Cells grow in response to nutrients or growth factors, whose presence is
detected and communicated by elaborate signaling pathways. Protein kinases play
crucial roles in processes such as cell cycle progression and gene expression, and
misregulation of such pathways has been correlated with various diseased states.
Signals intended to promote cell growth converge on ribosome biogenesis, as the ability
to produce cellular proteins is intimately tied to cell growth. Part of the response to
growth signals is therefore the coordinate expression of genes encoding ribosomal RNA
(rRNA) and ribosomal proteins (RP). A key player in regulating cell growth is the
Target of Rapamycin (TOR) kinase, one of the gatekeepers that prevent cell cycle
progression from G1 to S under conditions of nutritional stress. TOR is structurally and
functionally conserved in all eukaryotes. Under favorable growth conditions, TOR is
active and cells maintain a robust rate of ribosome biogenesis, translation initiation and
nutrient import. Under stress conditions, TOR signaling is suppressed, leading to cell
cycle arrest, while the failure of TOR to respond appropriately to environmental or
nutritional signals leads to uncontrolled cell growth. Emerging evidence from
Saccharomyces cerevisiae indicates that High Mobility Group (HMGB) proteins, nonsequence-
specific chromosomal proteins, participate in mediating responses to growth
signals. As HMGB proteins are distinguished by their ability to alter DNA topology,
they frequently function in the assembly of higher-order nucleoprotein complexes. We
review here recent evidence, which suggests that HMGB proteins may function to
coordinate TOR-dependent regulation of rRNA and RP gene expression.
Keywords: Rapamycin, TORC1, HMO1, high mobility group, yeast, RP gene,
rDNA.
