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

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

Aging of immune organs, termed as immunosenescence, is suspected to promote systemic inflammation and age-associated disease. The cause of immunosenescence and how it promotes disease, however, has remained unclear. We report that the Drosophila fat body, a major immune organ, undergoes immunosenescence andmounts strong systemic inflammation that leads to deregulation of immune deficiency (IMD) signaling in the midgut of old animals. Inflamed old fat bodies secrete circulating peptidoglycan recognition proteins that repress IMD activity in the midgut, thereby promoting gut hyperplasia. Further, fat body immunosenecence is caused by age-associated lamin-B reduction specifically in fat body cells, which then contributes to heterochromatin loss and derepression of genes involved in immune responses. As lamin-associated heterochromatin domains are enriched for genes involved in immune response in both Drosophila and mammalian cells, our findings may provide insights into the cause and consequence of immunosenescence during mammalian aging.

Cellular architectural proteins often participate in organ development and maintenance. Although functional decay of some of these proteins during aging is known, the cell-type-specific developmental role and the cause and consequence of their subsequent decay remain to be established especially in mammals. By studying lamins, the nuclear structural proteins, we demonstrate that lamin-B1 functions specifically in the thymic epithelial cells (TECs) for proper thymus organogenesis. An up-regulation of proinflammatory cytokines in the intra-thymic myeloid immune cells during aging accompanies a gradual reduction of lamin-B1 in adult TECs. We show that these cytokines can cause senescence and lamin-B1 reduction of the young adult TECs. Lamin-B1 supports the expression of TEC genes that can help maintain the adult TEC subtypes we identified by single-cell RNA-sequencing, thymic architecture, and function. Thus, structural proteins involved in organ building and maintenance can undergo inflammation-driven decay which can in turn contribute to age-associated organ degeneration.

We present the largest-ever sample of 79 Ly? emitters (LAEs) at z?7.0 selected in the COSMOS and CDFS fields of the LAGER project (the Lyman Alpha Galaxies in the Epoch of Reionization). Our newly amassed ultradeep narrowband exposure and deeper/wider broadband images have more than doubled the number of LAEs in COSMOS, and we have selected 30 LAEs in the second field CDFS. We detect two large-scale LAE-overdense regions in the COSMOS that are likely protoclusters at the highest redshift to date. We perform injection and recovery simulations to derive the sample incompleteness. We show that significant incompleteness comes from blending with foreground sources, which, however, has not been corrected in LAE luminosity functions (LFs) in the literature. The bright-end bump in the Ly? LF in COSMOS is confirmed with six (two newly selected) luminous LAEs (L-Ly? > 10(43.3) erg s(?1)). Interestingly, the bump is absent in CDFS, in which only one luminous LAE is detected. Meanwhile, the faint-end LFs from the two fields agree well with each other. The six luminous LAEs in COSMOS coincide with two LAE-overdense regions, while such regions are not seen in CDFS. The bright-end LF bump could be attributed to ionized bubbles in a patchy reionization. It appears associated with cosmic overdensities and thus supports an inside-out reionization topology at z?7.0, i.e., the high-density peaks were ionized earlier compared to the voids. An average neutral hydrogen fraction of x(H i)?0.2?0.4 is derived at z?7.0 based on the cosmic evolution of the Ly? LF.

Main conclusion This study demonstrates that brassinosteroid is essential for seedling and shoot growth in moso bamboo. The shoot of moso bamboo is known to grow extremely fast. The roles of phytohormones in such fast growth of bamboo shoot remain unclear. Here we reported that endogenous brassinosteroid (BR) is a major factor promoting bamboo shoot internode elongation. Reducing endogenous brassinosteroid level by its biosynthesis inhibitor propiconazole stunted shoot growth in seedling stage, whereas exogenous BR application promoted scale leaf elongation and the inclination of lamina joint of leaves and scale leaves. Genome-wide transcriptome analysis identified hundreds of genes whose expression levels are altered by BR and propiconazole in shoots and roots of bamboo seedling. The data show that BR regulates cell wall-related genes, hydrogen peroxide catabolic genes, and auxin-related genes. Our study demonstrates an essential role of BR in fast growth bamboo shoots and identifies a large number of BR-responsive genes in bamboo seedlings.