Abstract
We have shown that elevated expression of ribosomal protein L5 in Xenopus embryos results in the ectopic activation of 5 S rRNA genes that are normally inactive. This transcriptional stimulation mimics the effect of overexpressing transcription factor IIIA (TFIIIA), the 5 S rRNA gene-specific transcription factor. The results support a model in which a network of nucleic acid-protein interactions involving 5 S rRNA, the 5 S rRNA gene, TFIIIA, and L5 mediates both feedback inhibition of 5 S rRNA synthesis and coupling of 5 S rRNA synthesis to accumulation of a ribosomal protein, L5. We propose that these mechanisms contribute to the homeostatic control of ribosome assembly.
Highlights
We have shown that elevated expression of ribosomal protein L5 in Xenopus embryos results in the ectopic activation of 5 S rRNA genes that are normally inactive
Transcription factor IIIA (TFIIIA)1 is a 5 S rRNA genespecific transcription factor that binds to the internal control region of 5 S rRNA genes in the first step of transcription complex assembly [1, 2]
The feedback regulation model has been supported by experiments showing that expression in Xenopus embryos of mutant forms of TFIIIA that have reduced affinity for 5 S rRNA [7] leads to levels of 5 S rRNA synthesis that are considerably higher than is obtained with comparable expression of wildtype TFIIIA [8]
Summary
We have shown that elevated expression of ribosomal protein L5 in Xenopus embryos results in the ectopic activation of 5 S rRNA genes that are normally inactive.
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