PHA-4/FoxA senses nucleolar stress to regulate lipid accumulation in Caenorhabditis elegans

Jieyu Wu, Xue Jiang, Yamei Li, Tingting Zhu, Jingjing Zhang, Zhiguo Zhang, Linqiang Zhang, Yuru Zhang, Yanli Wang, Xiaoju Zou () and Bin Liang ()
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Jieyu Wu: Kunming Institute of Zoology, Chinese Academy of Sciences
Xue Jiang: Kunming Institute of Zoology, Chinese Academy of Sciences
Yamei Li: Kunming Institute of Zoology, Chinese Academy of Sciences
Tingting Zhu: Kunming Institute of Zoology, Chinese Academy of Sciences
Jingjing Zhang: Kunming Institute of Zoology, Chinese Academy of Sciences
Zhiguo Zhang: Kunming Institute of Zoology, Chinese Academy of Sciences
Linqiang Zhang: Kunming Institute of Zoology, Chinese Academy of Sciences
Yuru Zhang: Kunming Institute of Zoology, Chinese Academy of Sciences
Yanli Wang: Kunming Institute of Zoology, Chinese Academy of Sciences
Xiaoju Zou: Kunming University
Bin Liang: Kunming Institute of Zoology, Chinese Academy of Sciences

Nature Communications, 2018, vol. 9, issue 1, 1-17

Abstract: Abstract The primary function of the nucleolus is ribosome biogenesis, which is an extremely energetically expensive process. Failures in ribosome biogenesis cause nucleolar stress with an altered energy status. However, little is known about the underlying mechanism linking nucleolar stress to energy metabolism. Here we show that nucleolar stress is triggered by inactivation of RSKS-1 (ribosomal protein S6 kinase), RRP-8 (ribosomal RNA processing 8), and PRO-2/3 (proximal proliferation), all of which are involved in ribosomal RNA processing or inhibition of rDNA transcription by actinomycin D (AD), leading to excessive lipid accumulation in Caenorhabditis elegans. The transcription factor PHA-4/FoxA acts as a sensor of nucleolar stress to bind to and transactivate the expression of the lipogenic genes pod-2 (acetyl-CoA carboxylase), fasn-1 (fatty acid synthase), and dgat-2 (diacylglycerol O-acyltransferase 2), consequently promoting lipid accumulation. Importantly, inactivation of pha-4 or dgat-2 is sufficient to abolish nucleolar stress-induced lipid accumulation and prolonged starvation survival. The results revealed a distinct PHA-4-mediated lipogenesis pathway that senses nucleolar stress and shifts excessive energy for storage as fat.

Date: 2018
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DOI: 10.1038/s41467-018-03531-2

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