulator has so far been realized only with a gas of bosons, which lack the rich and peculiar nature of fermions. Here we report the formation of a Mott insulator of a repulsively interacting two-component Fermi gas in an optical lattice. It is identified by three features: a drastic suppression of doubly occupied lattice sites, a strong reduction of the compressibility inferred from the response of double occupancy to an increase in atom number, and the appearance of a gapped mode in the excitation spectrum. Direct control of the interaction strength allows us to compare the Mott insulating regime and the non-interacting regime without changing tunnel-coupling or confinement. Our results pave the way for further studies of the Mott insulator, including spin-ordering and ultimately the question of d-wave superfluidity.     

Multimodal fast optical interrogation of neural circuitry

Our understanding of the cellular implementation of systems-level neural processes like action, thought and emotion has been limited by the availability of tools to interrogate specific classes of neural cells within intact, living brain tissue. Here we identify and develop an archaeal light-driven chloride pump (NpHR) from Natronomonas pharaonis for temporally precise optical inhibition of neural activity. NpHR allows either knockout of single action potentials, or sustained blockade of spiking. NpHR is compatible with ChR2, the previous optical excitation technology we have described, in that the two opposing probes operate at similar light powers but with well-separated action spectra. NpHR, like ChR2, functions in mammals without exogenous cofactors, and the two probes can be integrated with calcium imaging in mammalian brain tissue for bidirectional optical modulation and readout of neural activity. Likewise, NpHR and ChR2 can be targeted together to Caenorhabditis elegans muscle and cholinergic motor neurons to control locomotion bidirectionally. NpHR and ChR2 form a complete system for multimodal, high-speed, genetically targeted, all-optical interrogation of living neural circuits.     

Clonally dominant cardiomyocytes direct heart morphogenesis

As vertebrate embryos develop to adulthood, their organs undergo marked changes in size and tissue architecture. The heart acquires muscle mass and matures structurally to fulfil increasing circulatory needs, a process that is incompletely understood. Here we used multicolour clonal analysis to define the contributions of individual cardiomyocytes as the zebrafish heart undergoes morphogenesis from a primitive embryonic structure into its complex adult form. We find that the single-cardiomyocyte-thick wall of the juvenile ventricle forms by lateral expansion of several dozen cardiomyocytes into muscle patches of variable sizes and shapes. As juvenile zebrafish mature into adults, this structure becomes fully enveloped by a new lineage of cortical muscle. Adult cortical muscle originates from a small number of cardiomyocytes--an average of approximately eight per animal--that display clonal dominance reminiscent of stem cell populations. Cortical cardiomyocytes initially emerge from internal myofibres that in rare events breach the juvenile ventricular wall, and then expand over the surface. Our results illuminate the dynamic proliferative behaviours that generate adult cardiac structure, revealing clonal dominance as a key mechanism that shapes a vertebrate organ.     

Tumorigenesis: RAF/RAS oncogenes and mismatch-repair status

Genes of the RAF family encode kinases that are regulated by Ras and mediate cellular responses to growth signals. Activating mutations in one RAF gene, BRAF, have been found in a high proportion of melanomas and in a small fraction of other cancers. Here we show that BRAF mutations in colorectal cancers occur only in tumours that do not carry mutations in a RAS gene known as KRAS, and that BRAF mutation is linked to the proficiency of these tumours in repairing mismatched bases in DNA. Our results not only provide genetic support for the idea that mutations in BRAF and KRAS exert equivalent effects in tumorigenesis, but also emphasize the role of repair processes in establishing the mutation spectra that underpin human cancer.