TY - JOUR
T1 - Drosophila Myc is oncogenic in mammalian cells and plays a role in the diminutive phenotype
AU - Schreiber-Agus, Nicole
AU - Stein, David
AU - Chen, Ken
AU - Goltz, Jason S.
AU - Stevens, Leslie
AU - DePinho, Ronald A.
PY - 1997/2/18
Y1 - 1997/2/18
N2 - Biochemical and biological activities of Myc oncoproteins are highly dependent upon their association with another basic region helix-loop- helix/leucine zipper (bHLH/LZ) protein, Max. Our previous observation that the DNA-binding/dimerization region of Max is absolutely conserved throughout vertebrate evolution provided the basis for a yeast two-hybrid interaction screen that led to the isolation of the Drosophila Myc (dMyc1) protein. Structural conservation in regions of known functional significance is consistent with the ability of dMyc1 to interact with vertebrate Max, to transactivate gene expression in yeast cells, and to cooperate with activated H-RAS to effect the malignant transformation of primary mammalian cells. The ability of P-element-mediated ectopic expression of dmyc1 to reverse a subset of the phenotypic alterations associated with the diminutive mutation suggests that diminutive may correspond to dmyc1. This finding, along with the localization of dmyc1 expression to zones of high proliferative activity in the embryo, implicates dMyc1 as an integral regulator of Drosophila growth and development.
AB - Biochemical and biological activities of Myc oncoproteins are highly dependent upon their association with another basic region helix-loop- helix/leucine zipper (bHLH/LZ) protein, Max. Our previous observation that the DNA-binding/dimerization region of Max is absolutely conserved throughout vertebrate evolution provided the basis for a yeast two-hybrid interaction screen that led to the isolation of the Drosophila Myc (dMyc1) protein. Structural conservation in regions of known functional significance is consistent with the ability of dMyc1 to interact with vertebrate Max, to transactivate gene expression in yeast cells, and to cooperate with activated H-RAS to effect the malignant transformation of primary mammalian cells. The ability of P-element-mediated ectopic expression of dmyc1 to reverse a subset of the phenotypic alterations associated with the diminutive mutation suggests that diminutive may correspond to dmyc1. This finding, along with the localization of dmyc1 expression to zones of high proliferative activity in the embryo, implicates dMyc1 as an integral regulator of Drosophila growth and development.
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U2 - 10.1073/pnas.94.4.1235
DO - 10.1073/pnas.94.4.1235
M3 - Article
C2 - 9037036
AN - SCOPUS:0031028183
SN - 0027-8424
VL - 94
SP - 1235
EP - 1240
JO - Proceedings of the National Academy of Sciences of the United States of America
JF - Proceedings of the National Academy of Sciences of the United States of America
IS - 4
ER -