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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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Scheme of bud development and its estimated timing,  as deduced from budding time assays, in a wild-type strain, haploid and diploid cdc15 mutants. Haploid cdc15 mutants fail to localize actin to the bud-daughter constriction at the end of mitosis  and display an arrest in the transition from anaphase to telophase. The mother cell fails to accomplish any morphogenetic response in a haploid background, but the daughter cell polarizes  growth with a delay of 45 min with respect to a wild-type daughter. Such polarization follows an incorrect distal pattern. This behavior leads to immediate cell lysis. In contrast, diploid cdc15/ cdc15 mutants are frequently able to develop a new bud at the  distal pole after overcoming mitotic arrest and the mother cell  also eventually starts a new round of the cell cycle.
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Figure 8: Scheme of bud development and its estimated timing, as deduced from budding time assays, in a wild-type strain, haploid and diploid cdc15 mutants. Haploid cdc15 mutants fail to localize actin to the bud-daughter constriction at the end of mitosis and display an arrest in the transition from anaphase to telophase. The mother cell fails to accomplish any morphogenetic response in a haploid background, but the daughter cell polarizes growth with a delay of 45 min with respect to a wild-type daughter. Such polarization follows an incorrect distal pattern. This behavior leads to immediate cell lysis. In contrast, diploid cdc15/ cdc15 mutants are frequently able to develop a new bud at the distal pole after overcoming mitotic arrest and the mother cell also eventually starts a new round of the cell cycle.

Mentions: As seen in Figs. 2 and 6, cells that express mutations that arrest the cell cycle in anaphase thus failing to locate actin to the cytokinesis site, develop a distal projection. Pringle and Hartwell (1981) had already noticed the appearance of elongated cells on their early work on the characterization of certain cell cycle mutants. Several observations indicate that this abnormal morphogenetic response may correspond to a new round of the cell cycle: i.e., recognition of the distal pole depends on the basic polarity signaling pathways for budding led by Bud1p (Chant, 1994); START-defective cdc15 mutants do not develop such projections and, apparently correlative with this morphogenetic response, nuclei start DNA replication. Thus, assuming that the observed phenomena constitute the development of a new bud in cytokinesis-defective cells, we found that this new budding process was delayed by ∼40 min as compared with normal budding. A comparison of a normal cell cycle to the abnormal morphogenetic response in cdc15 mutants is offered in Fig. 8.


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)

Scheme of bud development and its estimated timing,  as deduced from budding time assays, in a wild-type strain, haploid and diploid cdc15 mutants. Haploid cdc15 mutants fail to localize actin to the bud-daughter constriction at the end of mitosis  and display an arrest in the transition from anaphase to telophase. The mother cell fails to accomplish any morphogenetic response in a haploid background, but the daughter cell polarizes  growth with a delay of 45 min with respect to a wild-type daughter. Such polarization follows an incorrect distal pattern. This behavior leads to immediate cell lysis. In contrast, diploid cdc15/ cdc15 mutants are frequently able to develop a new bud at the  distal pole after overcoming mitotic arrest and the mother cell  also eventually starts a new round of the cell cycle.
© Copyright Policy
Related In: Results  -  Collection

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

Figure 8: Scheme of bud development and its estimated timing, as deduced from budding time assays, in a wild-type strain, haploid and diploid cdc15 mutants. Haploid cdc15 mutants fail to localize actin to the bud-daughter constriction at the end of mitosis and display an arrest in the transition from anaphase to telophase. The mother cell fails to accomplish any morphogenetic response in a haploid background, but the daughter cell polarizes growth with a delay of 45 min with respect to a wild-type daughter. Such polarization follows an incorrect distal pattern. This behavior leads to immediate cell lysis. In contrast, diploid cdc15/ cdc15 mutants are frequently able to develop a new bud at the distal pole after overcoming mitotic arrest and the mother cell also eventually starts a new round of the cell cycle.
Mentions: As seen in Figs. 2 and 6, cells that express mutations that arrest the cell cycle in anaphase thus failing to locate actin to the cytokinesis site, develop a distal projection. Pringle and Hartwell (1981) had already noticed the appearance of elongated cells on their early work on the characterization of certain cell cycle mutants. Several observations indicate that this abnormal morphogenetic response may correspond to a new round of the cell cycle: i.e., recognition of the distal pole depends on the basic polarity signaling pathways for budding led by Bud1p (Chant, 1994); START-defective cdc15 mutants do not develop such projections and, apparently correlative with this morphogenetic response, nuclei start DNA replication. Thus, assuming that the observed phenomena constitute the development of a new bud in cytokinesis-defective cells, we found that this new budding process was delayed by ∼40 min as compared with normal budding. A comparison of a normal cell cycle to the abnormal morphogenetic response in cdc15 mutants is offered in Fig. 8.

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