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Zraly, C.B., Marenda, D.R., Dingwall, A.K. (2004). SNR1 (INI1/SNF5) mediates important cell growth functions of the Drosophila Brahma (SWI/SNF) chromatin remodeling complex.  Genetics 168(1): 199--214.
FlyBase ID
FBrf0180290
Publication Type
Research paper
Abstract

SNR1 is an essential subunit of the Drosophila Brahma (Brm) ATP-dependent chromatin remodeling complex, with counterparts in yeast (SNF5) and mammals (INI1). Increased cell growth and wing patterning defects are associated with a conditional snr1 mutant, while loss of INI1 function is directly linked with aggressive cancers, suggesting important roles in development and growth control. The Brm complex is known to function during G1 phase, where it appears to assist in restricting entry into S phase. In Drosophila, the activity of DmcycE/CDK2 is rate limiting for entry into S phase and we previously found that the Brm complex can suppress a reduced growth phenotype associated with a hypomorphic DmcycE mutant. Our results reveal that SNR1 helps mediate associations between the Brm complex and DmcycE/CDK2 both in vitro and in vivo. Further, disrupting snr1 function suppressed DmcycEJP phenotypes, and increased cell growth defects associated with the conditional snr1E1 mutant were suppressed by reducing DmcycE levels. While the snr1E1-dependent increased cell growth did not appear to be directly associated with altered expression of G1 or G2 cyclins, transcription of the G2-M regulator string/cdc25 was reduced. Thus, in addition to important functions of the Brm complex in G1-S control, the complex also appears to be important for transcription of genes required for cell cycle progression.

PubMed ID
PubMed Central ID
PMC1448117 (PMC) (EuropePMC)
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    Language of Publication
    English
    Additional Languages of Abstract
    Parent Publication
    Publication Type
    Journal
    Abbreviation
    Genetics
    Title
    Genetics
    Publication Year
    1916-
    ISBN/ISSN
    0016-6731
    Data From Reference
    Aberrations (4)
    Alleles (17)
    Genes (17)
    Physical Interactions (7)
    Transgenic Constructs (1)