Lamin proteins form a meshwork beneath the nuclear envelope and contribute to many different cellular processes. Mutations in lamins cause defective organogenesis in mouse models and human diseases that affect adipose tissue, brain, skeletal muscle, and the heart. In vitro cell culture studies have shown that lamins help maintain nuclear shape and facilitate cell migration. However, whether these defects contribute to improper tissue building in vivo requires further clarification. By studying the heart epicardium during embryogenesis, we show that Lb1-null epicardial cells exhibit in vivo and in vitro migratory delay. Transcriptome analyses of these cells suggest that Lb1 influences the expression of cell adhesion genes, which could affect cell migration during epicardium development. These epicardial defects are consistent with incomplete development of both vascular smooth muscle and compact myocardium at later developmental stages in Lb1-null embryos. Further, we found that Lb1-null epicardial cells have a delayed nuclear morphology change in vivo, suggesting that Lb1 facilitates morphological changes associated with migration. These findings suggest that Lb1 contributes to nuclear shape maintenance and migration of epicardial cells and highlights the use of these cells for in vitro and in vivo study of these classic cell biological phenomena.

B-type lamins are major constituents of the nuclear lamina in all metazoan cells, yet have specific roles in the development of certain cell types. Although they are speculated to regulate gene expression in developmental contexts, a direct link between B-type lamins and developmental gene expression in an in vivo system is currently lacking. Here, we identify lamin B1 as a key regulator of gene expression required for the formation of functional olfactory sensory neurons. By using targeted knockout in olfactory epithelial stem cells in adult mice, we show that lamin B1 deficient neurons exhibit attenuated response to odour stimulation. This deficit can be explained by decreased expression of genes involved in mature neuron function, along with increased expression of genes atypical of the olfactory lineage. These results support that the broadly expressed lamin B1 regulates expression of a subset of genes involved in the differentiation of a specific cell type.

Increasing the thermostability of amorphous materials has been a long journey to improve their properties. The metastable nature of chalcogenide glasses limits their practical applications as an amorphous semiconductor in photovoltaic performance. Here, we report the formation and physical properties of ultrastable amorphous Sb2Se3 with an enhanced thermal stability compared to ordinary amorphous Sb2Se3 (Delta T-x= 17 K). By in situ high temperature-high energy synchrotron X-ray diffraction, the difference in structure relaxation between ordinary and ultrastable amorphous Sb2Se3 was manifested by local structure evolution. Ultrastable amorphous Sb2Se3 showed the smallest surface roughness and highest refractive index, the mechanism behind was further discussed in terms of fast molecular mobility and molecular orientation during vapor deposition. Formation of ultrastable amorphous Sb2Se3 demonstrated a promising avenue to obtain novel functional amorphous semiconductor with modulated structure and property.

Lamins are structural components of the nuclear lamina (NL) that regulate genome organization and gene expression, but the mechanism remains unclear. Using Hi-C, we show that lamins maintain proper interactions among the topologically associated chromatin domains (TADs) but not their overall architecture. Combining Hi-C with fluorescence in situ hybridization (FISH) and analyses of lamina-associated domains (LADs), we reveal that lamin loss causes expansion or detachment of specific LADs in mouse ESCs. The detached LADs disrupt 3D interactions of both LADs and interior chromatin. 4C and epigenome analyses further demonstrate that lamins maintain the active and repressive chromatin domains among different TADs. By combining these studies with transcriptome analyses, we found a significant correlation between transcription changes and the interaction changes of active and inactive chromatin domains These findings provide a foundation to further study how the nuclear periphery impacts genome organization and transcription in development and NL-associated diseases.

Genome-wide mapping of lamin-B1-genome interactions has shown that gene-poor and transcriptionally inactive genomic regions are associated with the nuclear lamina. Numerous studies have suggested that lamins, the major structural components of the nuclear lamina, play a role in global chromatin organization and gene expression. How lamins could influence the 3D genome organization and transcription from the nuclear periphery has, however, remained unclear. Our recent studies showed that lamins differentially regulate distinct lamina-associated chromatin domains (LADs) at the nuclear periphery, which can in turn influence global 3D genome organization and gene expression. In this Extra View, we discuss how by using various genomics tools, it has become possible to reveal the functions of lamins in orchestrating 3D genome organization and gene expression.

The genome-wide chromosome conformation capture (Hi-C) has revealed that the eukaryotic genome can be partitioned into A and B compartments that have distinctive chromatin and transcription features. Current Principle Component Analyses (PCA)-based method for the A/B compartment prediction based on Hi-C data requires substantial CPU time and memory. We report the development of a method, CscoreTool, which enables fast and memory-efficient determination of A/B compartments at high resolution even in datasets with low sequencing depth.

Bases are called using Illumina pipeline Casava 1.8.Reads are mapped to the drosophila genome using Tophat2. Refseq annotations of known exon junctions are provided with -G option.Number of reads on each gene were counted using custom script, and differentially expressed genes were called using edgeR.Genome_build: Dm3Supplementary_files_format_and_content: tab-delimited text file listing the number of reads on each gene

Bases are called using Illumina pipeline Casava 1.8.Reads are mapped to the drosophila genome using Tophat2. Refseq annotations of known exon junctions are provided with -G option.Number of reads on each gene were counted using custom script, and differentially expressed genes were called using edgeR.Genome_build: Dm3Supplementary_files_format_and_content: tab-delimited text file listing the number of reads on each gene

Bases are called using Illumina pipeline Casava 1.8.Reads are mapped to the drosophila genome using Tophat2. Refseq annotations of known exon junctions are provided with -G option.Number of reads on each gene were counted using custom script, and differentially expressed genes were called using edgeR.Genome_build: Dm3Supplementary_files_format_and_content: tab-delimited text file listing the number of reads on each gene

Bases are called using Illumina pipeline Casava 1.8.Reads are mapped to the drosophila genome using Tophat2. Refseq annotations of known exon junctions are provided with -G option.Number of reads on each gene were counted using custom script, and differentially expressed genes were called using edgeR.Genome_build: Dm3Supplementary_files_format_and_content: tab-delimited text file listing the number of reads on each gene