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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.

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(a–f) Morphological observations by phase  contrast microscopy of mutants in genes involved in late  mitotic events after 6 h of incubation at 37°C: (a) L119-7d  (dbf2-1); (b) RH1779 (cdc14-1); (c) EO156 (tem1-3); (d)  4965-3a (cdc16); (e) 4086-23-2a (cdc23); (f) 9002 (cdc27).  (g) L2C24d (cdc15-lyt1)  strain transformed with the  pGAL–CLB2 plasmid after  6 h of incubation at 37°C with  galactose as a carbon source.  (h) The same strain transformed with a pRS316 control plasmid under the same  conditions. Arrows, distal  projections. Bars, 5 μm.
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Figure 6: (a–f) Morphological observations by phase contrast microscopy of mutants in genes involved in late mitotic events after 6 h of incubation at 37°C: (a) L119-7d (dbf2-1); (b) RH1779 (cdc14-1); (c) EO156 (tem1-3); (d) 4965-3a (cdc16); (e) 4086-23-2a (cdc23); (f) 9002 (cdc27). (g) L2C24d (cdc15-lyt1) strain transformed with the pGAL–CLB2 plasmid after 6 h of incubation at 37°C with galactose as a carbon source. (h) The same strain transformed with a pRS316 control plasmid under the same conditions. Arrows, distal projections. Bars, 5 μm.

Mentions: There is genetic evidence that the products of the genes TEM1, CDC14, and DBF2 act in a common pathway with the Cdc15p protein kinase (Kitada et al., 1993, Shirayama et al., 1994, 1996). As in the case of CDC15, these genes are essential for viability and dysfunctions in them have been described to cause a late M phase arrest (Toyn and Johnston, 1994; Shirayama et al., 1994, 1996). By applying some of the same techniques as those described above for cdc15 mutants to strains EO156 (tem1-3), RH1779 (cdc14) and L119-7d (dbf2), we also detected a distal polarization pattern in these mutants (Fig. 6, a–c, Table IV). The data thus obtained are comparable to those obtained for cdc15-1 and cdc15-lyt1 in different backgrounds (Table II), suggesting that the eventual overcoming of mitotic arrest would not be restricted to cdc15 mutants, but that it would be common to other mutations in the pathway.


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)

(a–f) Morphological observations by phase  contrast microscopy of mutants in genes involved in late  mitotic events after 6 h of incubation at 37°C: (a) L119-7d  (dbf2-1); (b) RH1779 (cdc14-1); (c) EO156 (tem1-3); (d)  4965-3a (cdc16); (e) 4086-23-2a (cdc23); (f) 9002 (cdc27).  (g) L2C24d (cdc15-lyt1)  strain transformed with the  pGAL–CLB2 plasmid after  6 h of incubation at 37°C with  galactose as a carbon source.  (h) The same strain transformed with a pRS316 control plasmid under the same  conditions. Arrows, distal  projections. Bars, 5 μm.
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Figure 6: (a–f) Morphological observations by phase contrast microscopy of mutants in genes involved in late mitotic events after 6 h of incubation at 37°C: (a) L119-7d (dbf2-1); (b) RH1779 (cdc14-1); (c) EO156 (tem1-3); (d) 4965-3a (cdc16); (e) 4086-23-2a (cdc23); (f) 9002 (cdc27). (g) L2C24d (cdc15-lyt1) strain transformed with the pGAL–CLB2 plasmid after 6 h of incubation at 37°C with galactose as a carbon source. (h) The same strain transformed with a pRS316 control plasmid under the same conditions. Arrows, distal projections. Bars, 5 μm.
Mentions: There is genetic evidence that the products of the genes TEM1, CDC14, and DBF2 act in a common pathway with the Cdc15p protein kinase (Kitada et al., 1993, Shirayama et al., 1994, 1996). As in the case of CDC15, these genes are essential for viability and dysfunctions in them have been described to cause a late M phase arrest (Toyn and Johnston, 1994; Shirayama et al., 1994, 1996). By applying some of the same techniques as those described above for cdc15 mutants to strains EO156 (tem1-3), RH1779 (cdc14) and L119-7d (dbf2), we also detected a distal polarization pattern in these mutants (Fig. 6, a–c, Table IV). The data thus obtained are comparable to those obtained for cdc15-1 and cdc15-lyt1 in different backgrounds (Table II), suggesting that the eventual overcoming of mitotic arrest would not be restricted to cdc15 mutants, but that it would be common to other mutations in the pathway.

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