Sk. Koo et al., PKC PHOSPHORYLATION DISRUPTS GAP JUNCTIONAL COMMUNICATION AT G(0) S PHASE IN CLONE-9 CELLS/, Molecular and cellular biochemistry, 167(1-2), 1997, pp. 41-49
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.