regulation of translation involved in cellular response to UV

Definition

Target type: biologicalprocess

Any regulation of translation that is involved in cellular response to UV. [GO_REF:0000060, GOC:TermGenie, PMID:17369398]

Cellular response to UV radiation involves a complex interplay of regulatory mechanisms, including the modulation of translation. Upon UV exposure, cells activate a variety of signaling pathways that converge on the regulation of gene expression, including those governing the translation process.

One key aspect of this regulation is the activation of the p53 tumor suppressor protein. p53 is a transcription factor that plays a crucial role in DNA damage response and cell cycle arrest. Following UV exposure, p53 is stabilized and translocates to the nucleus, where it binds to specific DNA sequences and activates the transcription of genes involved in DNA repair, cell cycle control, and apoptosis.

The induction of p53 target genes often involves changes in the translation of their corresponding mRNAs. In some cases, p53 directly regulates the translation of its target genes by binding to their 5' untranslated regions (UTRs). These UTRs contain cis-acting regulatory elements that control the efficiency of translation initiation.

Another important regulatory mechanism involves the phosphorylation of eukaryotic initiation factor 2α (eIF2α). eIF2α is a key component of the translation initiation complex, and its phosphorylation inhibits the formation of this complex, thereby reducing the rate of translation initiation. UV irradiation can trigger the activation of various kinases that phosphorylate eIF2α, including PKR (double-stranded RNA-activated protein kinase), PERK (PKR-like endoplasmic reticulum kinase), and GCN2 (general control nonderepressible 2). The phosphorylation of eIF2α is thought to be a protective mechanism that allows cells to conserve resources during stress conditions, such as UV exposure.

In addition to the regulation of initiation, translation elongation can also be affected by UV exposure. UV-induced DNA damage can lead to the accumulation of misfolded proteins, which can trigger the unfolded protein response (UPR). The UPR is a signaling pathway that aims to restore protein homeostasis by reducing the rate of translation and promoting the degradation of misfolded proteins.

Furthermore, UV exposure can induce the formation of stress granules (SGs), which are cytoplasmic aggregates of mRNAs and translation initiation factors. SGs are thought to sequester mRNAs and translation factors, thereby reducing the overall rate of translation and promoting mRNA stability.

Overall, the regulation of translation in response to UV exposure is a complex and multifaceted process that involves the activation of signaling pathways, the phosphorylation of key translation factors, and the formation of stress granules. These regulatory mechanisms ensure that cells can effectively respond to UV damage and maintain cellular homeostasis.'
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Proteins (1)

Compounds (2)