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Mol. Cell. Biol., Mar 1995, 1479-1488, Vol 15, No. 3
SY Wu and M McLeod
In Schizosaccharomyces pombe, meiosis is initiated by conditions of
nutrient deprivation. Mutations in genes encoding elements of the cyclic
AMP-dependent protein kinase (cAPK) pathway interfere with meiosis.
Loss-of-function alleles of genes that stimulate the activity of cAPK allow
cells to bypass the normal requirement of starvation for conjugation and
meiosis. Alternatively, loss-of-function alleles of genes that inhibit cAPK
lead to the inability to undergo sexual differentiation. The cgs1+ gene
encodes the regulatory subunit of cAPK, and the cgs2+ gene encodes a cyclic
AMP phosphodiesterase. Thus, both genes encode proteins which negatively
regulate the activity of cAPK. Loss of either cgs1 or cgs2 prevents haploid
cells from conjugating and diploid cells from undergoing meiosis. In
addition to these defects, cells are unable to enter stationary phase. We
describe a novel gene, sak1+, which when present on a plasmid overcomes the
aberrant phenotypes associated with unregulated cAPK activity. Genetic
analysis of sak1+ (suppressor of A-kinase) reveals that it functions
downstream of cyclic AMP-dependent protein kinase to allow cells to exist
the mitotic cycle and enter either stationary phase or the pathway leading
to sexual differentiation. The sak1+ gene is essential for cell viability,
and a null allele causes multiple defects in cell morphology and nuclear
division. Thus, sak1+ is an important regulatory element in the life cycle
of S. pombe. Sequence analysis shows that the predicted product of the
sak1+ gene is an 87-kDa protein which shares homology to the RFX family of
DNA-binding proteins identified in humans and mice. One member of this
family, RFX1, is a transcription factor for a variety of viral and cellular
genes.
Copyright © 1995, American Society for Microbiology
The sak1+ gene of Schizosaccharomyces pombe encodes an RFX family DNA- binding protein that positively regulates cyclic AMP-dependent protein kinase-mediated exit from the mitotic cell cycle
State University of New York Health Science Center at Brooklyn, 11203.
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