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First published online January 12, 2006
doi: 10.1242/10.1242/jcs.02815

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Of Myc and Mnt

Shriners Hospitals for Children and Department of Cell and Developmental Biology, Oregon Health and Science University, 3101 SW Sam Jackson Park Rd, Portland, OR 97239, USA

View larger version (20K): [in a new window]   Fig. 1. Working model for the relationship between activating Myc-Max complexes and repressive Mnt-Max, Mxd-Max and Mga-Max complexes. Myc-Max complexes are postulated to affect global gene regulation through binding thousands of E-box, as well as non-E-box, sequences, where they would activate transcription. Myc targets include genes regulated by RNA polymerase (pol) II, as well as RNA pol I. Myc also regulates RNA pol III complexes by engaging the pol III basal machinery. Mnt-Max, Mxd-Max and Mga-Max complexes can bind to E-box sequences and repress transcription. Studies in Drosophila indicate that dMnt and dMyc bind at both shared and unique sites. The extent to which Mnt-Max, Mad-Max and Mga-Max complexes counter Myc-dependent global transcription and impinge on the various activities of Myc remains unclear. Not depicted is transcriptional repression by Myc-Max-Miz1 complexes, which might not be affected either by Mnt-Max, or Mad-Max or Mga-Max complexes. *CACGTG and related sequences.

View larger version (22K): [in a new window]   Fig. 2. Schematic diagrams showing theoretical relationships between different Max complexes during (A) cell-cycle exit, (B-D) cell-cycle entry and the proliferative cell cycle. Although Max can homodimerize, all Max is portrayed in a complex with its heterodimerization partners. Note that this model predicts that the relative levels of Max complexes change as a result of deregulated Myc (C) and loss of Mnt (D).

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