Limits...
Morphogenesis beyond cytokinetic arrest in Saccharomyces cerevisiae.

Jiménez J, Cid VJ, Cenamor R, Yuste M, Molero G, Nombela C, Sánchez M - J. Cell Biol. (1998)

Bottom Line: This morphogenetic response reflects entry into a new round of the cell cycle: the preference for polarization from the distal pole was lost in bud1 cdc15 double mutants; double cdc15-lyt1 cdc28-4 mutants, defective for START, did not develop apical projections and apical polarization was accompanied by DNA replication.Apical polarization was delayed in cdc15 mutants as compared with budding in control cells and this delay was abolished in a septin mutant.Our results suggest that the delayed M/G1 transition in cdc15 mutants is due to a septin-dependent checkpoint that couples initiation of the cell cycle to the completion of cytokinesis.

View Article: PubMed Central - PubMed

Affiliation: Departamento de Microbiología II, Facultad de Farmacia.

ABSTRACT
The budding yeast lyt1 mutation causes cell lysis. We report here that lyt1 is an allele of cdc15, a gene which encodes a protein kinase that functions late in the cell cycle. Neither cdc15-1 nor cdc15-lyt1 strains are able to septate at 37 degreesC, even though they may manage to rebud. Cells lyse after a shmoo-like projection appears at the distal pole of the daughter cell. Actin polarizes towards the distal pole but the septins remain at the mother-daughter neck. This morphogenetic response reflects entry into a new round of the cell cycle: the preference for polarization from the distal pole was lost in bud1 cdc15 double mutants; double cdc15-lyt1 cdc28-4 mutants, defective for START, did not develop apical projections and apical polarization was accompanied by DNA replication. The same phenomena were caused by mutations in the genes CDC14, DBF2, and TEM1, which are functionally related to CDC15. Apical polarization was delayed in cdc15 mutants as compared with budding in control cells and this delay was abolished in a septin mutant. Our results suggest that the delayed M/G1 transition in cdc15 mutants is due to a septin-dependent checkpoint that couples initiation of the cell cycle to the completion of cytokinesis.

Show MeSH

Related in: MedlinePlus

Flow cytometry plots of RNase-treated propidium iodide-stained cells of the VCY242d strain both untransformed  (left) and transformed with a CDC10-bearing plasmid (right).  Cells were incubated at 37°C in osmotically stabilized media.  Samples were taken at the times indicated. Peaks that appear at  15, 30, and 60 arbitrary fluorescence units (see the scale at the  bottom) correspond respectively to cells with DNA contents  equivalent to 1, 2, and 4 nuclei. Comparison of the two series reveals an earlier (∼30 min) and larger amount of cells included in  the third peak when both cdc10 and cdc15 mutations are coexpressed than when the cdc15 mutation is expressed alone.
© Copyright Policy
Related In: Results  -  Collection


getmorefigures.php?uid=PMC2132980&req=5

Figure 7: Flow cytometry plots of RNase-treated propidium iodide-stained cells of the VCY242d strain both untransformed (left) and transformed with a CDC10-bearing plasmid (right). Cells were incubated at 37°C in osmotically stabilized media. Samples were taken at the times indicated. Peaks that appear at 15, 30, and 60 arbitrary fluorescence units (see the scale at the bottom) correspond respectively to cells with DNA contents equivalent to 1, 2, and 4 nuclei. Comparison of the two series reveals an earlier (∼30 min) and larger amount of cells included in the third peak when both cdc10 and cdc15 mutations are coexpressed than when the cdc15 mutation is expressed alone.

Mentions: An experiment to demonstrate that rebudding runs parallel to a new S phase at nuclear level is shown in Fig. 7. FACS® analysis revealed that the evolution of the peak corresponding to 4n DNA content described above was delayed about 30 min in the transformant bearing a wild-type CDC10 with respect to the untransformed cdc10-11 cdc15-1 mutant. According to these results, the expression of a septin mutation prevents the temporal cell cycle arrest caused by the cytokinetic defects due to a loss of function in the CDC15 gene. A plausible explanation for this phenomenon is that the integrity of the septin ring would be essential for a putative cell cycle checkpoint (see Discussion), which would prevent the nucleus from starting a new round of the cell cycle unless cytokinesis has been committed.


Morphogenesis beyond cytokinetic arrest in Saccharomyces cerevisiae.

Jiménez J, Cid VJ, Cenamor R, Yuste M, Molero G, Nombela C, Sánchez M - J. Cell Biol. (1998)

Flow cytometry plots of RNase-treated propidium iodide-stained cells of the VCY242d strain both untransformed  (left) and transformed with a CDC10-bearing plasmid (right).  Cells were incubated at 37°C in osmotically stabilized media.  Samples were taken at the times indicated. Peaks that appear at  15, 30, and 60 arbitrary fluorescence units (see the scale at the  bottom) correspond respectively to cells with DNA contents  equivalent to 1, 2, and 4 nuclei. Comparison of the two series reveals an earlier (∼30 min) and larger amount of cells included in  the third peak when both cdc10 and cdc15 mutations are coexpressed than when the cdc15 mutation is expressed alone.
© Copyright Policy
Related In: Results  -  Collection

Show All Figures
getmorefigures.php?uid=PMC2132980&req=5

Figure 7: Flow cytometry plots of RNase-treated propidium iodide-stained cells of the VCY242d strain both untransformed (left) and transformed with a CDC10-bearing plasmid (right). Cells were incubated at 37°C in osmotically stabilized media. Samples were taken at the times indicated. Peaks that appear at 15, 30, and 60 arbitrary fluorescence units (see the scale at the bottom) correspond respectively to cells with DNA contents equivalent to 1, 2, and 4 nuclei. Comparison of the two series reveals an earlier (∼30 min) and larger amount of cells included in the third peak when both cdc10 and cdc15 mutations are coexpressed than when the cdc15 mutation is expressed alone.
Mentions: An experiment to demonstrate that rebudding runs parallel to a new S phase at nuclear level is shown in Fig. 7. FACS® analysis revealed that the evolution of the peak corresponding to 4n DNA content described above was delayed about 30 min in the transformant bearing a wild-type CDC10 with respect to the untransformed cdc10-11 cdc15-1 mutant. According to these results, the expression of a septin mutation prevents the temporal cell cycle arrest caused by the cytokinetic defects due to a loss of function in the CDC15 gene. A plausible explanation for this phenomenon is that the integrity of the septin ring would be essential for a putative cell cycle checkpoint (see Discussion), which would prevent the nucleus from starting a new round of the cell cycle unless cytokinesis has been committed.

Bottom Line: This morphogenetic response reflects entry into a new round of the cell cycle: the preference for polarization from the distal pole was lost in bud1 cdc15 double mutants; double cdc15-lyt1 cdc28-4 mutants, defective for START, did not develop apical projections and apical polarization was accompanied by DNA replication.Apical polarization was delayed in cdc15 mutants as compared with budding in control cells and this delay was abolished in a septin mutant.Our results suggest that the delayed M/G1 transition in cdc15 mutants is due to a septin-dependent checkpoint that couples initiation of the cell cycle to the completion of cytokinesis.

View Article: PubMed Central - PubMed

Affiliation: Departamento de Microbiología II, Facultad de Farmacia.

ABSTRACT
The budding yeast lyt1 mutation causes cell lysis. We report here that lyt1 is an allele of cdc15, a gene which encodes a protein kinase that functions late in the cell cycle. Neither cdc15-1 nor cdc15-lyt1 strains are able to septate at 37 degreesC, even though they may manage to rebud. Cells lyse after a shmoo-like projection appears at the distal pole of the daughter cell. Actin polarizes towards the distal pole but the septins remain at the mother-daughter neck. This morphogenetic response reflects entry into a new round of the cell cycle: the preference for polarization from the distal pole was lost in bud1 cdc15 double mutants; double cdc15-lyt1 cdc28-4 mutants, defective for START, did not develop apical projections and apical polarization was accompanied by DNA replication. The same phenomena were caused by mutations in the genes CDC14, DBF2, and TEM1, which are functionally related to CDC15. Apical polarization was delayed in cdc15 mutants as compared with budding in control cells and this delay was abolished in a septin mutant. Our results suggest that the delayed M/G1 transition in cdc15 mutants is due to a septin-dependent checkpoint that couples initiation of the cell cycle to the completion of cytokinesis.

Show MeSH
Related in: MedlinePlus