Anti-RPS9 (aa 1-50) polyclonal antibody

The degeneration of photoreceptors is a common hallmark of ocular diseases like retinitis pigmentosa (RP) or age-related macular degeneration (AMD). To experimentally induce photoreceptor degeneration, the light damage paradigm is frequently used. In this study we show that the exposure to high amounts of cool white light (10,000 lux, 1 h) resulted in a more than 11-fold higher apoptotic rate in the retina compared to light exposure with 5000 lux for 30 min. Consequently, exposure to intense light resulted in a significant downregulation of retinal mRNA expression levels of the reference genes Gapdh, Gnb2l, Rpl32, Rps9, Actb, Ubc or Tbp compared to untreated controls. Investigators performing light-induced photoreceptor degeneration should be aware of the fact that higher light intensities will result in a dysregulation of reference genes.

Ribosomal proteins are essential to life. While the functions of ribosomal protein-encoding genes (RPGs) are highly conserved, the evolution of their regulatory mechanisms is remarkably dynamic. In Saccharomyces cerevisiae, RPGs are unusual in that they are commonly present as two highly similar gene copies and in that they are over-represented among intron-containing genes. To investigate the role of introns in the regulation of RPG expression, we constructed 16 S. cerevisiae strains with precise deletions of RPG introns. We found that several yeast introns function to repress rather than to increase steady-state mRNA levels. Among these, the RPS9A and RPS9B introns were required for cross-regulation of the two paralogous gene copies, which is consistent with the duplication of an autoregulatory circuit. To test for similar intron function in animals, we performed an experimental test and comparative analyses for autoregulation among distantly related animal RPS9 orthologs. Overexpression of an exogenous RpS9 copy in Drosophila melanogaster S2 cells induced alternative splicing and degradation of the endogenous copy by nonsense-mediated decay (NMD). Also, analysis of expressed sequence tag data from distantly related animals, including Homo sapiens and Ciona intestinalis, revealed diverse alternatively-spliced RPS9 isoforms predicted to elicit NMD. We propose that multiple forms of splicing regulation among RPS9 orthologs from various eukaryotes operate analogously to translational repression of the alpha operon by S4, the distant prokaryotic ortholog. Thus, RPS9 orthologs appear to have independently evolved variations on a fundamental autoregulatory circuit.