In the developing eye of Drosophila melanogaster, cells become synchro
nized in the G(1) phase of the cell cycle just prior to the onset of c
ellular differentiation and morphogenesis. In rougher (rux) mutants, c
ells enter S phase precociously because of ectopic activation of a Cyc
lin A/Cdk complex in early G(1). This leads to defects in cell fate an
d pattern formation, and results in abnormalities in the morphology of
the adult eye. A screen for dominant suppressors of the rux eye pheno
type led to the identification of mutations in cyclin A, string (cdc25
), and new cell cycle genes. One of these genes, regulator of cyclin A
(real), encodes a novel protein required for both mitotic and meiotic
cell cycle progression. rca1 mutants arrest in G(2) of embryonic cell
cycle 16 with a phenotype very similar to cyclin A loss of function m
utants. Expression of real transgenes in G(1) or in postmitotic neuron
s promotes Cyclin A protein accumulation and drives cells into S phase
in a Cyclin A-dependent fashion.