B-myb rescues ras-induced premature senescence, which requires its transactivation domain

B-myb, a ubiquitously expressed member of the myb gene family, is highly re gulated throughout the cell cycle and appears to be required for cell cycle progression. In contrast to its relatives A-myb, c-Myb, and v-myb, no tran sforming activity of B-myb has been reported thus far. We report here that B-myb can rescue senescence induced by an activated ras onco.-ene in rodent cells in vitro. We show that transformation by B-Myb involves its ability to activate transcription. Similar to other oncogenic transcription factors , such as c-Myc and E2F, we show that B-Myb also has repression activity. W e demonstrate that the C-terminus of B-Myb can function as a repressor of t ranscription, that B-Myb interacts with the repressor molecules BS69 and N- CoR and that the repression function, like the transactivation domain, cont ributes to B-myb transformation. (C) 2001 Elsevier Science Ireland Ltd. All rights reserved.