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Title: Maternal starvation primes progeny response to nutritional stress
Authors: Voo, Kelly
Ching, Jeralyn Wen Hui
Lim, Joseph Wee Hao
Chan, Seow Neng
Ng, Amanda Yunn Ee
Heng, Jasmine Yi Ying
Lim, Shiao See
Pek, Jun Wei 
Issue Date: 29-Nov-2021
Publisher: Public Library of Science
Citation: Voo, Kelly, Ching, Jeralyn Wen Hui, Lim, Joseph Wee Hao, Chan, Seow Neng, Ng, Amanda Yunn Ee, Heng, Jasmine Yi Ying, Lim, Shiao See, Pek, Jun Wei (2021-11-29). Maternal starvation primes progeny response to nutritional stress. PLoS Genetics 17 (11) : e1009932. ScholarBank@NUS Repository.
Rights: Attribution 4.0 International
Abstract: Organisms adapt to environmental changes in order to survive. Mothers exposed to nutritional stresses can induce an adaptive response in their offspring. However, the molecular mechanisms behind such inheritable links are not clear. Here we report that in Drosophila, starvation of mothers primes the progeny against subsequent nutritional stress. We found that RpL10Ab represses TOR pathway activity by genetically interacting with TOR pathway components TSC2 and Rheb. In addition, starved mothers produce offspring with lower levels of RpL10Ab in the germline, which results in higher TOR pathway activity, conferring greater resistance to starvation-induced oocyte loss. The RpL10Ab locus encodes for the RpL10Ab mRNA and a stable intronic sequence RNA (sisR-8), which collectively repress RpL10Ab pre-mRNA splicing in a negative feedback mechanism. During starvation, an increase in maternally deposited RpL10Ab and sisR-8 transcripts leads to the reduction of RpL10Ab expression in the offspring. Our study suggests that the maternally deposited RpL10Ab and sisR-8 transcripts trigger a negative feedback loop that mediates intergenerational adaptation to nutritional stress as a starvation response. © 2021 Voo et al. This is an open access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
Source Title: PLoS Genetics
ISSN: 1553-7390
DOI: 10.1371/journal.pgen.1009932
Rights: Attribution 4.0 International
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