Abstract
The genome expression pattern is strongly modified during the heat shock response (HSR) to form an adaptive state. This may be partly achieved by modulating microRNA levels that control the expression of a great number of genes that are embedded within the gene circuitry. Here, we investigated the cross-talk between two highly conserved and universal house-keeping systems, the HSR and microRNA machinery, in Drosophila melanogaster. We demonstrated that pronounced interstrain differences in the microRNA levels are alleviated after heat shock (HS) to form a uniform microRNA pattern. However, individual strains exhibit different patterns of microRNA expression during the course of recovery. Importantly, HS-regulated microRNAs may target functionally similar HS-responsive genes involved in the HSR. Despite the observed general downregulation of primary microRNA precursor expression as well as core microRNA pathway genes after HS, the levels of many mature microRNAs are upregulated. This indicates that the regulation of miRNA expression after HS occurs at transcriptional and post-transcriptional levels. It was also shown that deletion of all hsp70 genes had no significant effect on microRNA biogenesis but might influence the dynamics of microRNA expression during the HSR.
Highlights
All living organisms depend on the interaction of a complex set of biochemical reactions directed at maintaining the dynamic homeostatic balance in cells [1]
We used three D. melanogaster strains in our experiments, including a strain carrying a deletion of all hsp70 genes [26]
Maximal Hsp70 synthesis was achieved 6 h after heat shock (HS) in the control strain. We considered this time interval (6 h after HS) as a pivotal time point that allows the miRNA expression pattern to be compared between strains, with specific attention on the hsp702 strain in the context of the strikingly different protein levels
Summary
All living organisms depend on the interaction of a complex set of biochemical reactions directed at maintaining the dynamic homeostatic balance in cells [1]. Even short-term drastic environmental changes such as temperature elevation (i.e. heat shock, HS) force the cells to adapt by adjusting the basic gene expression profile [1,2,3]. Processed or mature miRNAs bind to Argonaute (Ago) proteins and form the RNA-induced silencing complex (RISC), which is capable of recognizing complementary sites in the target mRNA located primarily in the 30 untranslated regions [4,5]. As miRNAs control protein synthesis by promoting either target mRNA degradation or translation inhibition, they play essential roles in various.
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