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Defining the roles of beta-catenin and plakoglobin in LEF/T-cell factor-dependent transcription using beta-catenin/plakoglobin-null F9 cells.

beta-Catenin functions as a transcriptional regulator in Wnt signaling. Its function is regulated by a specific destruction system. Plakoglobin is a close homologue of beta-catenin in mammalian cells and is regulated in a similar fashion. When beta-catenin or plakoglobin is exogenously expressed in cells, endogenous beta-catenin is stabilized, which complicates estimation of the transcriptional activities of exogenously expressed proteins. To facilitate the design of experiments aimed at investigating the transcriptional activities of beta-catenin and plakoglobin, we utilized F9 cells in which we knocked out endogenous beta-catenin and/or plakoglobin by gene deletion and exogenously expressed wild-type and mutant beta-catenin and/or plakoglobin. We show that C-terminally deleted beta-catenin, but not plakoglobin, has a strong dominant-negative effect on transcription without altering the nuclear accumulation of beta-catenin. Moreover, we show that Wnt-3a activation of LEF/T-cell factor (TCF)-dependent transcription depends on beta-catenin but not on plakoglobin. Using chimeras of beta-catenin and plakoglobin, we demonstrate that plakoglobin has the potential to function in transcriptional regulation but is not responsible for Wnt-3a signaling in F9 cells. Our data show that preferential nuclear accumulation of beta-catenin is not necessarily linked to its transcriptional activity. We also clearly demonstrate that plakoglobin is insufficient for LEF/TCF-dependent transcriptional activation by Wnt-3a in F9 cells.