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In recent years, several genes involved in complex neuron specification networks have been shown to control life span. However, information on these genes is scattered, and studies to discover new neuronal genes and gene cascades contributing to life span control are needed, especially because of the recognized role of the nervous system in governing homeostasis, aging, and longevity. Previously, we demonstrated that several genes that encode RNA polymerase II transcription factors and that are involved in the development of the nervous system affect life span in  Drosophila melanogaster . Among other genes,  escargot  ( esg ) was demonstrated to be causally associated with an increase in the life span of male flies. Here, we present new data on the role of  esg  in life span control. We show that  esg  affects the life spans of both mated and unmated males and females to varying degrees. By analyzing the survival and locomotion of the  esg  mutants, we demonstrate that  esg  is involved in the control of aging. We show that increased longevity is caused by decreased  esg  transcription. In particular, we demonstrate that  esg  knockdown in the nervous system increased life span, directly establishing the involvement of the neuronal  esg  function in life span control. Our data invite attention to the mechanisms regulating the  esg  transcription rate, which is changed by insertions of DNA fragments of different sizes downstream of the structural part of the gene, indicating the direction of further research. Our data agree with the previously made suggestion that alterations in gene expression during development might affect adult lifespan, due to epigenetic patterns inherited in cell lineages or predetermined during the development of the structural and functional properties of the nervous system.

Reduced Neuronal Transcription of Escargot, the Drosophila Gene Encoding a Snail-Type Transcription Factor, Promotes Longevity