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Metabolomics,Unknown,Transcriptomics,Genomics,Proteomics

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MML-1/Mondo complexes regulate HLH-30/TFEB via TOR inhibition to promote longevity in response to signals from the reproductive system

ABSTRACT: Comprehensive transcriptome analysis of hlh-30, mml-1 and mxl-2 in N2 (wildtype) and glp-1 background.

INSTRUMENT(S): Illumina HiSeq 2500

ORGANISM(S): Caenorhabditis elegans

SUBMITTER: Sven Templer

PROVIDER: E-MTAB-3686 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Mondo complexes regulate TFEB via TOR inhibition to promote longevity in response to gonadal signals.

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Project description:Accumulating evidence has demonstrated the presence of inter-tissue communication regulating systemic aging, but the underlying molecular network has not been fully explored. We and others previously showed that two basic helix-loop-helix transcription factors, MML-1 and HLH-30, are required for lifespan extension in several longevity paradigms, including germline-less Caenorhabditis elegans. However, it is unknown what tissues these factors target to promote longevity. Here, using tissue-specific knockdown experiments, we found that MML-1 and its heterodimer partners MXL-2 and HLH-30 act primarily in neurons to extend longevity in germline-less animals. Neuronal functions of MML-1/MXL-2 and HLH-30 are also essential to prevent aging in non-neuronal tissues, including muscle and the intestine. Interestingly, however, both the temporal requirement and the downstream function of MML-1 in neurons were distinct from those of HLH-30. MML-1 was active early, while HLH-30 functioned later in life to sustain longevity in germline-less animals. Moreover, neuronal RNA interference (RNAi)-based transcriptome analysis revealed that the glutamate transporter GLT-5 is a novel downstream target of MML-1 but not HLH-30. Furthermore, the MML-1–GTL-5 axis in neurons is critical to prevent an age-dependent collapse of proteostasis and increased oxidative stress through autophagy and peroxidase MLT-7, respectively, in long-lived animals. Collectively, our study revealed that systemic aging is regulated by a novel molecular network involving neuronal MML-1 function in both neural and peripheral tissues.

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