Xenbase Image ID: 173953

Fig. 9. Truncated versions of Bix1 cause apoptosis; the ability to cause apoptosis is not correlated with the ability of the protein to activate transcription but does require DNA binding. (A) RNA encoding truncated and deleted versions of Bix1 was injected into Xenopus embryos and the same constructs were introduced into COS cells to assess their transcriptional activity as described in Fig. 8. All transfected constructs generated protein in approximately equivalent amounts (not shown). Deletion of 25 C-terminal amino acids of Bix1 causes the protein to acquire apoptosis-inducing activity. Further deletions suggest that the apoptosis-inducing domain resides between amino acids 144 and 225 and that optimal apoptotic activity can be obtained in a construct [Bix1 (1-225)] in which 78% of transcriptional activity is lost. (B) Mutation of Q132 to E reduces transcriptional activation, substantially decreases the ability of the protein to cause apoptosis abolishes DNA binding (not shown). The ability of truncated Bix1 to induce apoptosis requires DNA binding. Bix1 (1-376) induces apoptosis, is a powerful activator of transcription and binds DNA (not shown). Image published in: Trindade M et al. (2003) Copyright © 2003. Image reproduced with permission of the publisher and the copyright holder. This is an Open Access article distributed under the terms of the Creative Commons Attribution License. Larger Image Printer Friendly View

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