Abstract
During suboptimal growth conditions, Caenorhabditis elegans larvae undergo a global developmental arrest called “dauer.” During this stage, the germline stem cells (GSCs) become quiescent in an AMP-activated Protein Kinase (AMPK)-dependent manner, and in the absence of AMPK, the GSCs overproliferate and lose their reproductive capacity, leading to sterility when mutant animals resume normal growth. These defects correlate with the altered abundance and distribution of a number of chromatin modifications, all of which can be corrected by disabling components of the endogenous small RNA pathway, suggesting that AMPK regulates germ cell integrity by targeting an RNA interference (RNAi)-like pathway during dauer. The expression of AMPK in somatic cells restores all the germline defects, potentially through the transmission of small RNAs. Our findings place AMPK at a pivotal position linking energy stress detected in the soma to a consequent endogenous small RNA–mediated adaptation in germline gene expression, thereby challenging the “permeability" of the Weismann barrier.
Highlights
It is becoming more widely accepted that life history can affect developmental and behavioural outcomes, either in a temporary, or often in a more permanent manner
We reveal the importance of the endogenous small RNA pathway and its regulation by AMPK
Defects in the dauer germ line result in post-dauer sterility in AMPK mutants
Summary
It is becoming more widely accepted that life history can affect developmental and behavioural outcomes, either in a temporary, or often in a more permanent manner These modifications can occur downstream of a broad spectrum of environmental factors, including temperature, light, resource availability, population density, and even the presence of predators; all of which can influence gene expression, often with dramatic phenotypic consequences [1, 2]. Because the transmission of these molecular memories can span one or several generations, these modifications must impinge in some way upon the germ line, providing some adaptive phenotypic change in the unexposed future generations [4,5,6,7] These epigenetic modifications in the germ cells can have a significant impact on successive generations, yet the molecular mechanisms through which “experience” is transduced to the genome across several generations remains ill-defined
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