MAPPING OF 2 GENES ENCODING MEMBERS OF A DISTINCT SUBFAMILY OF MAX INTERACTING PROTEINS - MAD TO HUMAN-CHROMOSOME-2 AND MOUSE CHROMOSOME-6,AND MXI1 TO HUMAN-CHROMOSOME-10 AND MOUSE CHROMOSOME-19

Both the MAD and the MXI1 genes encode basic-helix-loop-helix-leucine zipper (bHLH-Zip) transcription factors which bind Max in vitro, formi ng a sequence-specific DNA-binding complex similar to the Myc-Max hete rodimer. Mad and Myc compete for binding to Max. In addition, Mad has been shown to act as a transcriptional repressor while Myc appears to function as an activator. Mxi1 also appears to lack a transcriptional activation domain. Therefore, Mxi1 and Mad might antagonize Myc functi on and are candidate tumor suppressor genes. We report here the mappin g of the MAD and MXI1 genes in human and mouse by fluorescence in situ hybridization (FISH) and by recombination mapping. The MAD gene was m apped to human chromosome 2 at band p13 by FISH and to mouse chromosom e 6 by meiotic mapping. The MXI1 gene was mapped to human chromosome 1 0 at band q25 and on mouse chromosome 19 at region D by FISH. There wa s a second site of hybridization on mouse chromosome 2 at region C, wh ich may represent a pseudogene or a related sequence. The mapping resu lts confirm regions of conservation between human chromosome 2p13 and mouse chromosome 6 and between chromosome 10q25 and mouse chromosome 1 9D. Human chromosomes 2p13 and 10q25 have been involved in specific tu mors where the role of Mad and Mxi1 can now he investigated.