Host genetics and diet jointly shape the microbiome of Drosophila melanogaster but do not predict lifespan or age-related traits - Biogerontology

The microbiome is a key determinant of organismal health, yet inter-individual variability and heterogeneous responses to environmental conditions complicates the understanding of its effects on hosts. Here, we present a comprehensive analysis using the Drosophila Genetic Reference Panel (DGRP) to investigate how the interplay between host genetic variation and diet influences microbiome composition, and to assess whether microbiome features in young flies can be used to predict lifespan and age-related traits. Our findings show that adult flies reared on a nutritionally rich control diet exhibited higher microbial richness but lower evenness compared to those on a nutritionally poor restricted diet. Principal component analysis (PCA) highlighted substantial diversity among lines reared on the same diet, and this variation was evidenced by high heritability estimates for all measured α-diversity metrics, including Unique OTU counts, Shannon and Simpson indices, as well as the relative abundances of genera and species with relative abundances exceeding 1%. These results underscore the critical roles of both environmental factors and genetic variation in shaping microbiome composition under different dietary conditions. Moreover, we identified widespread genotype-by-diet interactions, suggesting that the genetic regulation of the microbiome is highly complex. Finally, we found that the microbiome features of young flies including diversity indices, taxonomic abundances, or ordination scores cannot predict age-associated phenotypes (lifespan, locomotor activity, dry weight, and heat knockdown time). Our findings offer valuable insights into the genetic architecture that governs microbiome composition, dietary responses, and aging in Drosophila melanogaster.

Cyst stem cell lineage GAL4 transgenes are robustly expressed in hub cells of the Drosophila testis stem cell niche | microPublication

Retrovirus insertions in host transcripts trigger de novo piRNA immunity - The EMBO Journal

How host organisms adapt their defense systems to newly invading transposable elements remains poorly understood. Here, we show how Drosophila melanogaster acquired PIWI-interacting RNA (piRNA)-mediated immunity against the endogenous retrovirus Tirant. We uncover two distinct modes of de novo piRNA biogenesis by combining genetics, small RNA profiling, and population genomics. The primary route involves antisense insertions into the flamenco cluster, a master locus for transposon control. Unexpectedly, a second, equally potent mechanism arises from antisense Tirant insertions within host gene 3′ UTRs. This process requires host gene transcription but is independent of host gene identity. Our findings challenge prevailing models that tie piRNA precursor specification to genomic origin or nuclear RNA processing context. Instead, they reveal a flexible mechanism that turns a critical vulnerability of transposons into an advantage for the host. When transposition occurs into host gene exons, chimeric antisense transcripts are exported to the cytoplasm, inadvertently initiating piRNA production and enabling rapid, adaptive genome defense against new invaders.