Brain representations of motion and position in the double-drift illusion.

In the 'double-drift' illusion, local motion within a window moving in the periphery of the visual field alters the window's perceived path. The illusion is strong even when the eyes track a target whose motion matches the window so that the stimulus remains stable on the retina. This implies that the illusion involves the integration of retinal signals with non-retinal eye-movement signals. To identify where in the brain this integration occurs, we measured BOLD fMRI responses in visual cortex while subjects experienced the double-drift illusion. We then used a combination of univariate and multivariate decoding analyses to identify (1) which brain areas were sensitive to the illusion and (2) whether these brain areas contained information about the illusory stimulus trajectory. We identified a number of cortical areas that responded more strongly during the illusion than a control condition that was matched for low-level stimulus properties. Only in area hMT+ was it possible to decode the illusory trajectory. We additionally performed a number of important controls that rule out possible low-level confounds. Concurrent eye tracking confirmed that subjects accurately tracked the moving target; we were unable to decode the illusion trajectory using eye position measurements recorded during fMRI scanning, ruling out explanations based on differences in oculomotor behavior. Our results provide evidence for a perceptual representation in human visual cortex that incorporates extraretinal information.

Spatiotopic and retinotopic memory in the context of natural images.

Neural responses throughout the visual cortex encode stimulus location in a retinotopic (i.e., eye-centered) reference frame, and memory for stimulus position is most precise in retinal coordinates. Yet visual perception is spatiotopic: objects are perceived as stationary, even though eye movements cause frequent displacement of their location on the retina. Previous studies found that, after a single saccade, memory of retinotopic locations is more accurate than memory of spatiotopic locations. However, it is not known whether various aspects of natural viewing affect the retinotopic reference frame advantage. We found that the retinotopic advantage may in part depend on a retinal afterimage, which can be effectively nullified through backwards masking. Moreover, in the presence of natural scenes, spatiotopic memory is more accurate than retinotopic memory, but only when subjects are provided sufficient time to process the scene before the eye movement. Our results demonstrate that retinotopic memory is not always more accurate than spatiotopic memory and that the fidelity of memory traces in both reference frames are sensitive to the presence of contextual cues.

Ferroptosis occurs through an osmotic mechanism and propagates independently of cell rupture.

Ferroptosis is a regulated form of necrotic cell death that is caused by the accumulation of oxidized phospholipids, leading to membrane damage and cell lysis1,2. Although other types of necrotic death such as pyroptosis and necroptosis are mediated by active mechanisms of execution3-6, ferroptosis is thought to result from the accumulation of unrepaired cell damage1. Previous studies have suggested that ferroptosis has the ability to spread through cell populations in a wave-like manner, resulting in a distinct spatiotemporal pattern of cell death7,8. Here we investigate the mechanism of ferroptosis execution and discover that ferroptotic cell rupture is mediated by plasma membrane pores, similarly to cell lysis in pyroptosis and necroptosis3,4. We further find that intercellular propagation of death occurs following treatment with some ferroptosis-inducing agents, including erastin2,9 and C' dot nanoparticles8, but not upon direct inhibition of the ferroptosis-inhibiting enzyme glutathione peroxidase 4 (GPX4)10. Propagation of a ferroptosis-inducing signal occurs upstream of cell rupture and involves the spreading of a cell swelling effect through cell populations in a lipid peroxide- and iron-dependent manner.

Target capture strategy selection in a simulated marksmanship task.

This paper examines how individuals track targets that move in relatively unpredictable trajectories. Gaze and behavioural data were captured as twenty two participants learned a simulated competitive marksmanship task known colloquially as the Death Star over six training days. Participants spontaneously selected one of two consistent target-tracking strategies with approximately equal probability. Participants employed either chasing behaviour, in which gaze follows a target's trajectory before a shot, or ambushing behaviour, wherein gaze anticipates the trajectory and the participant intercepts a moving target predictively. All participants improved in task performance measures (completion time and number of shots), but did so at the expense of accuracy in missed shot attempts. Surprisingly, neither behavioural strategy offered a significant advantage in task performance measures, indicating that either may be equally effective in tackling a hand-eye coordination task with complex target motion such as the Death Star.

SOX10 regulates an alternative promoter at the Charcot-Marie-Tooth disease locus MTMR2.

Schwann cells are the myelinating glia of the peripheral nervous system and dysfunction of these cells causes motor and sensory peripheral neuropathy. The transcription factor SOX10 is critical for Schwann cell development and maintenance, and many SOX10 target genes encode proteins required for Schwann cell function. Loss-of-function mutations in the gene encoding myotubularin-related protein 2 (MTMR2) cause Charcot-Marie-Tooth disease type 4B1 (CMT4B1), a severe demyelinating peripheral neuropathy characterized by myelin outfoldings along peripheral nerves. Previous reports indicate that MTMR2 is ubiquitously expressed making it unclear how loss of this gene causes a Schwann cell-specific phenotype. To address this, we performed computational and functional analyses at MTMR2 to identify transcriptional regulatory elements important for Schwann cell expression. Through these efforts, we identified an alternative, SOX10-responsive promoter at MTMR2 that displays strong regulatory activity in immortalized rat Schwann (S16) cells. This promoter directs transcription of a previously unidentified MTMR2 transcript that is enriched in mouse Schwann cells compared to immortalized mouse motor neurons (MN-1), and is predicted to encode an N-terminally truncated protein isoform. The expression of the endogenous transcript is induced in a heterologous cell line by ectopically expressing SOX10, and is nearly ablated in Schwann cells by impairing SOX10 function. Intriguingly, overexpressing the two MTMR2 protein isoforms in HeLa cells revealed that both localize to nuclear puncta and the shorter isoform displays higher nuclear localization compared to the longer isoform. Combined, our data warrant further investigation of the truncated MTMR2 protein isoform in Schwann cells and in CMT4B1 pathogenesis.