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Background <p>Insulin signaling is a conserved regulator of growth, metabolism, and lifespan across metazoans. While its systemic roles are well established, the mechanisms by which insulin coordinates tissue-specific transcriptional programs that underlie distinct functional demands remain incompletely understood. In particular, the differential impact of reduced insulin signaling on different tissues has not been systematically explored.</p> Results <p>We performed a comparative transcriptomic analysis of <i>Drosophila melanogaster</i> olfactory sensory neurons (OSNs) and fat body (Fb) to investigate how reduced insulin signaling remodels gene expression in neural and metabolic tissues. Across both tissue types, insulin reduction suppressed key pathways involved in protein synthesis and mRNA surveillance, indicating shared regulatory responses. However, distinct tissue-specific transcriptional adaptations were also observed. In OSNs, insulin reduction led to the upregulation of synaptic and signaling genes, alongside the downregulation of proteostasis-related factors, suggesting enhanced neural plasticity that may come at the cost of long-term neuronal maintenance. In contrast, the Fb exhibited widespread metabolic suppression accompanied by feedback activation of stress-responsive insulin-like peptide genes, consistent with a shift toward hypometabolic adaptation. Network and pathway analyses revealed that these tissue-specific responses involved distinct regulatory architectures affecting core insulin pathway components and gene families.</p> Conclusions <p>Our findings demonstrate that reduced insulin signaling elicits both shared and divergent transcriptional programs in neural and metabolic tissues of <i>Drosophila melanogaster</i>. These findings reveal how insulin signaling orchestrates tissue-specific transcriptional landscapes that may underlie differential resilience or vulnerability to cognitive and metabolic decline.</p>

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Insulin signaling engages divergent transcriptional mechanisms in neural and metabolic tissues

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2026年2月19日

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  • Roshni Jain,
  • Rutuj Kolhe,
  • Cassandra Hui,
  • Juli Petereit,
  • Dennis Mathew

摘要

Background

Insulin signaling is a conserved regulator of growth, metabolism, and lifespan across metazoans. While its systemic roles are well established, the mechanisms by which insulin coordinates tissue-specific transcriptional programs that underlie distinct functional demands remain incompletely understood. In particular, the differential impact of reduced insulin signaling on different tissues has not been systematically explored.

Results

We performed a comparative transcriptomic analysis of Drosophila melanogaster olfactory sensory neurons (OSNs) and fat body (Fb) to investigate how reduced insulin signaling remodels gene expression in neural and metabolic tissues. Across both tissue types, insulin reduction suppressed key pathways involved in protein synthesis and mRNA surveillance, indicating shared regulatory responses. However, distinct tissue-specific transcriptional adaptations were also observed. In OSNs, insulin reduction led to the upregulation of synaptic and signaling genes, alongside the downregulation of proteostasis-related factors, suggesting enhanced neural plasticity that may come at the cost of long-term neuronal maintenance. In contrast, the Fb exhibited widespread metabolic suppression accompanied by feedback activation of stress-responsive insulin-like peptide genes, consistent with a shift toward hypometabolic adaptation. Network and pathway analyses revealed that these tissue-specific responses involved distinct regulatory architectures affecting core insulin pathway components and gene families.

Conclusions

Our findings demonstrate that reduced insulin signaling elicits both shared and divergent transcriptional programs in neural and metabolic tissues of Drosophila melanogaster. These findings reveal how insulin signaling orchestrates tissue-specific transcriptional landscapes that may underlie differential resilience or vulnerability to cognitive and metabolic decline.