Knockdown of the Ribosomal Protein eL29 in Mammalian Cells Leads to Significant Changes in Gene Expression at the Transcription Level

Cells. 2020 May 15;9(5):1228. doi: 10.3390/cells9051228.

Abstract

An imbalance in the synthesis of ribosomal proteins can lead to the disruption of various cellular processes. For mammalian cells, it has been shown that the level of the eukaryote-specific ribosomal protein eL29, also known as the one interacting with heparin/heparan sulfate, substantially affects their growth. Moreover, in animals lacking this protein, a number of anatomical abnormalities have been observed. Here, we applied next-generation RNA sequencing to HEK293 cells transfected with siRNAs specific for the mRNA of eL29 to determine what changes occur in the transcriptome profile with a decrease in the level of the target protein. We showed that an approximately 2.5-fold decrease in the content of eL29 leads to statistically significant changes in the expression of more than a thousand genes at the transcription level, without a noticeable effect on cell viability, rRNA level, and global translation. The set of eL29-dependent genes included both up-regulated and down-regulated ones, among which there are those previously identified as targets for proteins implicated in oncogenesis. Thus, our findings demonstrate that an insufficiency of eL29 in mammalian cells causes a significant reorganization of gene expression, thereby highlighting the relationship between the cellular balance of eL29 and the activities of certain genes.

Keywords: HEK293 cells; RNA-seq; differential gene expression; eL29-dependent genes; eL29-related processes; knockdown of ribosomal protein eL29; next-generation sequencing.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Gene Expression Regulation*
  • Gene Knockdown Techniques
  • Gene Ontology
  • HEK293 Cells
  • Humans
  • Mammals / metabolism*
  • Proto-Oncogene Proteins c-myc / metabolism
  • RNA-Binding Proteins / metabolism*
  • RNA-Seq
  • Ribosomal Proteins / metabolism*
  • Transcription, Genetic*
  • Transcriptome
  • Tumor Suppressor Protein p53 / metabolism

Substances

  • Proto-Oncogene Proteins c-myc
  • RNA-Binding Proteins
  • RPL29 protein, human
  • Ribosomal Proteins
  • Tumor Suppressor Protein p53