Microscopic image showing localization of the YOX1 transcript at P-bodies in the cytoplasm of budding yeast cells. YOX1 mRNA was tagged with MS2 repeats and visualized using the MS2 coat protein fused to GFP, and P-bodies were detected using Pat1 tagged with mCherry.
Raphael Loll-Krippleber from the Brown lab describes how yeast cells exposed to DNA replication stress induced by the anti-cancer drug hydroxyurea use RNA decay to reprogram gene expression. Using complementary functional genomics approaches Raphael found that a specific mRNA encoding the transcriptional repressor Yox1 is degraded at P-bodies sites to prevent accumulation of the Yox1 repressor in the nucleus. Up-regulation of YOX1 expression, as observed when P-body function is impaired, causes transcriptional down-regulation of a network of genes that is important for hydroxyurea resistance. One effector of this network, acetaldehyde dehydrogenase, prevents toxic accumulation of acetaldehyde and promotes replication stress resistance. This work, published in Nature Communications, identifies key targets of RNA decay that are important when DNA replication is perturbed.
Reference
Raphael Loll-Krippleber and Grant W. Brown. P-body proteins regulate transcriptional rewiring to promote DNA replication stress resistance. Nature Communications 8: 558 (2017) doi:10.1038/s41467-017-00632-2
