Bee mechanosensory hairs respond to electric fields
Bumblebee showing the array of hairs on its body.
Electroreception is common in aquatic mammals, which evolved in the conductive medium of saltwater. However, how bees respond to weak electric fields remains poorly understood. Focusing on the Bombus terrestris bumblebee, Gregory Sutton et al. (pp. 7261–7265) tested two potential mechanisms that would allow insects to detect electric fields through the insulating medium of dry air: deflections of either the antenna or mechanosensory hairs. Using noncontact laser vibration measurements, the authors found that both antenna and hairs deflect in response to an electric field, but hairs move more rapidly and with overall greater displacements. In addition, electrophysiology measurements reveal that deflections in hairs trigger neural activity in bumblebees, with no corresponding nervous system response for the antenna. This ability may arise from the low mass and high stiffness of bumblebee mechanosensory hairs, the rigid, lever-like motion of which resembles acoustically sensitive spider hairs and mosquito antennae. Noting that mechanosensory hairs are common in arthropods, the authors suggest that electroreception could be a widespread phenomenon that provides insects with a variety of currently unrecognized abilities. — T.J.
Treating prostate cancer via protein degradation

ARV-771, a von Hippel–Landau super-enzyme complex.
Androgen deprivation by surgical or chemical castration can lead to initial remission of prostate cancer, but the disease often progresses to castration-resistant prostate cancer (CRPC), in which androgen receptor (AR) signaling continues despite low androgen levels. Drugs that block AR signaling can improve survival among CRPC patients, but patients invariably acquire secondary resistance to these drugs. As an alternative approach, Kanak Raina et al. (pp. 7124–7129) developed the small molecule proteolysis-targeting chimera, ARV-771, that enhances the degradation of bromodomain and extra-terminal (BET) proteins by binding simultaneously to a BET protein and an enzyme that tags proteins for degradation. BET inhibitors have been shown to inhibit tumor growth in preclinical models of CRPC, but the efficacy of BET degradation has not been demonstrated in vivo. The authors found that treating CRPC cells in culture with ARV-771 reduced both AR levels and AR signaling and led to increased caspase activation, indicative of cell death. Treatment of CRPC mouse models with ARV-771 led to reduced AR levels and dose-dependent inhibition or regression of tumor growth. The results suggest that enhancing BET protein degradation might be an effective therapeutic strategy for CRPC, according to the authors. — B.D.
Silicic volcanism on Mars
In August 2015, the Mars Science Laboratory rover Curiosity detected the mineral tridymite at the silica-rich Buckskin drill site in Gale crater on Mars. The discovery was unexpected because this mineral on Earth usually results from silicic volcanism, a high-temperature volcanic process not typically associated with rock formation on Mars. Using Curiosity’s onboard chemistry and mineralogy instrument, which possesses X-ray diffraction capabilities, Richard Morris et al. (pp. 7071–7076) analyzed the tridymite-bearing sample and determined its composition and structure. Based on the results, as well as the geologic setting in Gale crater, the authors suggest a scenario in which material from silicic volcanism was carried by water into a formation known as “Lake Gale” and deposited as sediment that gradually became mudstone rock. The findings may represent the first in situ evidence of silicic volcanism on Mars and support a growing body of research that points to the planet’s complex geologic history, according to the authors. — T.J.
Tau protein, stress, and cognitive deficits
Chronic stress can induce depressive behavior and memory deficits in addition to neuronal atrophy implicated in the development of neurological disorders. For example, both stress and Alzheimer’s disease (AD) are marked by abnormalities in the Tau protein, which plays a key role in stabilizing the cytoskeleton to help neurons maintain shape and function properly. Sofia Lopes et al. (pp. E3755–E3763) report that Tau is a key molecular mediator of the effects of chronic stress on cognitive, mood, and neuronal deficits. The authors exposed mice to stressful conditions, such as restraint, a vibrating platform, overcrowding, or a hot air stream, for 6 weeks. Exposure to chronic unpredictable stress caused anxiety, depressive-like behavior, and impaired memory in control mice. However, mice that were genetically modified to lack Tau were protected from these stress-induced mood and cognitive deficits. Moreover, Tau-deficient mice showed relatively less stress-induced disruption of neuronal activity in the hippocampus, a brain region that plays a key role in emotion and memory. Taken together, the findings suggest that shared Tau-dependent neurobiological mechanisms may underlie both AD and stress-induced mood and cognitive impairments. According to the authors, the study supports the idea that Tau-targeting therapies could potentially benefit patients with AD and other stress-related disorders. — J.W.
Glycolysis and visual–motor learning
Glucose metabolism supports the brain’s energy needs, mainly through an oxygen-consuming process known as oxidative phosphorylation. However, around 10–15% of glucose used by the adult brain is metabolized through glycolysis, which does not require oxygen and generates little energy. Because glycolysis produces molecules required for learning, Benjamin Shannon et al. (pp. E3782–E3791) examined the role of glycolysis in learning-associated changes in the human brain using PET and fMRI. Forty-six healthy participants were trained on an out-and-back reaching task using a stylus, a tablet, and a visual display screen. In each trial, the participants saw a circle projected on the center of the screen, along with eight equally spaced circles in the periphery of the screen. Using the tablet, the participants moved a stylus first to a flashing circle in the periphery and then back to the center of the screen. However, half of the participants experienced a gradually imposed mismatch between the actual movement made by their hand and the stylus movement projected on the screen. Participants who experienced the rotational mismatch adapted to this deviation and showed elevated levels of glycolysis in the brain region called Brodmann Area 44. According to the authors, glycolysis might enable learning-required adjustments in the human brain. — J.W.

