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Aratani, S., Kageyama, Y., Nakamura, A., Fujita, H., Fujii, R., Nishioka, K., Nakajima, T. (2008). MLE activates transcription via the minimal transactivation domain in Drosophila.  Int. J. Mol. Med. 21(4): 469--476.
FlyBase ID
FBrf0204293
Publication Type
Research paper
Abstract
Transcription levels of the genes on X chromosome are regulated through the dosage compensation mechanisms. The dosage compensation complex (DCC) localizes to X chromosome and activates the transcription of target genes in male 2-fold more than in female. Drosophila maleless (MLE), an ATPase/helicase, is a component of the DCC and essential for the viability of male flies. However, the functions of MLE on gene expression are not clear. RNA helicase A (RHA) is a homologue of Drosophila MLE and mediates the expression of several genes. RHA recruits preinitiation complex via the minimal transactivation domain (MTAD), consisting of 50 amino acids to target promoters. The tryptophan residues in MTAD are important for transactivation via RHA. The amino acid sequence of MTAD is conserved in MLE. In this study, we assessed whether the functions of MTAD are conserved in fruit fly by investigating the transcriptional activity of MLE. Transactivation assay indicated the MTAD of MLE had transcriptional activity in Schneider's cells. In vitro binding assays revealed that MLE recruited RNA polymerase II (Pol II) complexes through MTAD. Reporter assays showed that the MTAD, especially tryptophan residues, is important for transcription from roX promoter, similar to RHA. The results confirm that MTAD of MLE mediates the expression of MLE target genes through recruitment of Pol II.
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    Language of Publication
    English
    Additional Languages of Abstract
    Parent Publication
    Publication Type
    Journal
    Abbreviation
    Int. J. Mol. Med.
    Title
    International journal of molecular medicine
    Publication Year
    1998-
    ISBN/ISSN
    1107-3756
    Data From Reference
    Alleles (3)
    Genes (5)
    Physical Interactions (1)
    Cell Lines (1)
    Natural transposons (1)
    Transgenic Constructs (2)