The human WBSCR22 protein is involved in the biogenesis of the 40S ribosomal subunits in mammalian cells

PLoS One. 2013 Sep 23;8(9):e75686. doi: 10.1371/journal.pone.0075686. eCollection 2013.

Abstract

The human WBSCR22 protein was previously shown to be up-regulated in invasive breast cancer and its ectopic expression enhances tumor cell survival in the vasculature. In the current study, we show that the WBSCR22 protein is important for cell growth. Knock-down of WBSCR22 with siRNA results in slower growth of WBSCR22-depleted cells. Treatment with siWBSCR22 causes defects in the processing of pre-rRNAs and reduces the level of free 40S ribosomal subunit, suggesting that WBSCR22 is involved in ribosome small subunit biosynthesis. The human WBSCR22 partially complements the growth of WBSCR22 yeast homologue, bud23 deletion mutant suggesting that the human WBSCR22 is a functional homologue of yeast Bud23. WBSCR22 is localized throughout the cell nucleus and is not stably associated with ribosomal subunits within the cell nucleus. We also show that the WBSCR22 protein level is decreased in lymphoblastoid cell lines derived from William-Beuren Syndrome (WBS) patients compared to healthy controls. Our data suggest that the WBSCR22 protein is a ribosome biogenesis factor involved in the biosynthesis of 40S ribosomal particles in mammalian cells.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Cell Line
  • Cell Line, Tumor
  • Cell Nucleus / genetics
  • Cell Nucleus / metabolism
  • Fungal Proteins / genetics
  • Fungal Proteins / metabolism
  • HEK293 Cells
  • HeLa Cells
  • Humans
  • Methyltransferases / genetics*
  • Methyltransferases / metabolism*
  • RNA Precursors / genetics
  • RNA Precursors / metabolism
  • Ribosome Subunits, Small, Eukaryotic / genetics*
  • Ribosome Subunits, Small, Eukaryotic / metabolism*
  • Sequence Deletion / genetics
  • Yeasts / genetics
  • Yeasts / metabolism

Substances

  • Fungal Proteins
  • RNA Precursors
  • BUD23 protein, human
  • Methyltransferases

Grants and funding

This work was supported by research programmes (SF0180175; SF0180027s10) from Estonian Ministry of Education and Research; and by the European Regional Development Fund through the Center of Excellence in Chemical Biology. The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.