Please use this identifier to cite or link to this item:http://hdl.handle.net/20.500.12105/6497
Title
MAZ induces MYB expression during the exit from quiescence via the E2F site in the MYB promoter
Author(s)
Alvaro-Blanco, Josue | Urso, Katia CNIC | Chiodo, Yuri | Martin-Cortazar, Carla | Kourani, Omar | Gomez-del Arco, Pablo CNIC | Rodriguez-Martinez, Maria | Calonge, Esther ISCIII | Alcamí, José ISCIII | Redondo, Juan Miguel CNIC | Iglesias, Teresa | Campanero, Miguel R.
Date issued
2017
Citation
Nucleic Acids Res. 2017; 45(17):9960-9975
Language
Inglés
Document type
journal article
Abstract
Most E2F-binding sites repress transcription through the recruitment of
Retinoblastoma (RB) family members until the end of the G1 cell-cycle
phase. Although the MYB promoter contains an E2F-binding site, its
transcription is activated shortly after the exit from quiescence,
before RB family members inactivation, by unknown mechanisms. We had
previously uncovered a nuclear factor distinct from E2F, Mybsp, whose
DNA-binding site overlapped the E2F element and had hypothesized that
this factor might overcome the transcriptional repression of MYB by
E2F-RB family members. We have purified Myb-sp and discovered that
Myc-associated zinc finger proteins (MAZ) are major components. We show
that various MAZ isoforms are present in Myb-sp and activate
transcription via the MYB-E2F element. Moreover, while forced RB or p130
expression repressed the activity of a luciferase reporter driven by the
MYB-E2F element, co-expression of MAZ proteins not only reverted
repression, but also activated transcription. Finally, we show that MAZ
binds the MYB promoter in vivo, that its binding site is critical for
MYB transactivation, and that MAZ knockdown inhibits MYB expression
during the exit from quiescence. Together, these data indicate that MAZ
is essential to bypass MYB promoter repression by RB family members and
to induce MYB expression.
Subject
ZINC-FINGER PROTEIN | CELL-CYCLE CONTROL | C-MYB | TRANSCRIPTION FACTORS | BINDING-SITES | NEGATIVE REGULATION | SIGNALING PATHWAY | GENE-EXPRESSION | SPLICE VARIANT | RECEPTOR GENE
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