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

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.