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E Warbrick

Publications and source records attributed to E Warbrick.

25 records · Page 2Linked to original sources
PubMed1994

A Drosophila melanogaster homolog of the TIS11 family of immediate early genes that can rescue a cdr1 cdc25 mutant strain of fission yeast.

A Drosophila melanogaster (Dm) embryonic cDNA library was screened for genes capable of inhibiting wee1+/mik1+ protein kinase (Pk) function. We expected to identify homologs of the Schizosaccharomyces pombe gene nim1+. This gene encodes a Pk capable of phosphorylating and so inhibiting the wee1+ Pk that in turn inhibits p34cdc2. Dm cDNAs capable of complementing the temperature-sensitive phenotype of a nim1/cdr1 cdc25 double mutant strain were identified and found to fall into two classes. One class encodes the Dm Cdc2 protein. The second cDNA class encodes a novel protein containing a central motif consisting of two tandem repeats of a putative Zn(2+)-finger motif. This region is highly conserved in the TIS11 family of immediate early genes, which in mammalian cells are rapidly and transiently induced in response to 12-O-tetradecanoyl phorbol-13-acetate (TPA) and to mitogens such as epidermal growth factor and fibroblast growth factor.

Amino Acid Sequence↗
PubMed1994

A Drosophila gene encoding a DEAD box RNA helicase can suppress loss of wee1/mik1 function in Schizosaccharomyces pombe.

We describe a screen to isolate cDNAs encoding Drosophila mitosis inhibitors capable of suppressing the mitotic catastrophe phenotype resulting in Schizosaccharomyces pombe from the combination of the wee1-50 mutation with either a deletion allele of mik1, or with overexpression of cdc25+. One plasmid was isolated which could suppress the temperature sensitive lethality of both these strains. The cDNA in this plasmid encodes a protein highly homologous to the DEAD-box family of ATP-dependent RNA helicases, rather than to protein kinases as might be expected. It is possible that the RNA helicase described here may regulate entry into mitosis by down regulating the expression of other genes whose activity may be rate-limiting for entry into mitosis.

Amino Acid Sequence↗
PubMed1992

Five novel elements involved in the regulation of mitosis in fission yeast.

Five new elements of the mitotic control in the fission yeast Schizosaccharomyces pombe were isolated from gene libraries as multicopy suppressors of the conditional lethal phenotype of win1-1 wee1ts cdc25ts triple mutant strains. These genes were designated wis1(+)-wis5+ for win suppressing, and do not correspond to win1+ or any of the previously characterised mitotic control genes. None of the wis genes is capable of suppressing the cdc phenotype of cdc25ts strains, suggesting that their effect is not simply to reverse the effect of loss of cdc25 function. wis1+ has been previously reported to encode a putative serine/threonine protein kinase that acts as a dosage-dependent inducer of mitosis. wis4+ appears to be a specific suppressor of the win1-1 mutation. wis2+ and wis3+ are capable of suppressing a wide range of cdc phenotypes arising from the combination of various mutations with wee1ts and cdc25ts, suggesting that the wis2+ and wis3+ products may interact with elements central to the mitotic control.

Cell Cycle↗
PubMed1991

The wis1 protein kinase is a dosage-dependent regulator of mitosis in Schizosaccharomyces pombe.

The wis1+ gene encodes a newly identified mitotic control element in Schizosaccharomyces pombe. It was isolated by virtue of its interaction with the mitotic control genes cdc25, wee1 and win1. The wis1+ gene potentially encodes a 66 kDa protein with homology to the serine/threonine family of protein kinases. wis1+ plays an important role in the regulation of entry into mitosis, as it shares with cdc25+ and nim1+/cdr1+ the property of inducing mitosis in a dosage-dependent manner. Increased levels of wis1+ expression cause mitotic initiation to occur at a reduced cell size. Loss of wis1+ function does not prevent vegetative growth and division, though wis1- cells show an elongated morphology, indicating that their entry into mitosis and cell division is delayed relative to wild type cells. wis1- cells undergo a rapid reduction of viability upon entry into stationary phase, suggesting a role for wis1+ in the integration of nutritional sensing with the control over entry into mitosis.

Amino Acid Sequence↗
PubMed1991

Controlling cell cycle progress in the fission yeast Schizosaccharomyces pombe.

The suitability of fission yeast as a model for understanding the eukaryotic cell cycle has been validated in five years of exciting developments. We review recent advances in understanding the nature of the controls that regulate progression through the cell cycle and the coordination of DNA replication and mitosis.

CDC2 Protein Kinase↗
PubMed1991

New elements in the mitotic control of the fission yeast Schizosaccharomyces pombe.

The p107wee1 protein kinase plays a central role in regulating the cell cycle of fission yeast. It mediates transmission of signal(s) related to the nutritional status of the cell to the p34cdc2 protein kinase, which is an active component of the MPF complex driving cells into mitosis. p107wee1 is itself subject to control by the products of other genes such as nim1+/cdr1+, win1+, and perhaps wis1+ and other wis+ genes. At present, the relationships between these genes and their possible roles in the mitotic control are unclear and must await further analysis (Fig. 5). It is likely that some of the gene products are concerned with the sensing and/or transmission of nutritional signals. p107wee1 negatively regulates the activity of p34cdc2, probably by direct tyrosine phosphorylation, and also appears to regulate the activities of the cdc1+ and cdc27+ gene products. The effects of nitrogen starvation and of wee1 mutations on conditional lethal mutations at the cdc1, cdc2, and cdc27 loci, taken together, support the largely speculative model shown in Figure 5. During the normal cycle, the balance between phosphorylated and dephosphorylated p34cdc2 changes such that at the appropriate time, p34cdc2 is activated and the cell enters mitosis. We suggest that the cdc1+ and cdc27+ products may be regulated in a similar way. Such a mechanism would ensure coordinated activation of these and perhaps other proteins required for the G2/M transition. There are, of course, many uncertainties, and these must await elucidation by biochemical and genetic analysis.

CDC2 Protein Kinase↗