AJP - Cell Physiology, Vol 253, Issue 4 C575-C579, Copyright © 1987 by American Physiological Society
Control of late G0/G1 progression and protein modification by SmC/IGF I
N. E. Olashaw, J. J. Van Wyk and W. J. Pledger
Department of Cell Biology, Vanderbilt University School of Medicine, Nashville, Tennessee 37232.
Somatomedin C/insulin-like growth factor I (SmC/IGF I) mediates traverse of
late G0/G1 in density-arrested BALB/c-3T3 cells from a distinct growth
arrest point in mid-G0/G1 (the V point) to the initiation of DNA synthesis.
As a prelude to future studies aimed at defining the mechanism of action of
SmC/IGF I, we investigated the level (e.g., transcriptional, translational)
at which SmC/IGF I modulates V to S traverse. The post-V point progression
of cells arrested at the V point by amino acid starvation and released into
amino acid-replenished medium containing SmC/IGF I, insulin, or
platelet-poor plasma (PPP) did not require either mRNA synthesis or an
increase in the overall level of protein synthesis. Although
two-dimensional gel analysis of proteins prepared from SmC/IGF I-treated
cells did not reveal any preferentially synthesized proteins, several
SmC/IGF I-induced protein modifications, which result in an increase in
isoelectric point (pI) and occur in the absence of mRNA synthesis, were
evident. These findings suggest that SmC/IGF I modulates late G0/G1
progression by a posttranscriptional process that may involve protein
modification.
