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Cyclic‐AMP deficient MDCK cells form tubules
Author(s) -
Klebe Robert J.,
Grant Anne,
Grant George,
Ghosh Paramita
Publication year - 1995
Publication title -
journal of cellular biochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.028
H-Index - 165
eISSN - 1097-4644
pISSN - 0730-2312
DOI - 10.1002/jcb.240590406
Subject(s) - staurosporine , tubule , microbiology and biotechnology , population , protein kinase c , adenylate kinase , forskolin , biology , protein kinase a , chemistry , kinase , stimulation , biochemistry , receptor , endocrinology , kidney , demography , sociology
It has known for many years that MDCK cells blister structures, termed domes. During an examination of the morphbology of a large number of MDCK clones, we found that two stable morphotypes exist in an MDCK cell population namely, dome‐forming and tubule‐forming clones. When maintained at high cell density, tubule‐forming clones displayed large numbers of anastomosing tubules which contained lumens. The frequency of obseration of the tubule forming clones in an MDCK population was 0.7% Tubule‐forming MDCK clones should be useful in studying tubule morphogenesis. While agents that affect protein kinase A actiity increased dome formation, the same agents abolished the formation of tubules in all tubule‐forming clones. In contrast, drugs that stimulate protein kinase C actity (phorbol esters and staurosporine) decreased dome formation and increased tubule morphogenesis in all MDCK morphotyes. Tubules‐forming clones were found to have lower resting levels of cyclic‐AMP and to respond to forskolin stimulation of adenylate cyclase readily. Hence, sigals transmitted by the protein kinase C pathway appear to lead to tubule formation MDCK cells, while signals transmitted through the protein A pathway lead to dome formation. © 1995 Wiley‐Liss, Inc.