High impact information on rux

• Rather, rux appears to act through cyclin A during premeiotic G2 to regulate meiosis II [1].
• Although cell cycle synchronization occurs in roughex (rux) mutants, cells circumvent G1 and all cells enter S phase, including cells that would normally differentiate [2].
• Conversely, germ cells with excess rux function fail to undergo meiosis II. rux does not appear to act directly at meiosis II [1].
• We show that the gene roughex (rux) is a dose-dependent regulator of meiosis II during Drosophila spermatogenesis. rux mutant germ cells execute the two meiotic divisions, but then undergo an additional M phase resembling an extra meiosis II [1].
• Cell cycle progression in the developing Drosophila eye: roughex encodes a novel protein required for the establishment of G1 [2].

Biological context of rux

• Observations of fixed and living embryos show that metaphase is significantly longer in rux mutants than in wild-type embryos [3].
• Roughex is a nuclear protein, while cyclin A was previously shown to be exclusively cytoplasmic during interphase in the embryo [4].
• A screen for dominant suppressors of the rux eye phenotype led to the identification of mutations in cyclin A, string (cdc25), and new cell cycle genes [5].
• roughex is a dose-dependent regulator of the second meiotic division during Drosophila spermatogenesis [1].
• When Roughex is overexpressed in S/G2 cells, Cyclin A is mislocalized to the nucleus and degraded, preventing mitosis [6].

Physical interactions of rux

• Results: Rux interacted with CycA and CycB in coprecipitation experiments [7].

Regulatory relationships of rux

• The roughex gene product plays a key role in this synchronization by negatively regulating cyclin A protein levels in G(1) [4].

Other interactions of rux

• Roughex mediates G(1) arrest through a physical association with cyclin A [4].
• The cyclin-dependent kinase inhibitor Roughex is involved in mitotic exit in Drosophila [3].
• Cdk1 inhibition by Rux did not rely on inhibitory phosphorylation, disruption of cyclin-Cdk complex formation or changes in subcellular localization [7].
• Following induction of a Rux transgene in Cyclin E mutant embryos during G2 of cell cycle 14 (G2(14)), Cyclins A, B, and B3 disappeared and cells reentered S phase [8].

References