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Abstract Given the surpassing of the Shockley-Quiesser efficiency limit in conventional p-n junction photovoltaic effect, bulk photovoltaic effect (BPVE) has garnered significant research interest. However, the BPVE primarily focuses on a narrow wavelength range, limiting its potential applications. Here we report a giant infrared bulk photovoltaic effect in tellurene (Te) for broad-spectrum neuromodulation. The generated photocurrent in uniformly illuminated Te excludes other photoelectric effects and is attributed to the BPVE. The bulk photovoltaic wavelength in Te spans a wide range from the ultraviolet (390 nm) to the mid-infrared (3.8 µm). Moreover, the photocurrent density of 70.4 A cm−2 under infrared light simulation outperforms that in previous ultraviolet and visible semiconductors as well as infrared semimetals. Te attached to the dendrites or somata of the cortical neurons successfully elicit action potentials under broad-spectrum light irradiation. This work lays the foundation for the further development of infrared BPVE in narrow bandgap materials.

Abstract Haploinsufficient mutation in arginine and glutamine-rich protein 1 (Arglu1), a newly identified pre-mRNA splicing regulator, may be linked to neural developmental disorders associated with mental retardation and epilepsy in human patients, but the underlying causes remain elusive. Here we show that ablation of Arglu1 promotes radial glial cell (RG) detachment from the ventricular zone (VZ), leading to ectopic localized RGs in the mouse embryonic cortex. Although they remain proliferative, ectopic progenitors, as well as progenitors in the VZ, exhibit prolonged mitosis, p53 upregulation and cell apoptosis, leading to reduced neuron production, neuronal loss and microcephaly. RNA seq analysis reveals widespread changes in alternative splicing in the mutant mouse embryonic cortex, preferentially affecting genes involved in neuronal functions. Mdm2 and Mdm4 are found to be alternatively spliced at the exon 3 and exon 5 respectively, leading to absence of the p53-binding domain and nonsense-mediated mRNA decay (NMD) and thus relieve inhibition of p53. Removal of p53 largely rescues the microcephaly caused by deletion of Arglu1. Our findings provide mechanistic insights into cortical malformations of human patients with Arglu1 haploinsufficient mutation.

Abstract Spinal motor neurons deficiency results in a series of devastating disorders such as amyotrophic lateral sclerosis (ALS), spinal muscular atrophy (SMA) and spinal cord injury (SCI). These disorders are currently incurable, while human pluripotent stem cells (hPSCs)-derived spinal motor neurons are promising but suffered from inappropriate regional identity and functional immaturity for the study and treatment of posterior spinal cord related injuries. In this study, we have established human spinal cord neural progenitor cells (hSCNPCs) via hPSCs differentiated neuromesodermal progenitors (NMPs) and demonstrated the hSCNPCs can be continuously expanded up to 40 passages. hSCNPCs can be rapidly differentiated into posterior spinal motor neurons with high efficiency. The functional maturity has been examined in detail. Moreover, a co-culture scheme which is compatible for both neural and muscular differentiation is developed to mimic the neuromuscular junction (NMJ) formation in vitro. Together, these studies highlight the potential avenues for generating clinically relevant spinal motor neurons and modeling neuromuscular diseases through our defined hSCNPCs.