PKC PHOSPHORYLATION DISRUPTS GAP JUNCTIONAL COMMUNICATION AT G(0) S PHASE IN CLONE-9 CELLS/

Gap junctional communication during the progression of cell cycle from quiescent G(0) to S phase was examined in cultured clone 9 rat liver cells. The transfer of scrape-loaded fluorescent dye was suppressed im mediately after the stimulation of cell cycle progression in a synchro nized cell population. Northern blot analysis showed that the temporal disturbance of gap junctional communication in cells passing from G(0 ) to S phase did not result from transcriptional down-regulation of co nnexin 43. It was also found that the PKC inhibitor, calphostin C, was able to restore intercellular communication in serum stimulated cells . Data suggest a control mechanism by PKC mediated phosphorylation in the regulation of gap junction function which is vulnerable to cell cy cling. The loss of gap junctional communication correlated with the in creased phosphorylation of connexin 43 on serine residues in clone 9 c ells.