Eukaryotic Ribosomes Lacking Rpl1 Are Hypersensitive to Defects in the Ubiquitin-Proteasome System
2011

Eukaryotic Ribosomes Lacking Rpl1

Sample size: 13 publication 10 minutes Evidence: moderate

Author Information

Author(s): McIntosh Kerri B., Bhattacharya Arpita, Willis Ian M., Warner Jonathan R.

Primary Institution: Albert Einstein College of Medicine

Hypothesis

Deficiency of ribosomal protein L1 (Rpl1) leads to the production of defective ribosomes that affect cell growth and sensitivity to the ubiquitin-proteasome system.

Conclusion

Cells lacking Rpl1 produce defective ribosomes that can be exported to the cytoplasm but lead to slow growth and increased sensitivity to proteasome inhibitors.

Supporting Evidence

  • Cells deficient in Rpl1 produce ribosomes lacking Rpl1 that can be incorporated into polyribosomes.
  • The presence of defective ribosomes leads to slow growth and hypersensitivity to the proteasome inhibitor MG132.
  • Deletion of RPL1B had a greater effect on growth than all but one of the RP paralogues.
  • 60S subunits lacking Rpl1 can be exported to the cytoplasm and potentially participate in translation.

Takeaway

This study shows that when cells don't have enough of a specific protein needed for making ribosomes, they can still make some ribosomes, but these don't work as well and make the cells sick.

Methodology

The study used Synthetic Genetic Array analyses and growth rate measurements in yeast strains with deletions of ribosomal protein genes.

Limitations

The study primarily focuses on yeast models, which may not fully represent ribosomal behavior in higher organisms.

Digital Object Identifier (DOI)

10.1371/journal.pone.0023579

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