TY - JOUR
T1 - Potassium-enhanced receptor-mediated endocytosis in oocyte maturation in polychaete, Pseudopotamilla occelata
AU - Chung, Jun Mo
AU - Lee, Sang Hyun
PY - 1996/12/31
Y1 - 1996/12/31
N2 - Using a confocal-laser scanning microscopy in this study, we investigated the underlying mechanism for the receptor-mediated endocytosis (RME) of coelomic fluid proteins into polychaete oocytes that was dramatically enhanced by potassium ion (K)-induced depolarization. Decrease of extracellular sodium ion (Na) did not have any effect on the K-induced RME. On the other hand, either removal of extracellular calcium ion (Ca) or addition of 10 μM nifedipine, an L-type Ca channel blocker, led to a profound decrease of the event, indicating that extracellular Ca that flowed in an oocyte through L-like Ca channels might be responsible for the process. Twenty mM of caffeine that probably increased intracellular Ca from an intracellular pool in an oocyte did not enhance the RME at all, emphasizing the importance of extracellular Ca for the event. However, 100 nM of phorbol myristate acetate (PMA), a protein kinase C (PKC) activator, could also enhance the RME markedly even in the absence of extracellular Ca. Therefore, we tentatively conclude here that intracellular Ca from an extracellular source through L-like channels may participate in RME by triggering a signal transduction pathway such as a PKC system that is in charge with the process in polychaete oocytes.
AB - Using a confocal-laser scanning microscopy in this study, we investigated the underlying mechanism for the receptor-mediated endocytosis (RME) of coelomic fluid proteins into polychaete oocytes that was dramatically enhanced by potassium ion (K)-induced depolarization. Decrease of extracellular sodium ion (Na) did not have any effect on the K-induced RME. On the other hand, either removal of extracellular calcium ion (Ca) or addition of 10 μM nifedipine, an L-type Ca channel blocker, led to a profound decrease of the event, indicating that extracellular Ca that flowed in an oocyte through L-like Ca channels might be responsible for the process. Twenty mM of caffeine that probably increased intracellular Ca from an intracellular pool in an oocyte did not enhance the RME at all, emphasizing the importance of extracellular Ca for the event. However, 100 nM of phorbol myristate acetate (PMA), a protein kinase C (PKC) activator, could also enhance the RME markedly even in the absence of extracellular Ca. Therefore, we tentatively conclude here that intracellular Ca from an extracellular source through L-like channels may participate in RME by triggering a signal transduction pathway such as a PKC system that is in charge with the process in polychaete oocytes.
UR - http://www.scopus.com/inward/record.url?scp=2842556031&partnerID=8YFLogxK
U2 - 10.1016/s1016-8478(23)10919-8
DO - 10.1016/s1016-8478(23)10919-8
M3 - Article
AN - SCOPUS:2842556031
SN - 1016-8478
VL - 6
SP - 759
EP - 765
JO - Molecules and Cells
JF - Molecules and Cells
IS - 6
ER -