TY - JOUR
T1 - Positive or negative MARE-dependent transcriptional regulation is determined by the abundance of small Maf proteins
AU - Motohashi, Hozumi
AU - Katsuoka, Fumiki
AU - Shavit, Jordan A.
AU - Engel, James Douglas
AU - Yamamoto, Masayuki
N1 - Funding Information:
We are grateful to Drs. K.-C. Lim, M. Nishizawa, S. Takahashi, and K. Igarashi for discussion and advice. We also thank Drs. T. Nagasawa and T. Komeno for instruction in megakaryocyte analysis, and Ms. N. Kaneko for technical support in histological examination. This work was supported by an NIH grant (R01 CA80088; J. D. E.) and grants from the Ministry of Education, Science, Sports and Culture (H. M. and M. Y.), PROBRAIN (H. M.), JSPS-RFTF, and CREST (M. Y.).
PY - 2000
Y1 - 2000
N2 - The small Maf transcription factor proteins bind to Maf Recognition Elements (MAREs) by dimerizing with CNC proteins or themselves. We undertook experiments to clarify the functional relationship between the small Mafs and their partners in vivo. Embryos expressing abundant transgene-derived MafK died of severe anemia, while lines expressing lower levels of small Maf lived to adulthood. Megakaryocytes from the latter overexpressing lines exhibited reduced proplatelet formation and MARE-dependent transcription, phenocopying mafG null mutant mice. When the mafG null mutants were bred to small Maf-overexpressing transgenic animals, both loss- and gain-of-function phenotypes were reversed. These results provide direct in vivo evidence that transcriptional regulation through MARE elements hinges on an exquisitely sensitive balance of activating CNC molecules and their small Maf partners.
AB - The small Maf transcription factor proteins bind to Maf Recognition Elements (MAREs) by dimerizing with CNC proteins or themselves. We undertook experiments to clarify the functional relationship between the small Mafs and their partners in vivo. Embryos expressing abundant transgene-derived MafK died of severe anemia, while lines expressing lower levels of small Maf lived to adulthood. Megakaryocytes from the latter overexpressing lines exhibited reduced proplatelet formation and MARE-dependent transcription, phenocopying mafG null mutant mice. When the mafG null mutants were bred to small Maf-overexpressing transgenic animals, both loss- and gain-of-function phenotypes were reversed. These results provide direct in vivo evidence that transcriptional regulation through MARE elements hinges on an exquisitely sensitive balance of activating CNC molecules and their small Maf partners.
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U2 - 10.1016/s0092-8674(00)00190-2
DO - 10.1016/s0092-8674(00)00190-2
M3 - Article
C2 - 11136972
AN - SCOPUS:0033637756
SN - 0092-8674
VL - 103
SP - 865
EP - 876
JO - Cell
JF - Cell
IS - 6
ER -