Dominant effects of the histone mutant H3-L61R on Spt16-gene interactions in budding yeast.

Recent studies have unveiled an association between an L61R substitution within the human histone H3.3 protein and the presentation of neurodevelopmental disorders in two patients. In both cases, the mutation responsible for this substitution is encoded by one allele of the H3F3A gene and, if this mutation is indeed responsible for the disease phenotypes, it must act in a dominant fashion since the genomes of these patients also harbour three other alleles encoding wild-type histone H3.3. In our previous work in yeast, we have shown that most amino acid substitutions at H3-L61 cause an accumulation of the Spt16 component of the yFACT histone chaperone complex at the 3' end of transcribed genes, a defect we have attributed to impaired yFACT dissociation from chromatin following transcription. In those studies, however, the H3-L61R mutant had not been tested since it does not sustain viability when expressed as the sole source of histone H3 in cells. In the present work, we show that H3-L61R impairs proper Spt16 dissociation from genes when co-expressed with wild-type histone H3 in haploid cells as well as in diploid cells that express the mutant protein from one of four histone H3-encoding alleles. These results, combined with other studies linking loss of function mutations in human Spt16 and neurodevelopmental disorders, provide a possible molecular mechanism underlying the neurodevelopmental disorders seen in patients expressing the histone H3.3 L61R mutant.

Experimental demonstration of broadband solar absorption beyond the lambertian limit in certain thin silicon photonic crystals.

The tantalizing possibility of 31% solar-to-electric power conversion efficiency in thin film crystalline silicon solar cell architectures relies essentially on solar absorption well beyond the Lambertian light trapping limit (Bhattacharya and John in Nat Sci Rep 9:12482, 2019). Up to now, no solar cell architecture has exhibited above-Lambertian solar absorption, integrated over the broad solar spectrum. In this work, we experimentally demonstrate two types of photonic crystal (PhC) solar cells architectures that exceed Lambertian light absorption, integrated over the entire 300-1,200 nm wavelength band. These measurements confirm theoretically predicted wave-interference-based optical resonances associated with long lifetime, slow-light modes and parallel-to-interface refraction. These phenomena are beyond the realm of ray optics. Using two types of 10-µm thick PhC's, first an Inverted Pyramid PhC with lattice constant a = 2,500 nm and second a Teepee PhC with a = 1,200 nm, we observe solar absorption well beyond the Lambertian limit over λ = 950-1,200 nm. Our absorption measurements correspond to the maximum-achievable-photocurrent-density (MAPD), under AM1.5G illumination at 4-degree incident angle, 41.29 and 41.52 mA/cm2 for the Inverted Pyramid and Teepee PhC, respectively, in agreement with wave-optics, numerical simulations. Both of these values exceed the MAPD (= 39.63 mA/cm2) corresponding to the Lambertian limit for a 10-µm thick silicon for solar absorption over the 300-1,200 nm band.

Synaptic depression depends on charge delivered to network.

In vitro neuronal networks cultured on microelectrode arrays enable the study of network electrophysiology on a fundamental level. Neuronal response to electrical stimulation is an area of interest at the laboratory bench and in the clinic, given its wide application for remedying neurological disorders. Here we investigated the change in cortical network response over time to varied amounts of charge used for stimulation, which may lead to a phenomenon known as selective adaptation. There is a charge threshold that invokes a reverberating network response; when stimulating at 900 mV, five stimulation electrodes were required to elicit a response across the entire network. Stimulating with more charge leads to greater synaptic depression over time when constant periodic stimulation is applied. Stimulating with 5 electrodes led to a decrease in network response to stimulation, whereas stimulating with 12 electrodes led to an extinction of network response. The previously hypothesized selective adaptation mechanism was not observed, implying that our random cortical assemblies have homogeneous excitatory and inhibitory subnetworks.