(i) In a wide variety of eukaryotes, many stress conditions including heat stress lead to a repression of translation initiation and an accumulation of translationally repressed mRNA in either so-called stress granules or in the nucleus.
As part of this work, we identified a novel mechanism of CFNS pathogenesis, involving the predicted translational readthrough of a conserved uORF, leading to repression of translation of EFNB1 from the main dORF.
Though many miRNA targets were affected by both repression of translation and mRNA degradation, a number of targets were predominantly regulated by translational repression [40].
Of special interest are microRNAs (miRNAs), small RNAs that regulate gene expression by mRNA cleavage or repression of translation.
They modulate gene function through their binding to complementary regions within the 3'-UTRs of target mRNAs, leading to mRNA degradation or repression of translation.
Similarly, PABPC1 is involved in both activation and repression of translation at the level of initiation.
This regulation occurs post-transcriptionally, involving destabilizing modifications of the CELF1 protein and microRNA-mediated repression of translation of CELF1 and CELF2 transcripts [7], [8].
The processed microRNAs are finally incorporated into the RNA-induced silencing complex (RISC) to mediate target mRNA repression of translation and/or degradation.
Hfq-dependent sRNAs typically act by binding to the 5'-region of target mRNAs, leading to repression of translation initiation and degradation of the mRNA.
Alternatively, this could be due to residual eIF2α phosphorylation, since as little as 10% of eIF2α phosphorylation can cause a strong repression of translation [12], [22].
