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Mohan, R.D., Dialynas, G., Weake, V.M., Liu, J., Martin-Brown, S., Florens, L., Washburn, M.P., Workman, J.L., Abmayr, S.M. (2014). Loss of Drosophila Ataxin-7, a SAGA subunit, reduces H2B ubiquitination and leads to neural and retinal degeneration.  Genes Dev. 28(3): 259--272.
FlyBase ID
FBrf0223974
Publication Type
Research paper
Abstract

The Spt-Ada-Gcn5-acetyltransferase (SAGA) chromatin-modifying complex possesses acetyltransferase and deubiquitinase activities. Within this modular complex, Ataxin-7 anchors the deubiquitinase activity to the larger complex. Here we identified and characterized Drosophila Ataxin-7 and found that reduction of Ataxin-7 protein results in loss of components from the SAGA complex. In contrast to yeast, where loss of Ataxin-7 inactivates the deubiquitinase and results in increased H2B ubiquitination, loss of Ataxin-7 results in decreased H2B ubiquitination and H3K9 acetylation without affecting other histone marks. Interestingly, the effect on ubiquitination was conserved in human cells, suggesting a novel mechanism regulating histone deubiquitination in higher organisms. Consistent with this mechanism in vivo, we found that a recombinant deubiquitinase module is active in the absence of Ataxin-7 in vitro. When we examined the consequences of reduced Ataxin-7 in vivo, we found that flies exhibited pronounced neural and retinal degeneration, impaired movement, and early lethality.

PubMed ID
PubMed Central ID
PMC3923968 (PMC) (EuropePMC)
Related Publication(s)
Note

Drosophila models reveal novel insights into mechanisms underlying neurodegeneration.
Mohan et al., 2014, Fly 8(3): 148--152 [FBrf0227086]

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Secondary IDs
    Language of Publication
    English
    Additional Languages of Abstract
    Parent Publication
    Publication Type
    Journal
    Abbreviation
    Genes Dev.
    Title
    Genes & Development
    Publication Year
    1987-
    ISBN/ISSN
    0890-9369
    Data From Reference
    Aberrations (1)
    Alleles (5)
    Genes (22)
    Human Disease Models (1)
    Physical Interactions (24)
    Cell Lines (1)
    Natural transposons (1)
    Insertions (1)
    Experimental Tools (1)
    Transgenic Constructs (4)