Abstract
Ribosomal RNA gene (rDNA) copy number variation modulates heterochromatin formation and influences the expression of a large fraction of the Drosophila ge-nome. This discovery, along with the link between rDNA, aging, and disease, high-lights the importance of understanding how natural rDNA copy number variation arises. Pursuing the relationship between rDNA expression and stability, we have discovered that increased dietary yeast concentration, emulating periods of dietary excess during life, results in somatic rDNA instability and copy number reduction. Modulation of Insulin/TOR signaling produces similar results, indicating a role for known nutrient sensing signaling pathways in this process. Furthermore, adults fed elevated dietary yeast concentrations produce offspring with fewer rDNA copies demonstrating that these effects also occur in the germline, and are transgenera-tionally heritable. This finding explains one source of natural rDNA copy number variation revealing a clear long-term consequence of diet.
Highlights
It is clear that an organism’s gene expression patterns are responsive to environmental input
We show that altering the nutritional medium of Drosophila cultures, emulating dietary largess in the wild, increases expression of the high copy-number ribosomal RNA genes and results in ribosomal DNA (rDNA) instability and loss
Previous work from yeast and filamentous fungi, Drosophila, plants, and experimental mammal systems have suggested that rDNA expression increases in response to diet, while other work has shown that derepression of the rDNA results in instability and loss
Summary
It is clear that an organism’s gene expression patterns are responsive to environmental input Often, this influence is not limited to short-term regulatory changes, but can persist through multiple cell divisions and can, in some cases, be transmitted to offspring. Because genome stability, of highly-repetitive (e.g., pentameric repeat) sequences or middle-repetitive transposable elements, is modified by silencing involving repressive histone modifications, “epigenetic” perturbations may have both direct and long-term consequences: the former caused by disruption of silencing leading to “epigenetic instability,” and the latter by creating transmissible changes to chromosomes that themselves may affect gene regulation in subsequent generations This consideration significantly adds to models of epigenetic inheritance that often overlook the ease with which histones and DNA methylation can be modified and the rapid rate at which they are turned over in non-dividing cells [9, 10]. Recent [11,12,13,14] and previous [15] findings show epigenetic silencing is unstable even in non-dividing cells, making it a difficult challenge to reconcile models of chromatin (e.g., histone) mediated epigenetic silencing with transgenerational (i.e., mitotic and/or meiotic) inheritance
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