scholarly journals ISOLATION OF ANEUPLOID-GENERATING MUTANTS OF ASPERGILLUS NIDULANS, ONE OF WHICH IS DEFECTIVE IN INTERPHASE OF THE CELL CYCLE

Genetics ◽  
1984 ◽  
Vol 108 (1) ◽  
pp. 107-121
Author(s):  
A Upshall ◽  
I D Mortimore
Keyword(s):  
Cell Cycle ◽  
Chromosome Segregation ◽  
High Frequency ◽  
Mitotic Chromosome ◽  
Meiotic Chromosome ◽  
Restrictive Temperature ◽  
Single Mutation ◽  
Chromosome Type ◽  
Temperature Exchange ◽  
And Behavior

ABSTRACT A method is described for isolating mutants potentially defective in loci involved in mitotic chromosome segregation. Conditional lethal, heat-sensitive (42°) mutants were assayed at a subrestrictive temperature of 37° for an inflated production of colonies displaying phenotypes and behavior patterns of whole chromosome aneuploids. Of 14 mutants, three showed specificity for one disomic phenotype, whereas 11 generated colonies mosaic for different aneuploid phenotypes. This latter group is designated hfa (high frequency of aneuploid). For ten of the 11 mutants temperature sensitivity and aneuploid production cosegregated, indicating a single mutation in each. These mutations were recessive and nonallelic. Analysis was concentrated on the hfaB3 mutation which is mapped to chromosome VI tightly linked to the methB and tsB loci. The disruptive influence of hfaB3 on mitosis at 37° was shown by (1) ploidy and whole chromosome-type segregation of markers in the breakdown sectors of phenotypically aneuploid colonies obtained from multiply marked homozygous hfaB3 disploids; (2) a high frequency of haploid and nondisjunctional diploid segregants among spontaneous yellow-spored parasexual recombinants taken from green-spored homozygous hfaB3 diploids. The mutation had no effect on meiotic chromosome segregation at 37°. The single interphase nucleus in germlings at 42°, coupled with changes in the mitotic index in temperature exchange experiments, showed hfaB3 to arrest the cell cycle in interphase at restrictive temperature. A conclusion drawn is that the hfaB gene product is required both for entry into mitosis and for normal chromosome segregation in dividing nuclei.

CSE1 and CSE2, two new genes required for accurate mitotic chromosome segregation in Saccharomyces cerevisiae

1993 ◽  
Vol 13 (8) ◽  
pp. 4691-4702 ◽  
Author(s):  
Z Xiao ◽  
J T McGrew ◽  
A J Schroeder ◽  
M Fitzgerald-Hayes
Keyword(s):  
Chromosome Segregation ◽  
Leucine Zipper ◽  
Mitotic Chromosome ◽  
Restrictive Temperature ◽  
Permissive Temperature ◽  
New Genes ◽  
Marked Chromosome ◽  
Cold Sensitive ◽  
Basic Region ◽  
Segregation Of Chromosomes

By monitoring the mitotic transmission of a marked chromosome bearing a defective centromere, we have identified conditional alleles of two genes involved in chromosome segregation (cse). Mutations in CSE1 and CSE2 have a greater effect on the segregation of chromosomes carrying mutant centromeres than on the segregation of chromosomes with wild-type centromeres. In addition, the cse mutations cause predominantly nondisjunction rather than loss events but do not cause a detectable increase in mitotic recombination. At the restrictive temperature, cse1 and cse2 mutants accumulate large-budded cells, with a significant fraction exhibiting aberrant binucleate morphologies. We cloned the CSE1 and CSE2 genes by complementation of the cold-sensitive phenotypes. Physical and genetic mapping data indicate that CSE1 is linked to HAP2 on the left arm of chromosome VII and CSE2 is adjacent to PRP2 on chromosome XIV. CSE1 is essential and encodes a novel 109-kDa protein. CSE2 encodes a 17-kDa protein with a putative basic-region leucine zipper motif. Disruption of CSE2 causes chromosome missegregation, conditional lethality, and slow growth at the permissive temperature.

scholarly journals Differential requirement for Bub1 and Bub3 in regulation of meiotic versus mitotic chromosome segregation

2020 ◽  
Vol 219 (4) ◽  
Author(s):  
Gisela Cairo ◽  
Anne M. MacKenzie ◽  
Soni Lacefield
Keyword(s):  
Chromosome Segregation ◽  
Protein Phosphatase ◽  
Mitotic Chromosome ◽  
Budding Yeast ◽  
Meiotic Chromosome ◽  
Protein Phosphatase 1 ◽  
Aurora B ◽  
Chromosome Missegregation ◽  
Anaphase Onset ◽  
Spindle Microtubules

Accurate chromosome segregation depends on the proper attachment of kinetochores to spindle microtubules before anaphase onset. The Ipl1/Aurora B kinase corrects improper attachments by phosphorylating kinetochore components and so releasing aberrant kinetochore–microtubule interactions. The localization of Ipl1 to kinetochores in budding yeast depends upon multiple pathways, including the Bub1–Bub3 pathway. We show here that in meiosis, Bub3 is crucial for correction of attachment errors. Depletion of Bub3 results in reduced levels of kinetochore-localized Ipl1 and concomitant massive chromosome missegregation caused by incorrect chromosome–spindle attachments. Depletion of Bub3 also results in shorter metaphase I and metaphase II due to premature localization of protein phosphatase 1 (PP1) to kinetochores, which antagonizes Ipl1-mediated phosphorylation. We propose a new role for the Bub1–Bub3 pathway in maintaining the balance between kinetochore localization of Ipl1 and PP1, a balance that is essential for accurate meiotic chromosome segregation and timely anaphase onset.

scholarly journals Impact of Global Transcriptional Silencing on Cell Cycle Regulation and Chromosome Segregation in Early Mammalian Embryos

2021 ◽  
Vol 22 (16) ◽  
pp. 9073
Author(s):  
Martin Anger ◽  
Lenka Radonova ◽  
Adela Horakova ◽  
Diana Sekach ◽  
Marketa Charousova
Keyword(s):  
Cell Cycle ◽  
Chromosome Segregation ◽  
Significant Proportion ◽  
Transcriptional Silencing ◽  
Early Embryo ◽  
Global Changes ◽  
Embryonic Genome ◽  
Mammalian Embryos ◽  
A Cell ◽  
And Behavior

The onset of an early development is, in mammals, characterized by profound changes of multiple aspects of cellular morphology and behavior. These are including, but not limited to, fertilization and the merging of parental genomes with a subsequent transition from the meiotic into the mitotic cycle, followed by global changes of chromatin epigenetic modifications, a gradual decrease in cell size and the initiation of gene expression from the newly formed embryonic genome. Some of these important, and sometimes also dramatic, changes are executed within the period during which the gene transcription is globally silenced or not progressed, and the regulation of most cellular activities, including those mentioned above, relies on controlled translation. It is known that the blastomeres within an early embryo are prone to chromosome segregation errors, which might, when affecting a significant proportion of a cell within the embryo, compromise its further development. In this review, we discuss how the absence of transcription affects the transition from the oocyte to the embryo and what impact global transcriptional silencing might have on the basic cell cycle and chromosome segregation controlling mechanisms.

scholarly journals CSE1 and CSE2, two new genes required for accurate mitotic chromosome segregation in Saccharomyces cerevisiae.

1993 ◽  
Vol 13 (8) ◽  
pp. 4691-4702 ◽  
Author(s):  
Z Xiao ◽  
J T McGrew ◽  
A J Schroeder ◽  
M Fitzgerald-Hayes
Keyword(s):  
Chromosome Segregation ◽  
Leucine Zipper ◽  
Mitotic Chromosome ◽  
Restrictive Temperature ◽  
Permissive Temperature ◽  
New Genes ◽  
Marked Chromosome ◽  
Cold Sensitive ◽  
Basic Region ◽  
Segregation Of Chromosomes

By monitoring the mitotic transmission of a marked chromosome bearing a defective centromere, we have identified conditional alleles of two genes involved in chromosome segregation (cse). Mutations in CSE1 and CSE2 have a greater effect on the segregation of chromosomes carrying mutant centromeres than on the segregation of chromosomes with wild-type centromeres. In addition, the cse mutations cause predominantly nondisjunction rather than loss events but do not cause a detectable increase in mitotic recombination. At the restrictive temperature, cse1 and cse2 mutants accumulate large-budded cells, with a significant fraction exhibiting aberrant binucleate morphologies. We cloned the CSE1 and CSE2 genes by complementation of the cold-sensitive phenotypes. Physical and genetic mapping data indicate that CSE1 is linked to HAP2 on the left arm of chromosome VII and CSE2 is adjacent to PRP2 on chromosome XIV. CSE1 is essential and encodes a novel 109-kDa protein. CSE2 encodes a 17-kDa protein with a putative basic-region leucine zipper motif. Disruption of CSE2 causes chromosome missegregation, conditional lethality, and slow growth at the permissive temperature.

scholarly journals Topoisomerase IIα is essential for maintenance of mitotic chromosome structure

2020 ◽  
Vol 117 (22) ◽  
pp. 12131-12142 ◽  
Author(s):  
Christian F. Nielsen ◽  
Tao Zhang ◽  
Marin Barisic ◽  
Paul Kalitsis ◽  
Damien F. Hudson
Keyword(s):  
Cell Cycle ◽  
Chromosome Segregation ◽  
Mitotic Chromosome ◽  
Chromosome Structure ◽  
Chromatin Condensation ◽  
Chromosome Condensation ◽  
Mitotic Chromosomes ◽  
Topoisomerase Iiα ◽  
Mitotic Chromosome Condensation

Topoisomerase IIα (TOP2A) is a core component of mitotic chromosomes and important for establishing mitotic chromosome condensation. The primary roles of TOP2A in mitosis have been difficult to decipher due to its multiple functions across the cell cycle. To more precisely understand the role of TOP2A in mitosis, we used the auxin-inducible degron (AID) system to rapidly degrade the protein at different stages of the human cell cycle. Removal of TOP2A prior to mitosis does not affect prophase timing or the initiation of chromosome condensation. Instead, it prevents chromatin condensation in prometaphase, extends the length of prometaphase, and ultimately causes cells to exit mitosis without chromosome segregation occurring. Surprisingly, we find that removal of TOP2A from cells arrested in prometaphase or metaphase cause dramatic loss of compacted mitotic chromosome structure and conclude that TOP2A is crucial for maintenance of mitotic chromosomes. Treatments with drugs used to poison/inhibit TOP2A function, such as etoposide and ICRF-193, do not phenocopy the effects on chromosome structure of TOP2A degradation by AID. Our data point to a role for TOP2A as a structural chromosome maintenance enzyme locking in condensation states once sufficient compaction is achieved.

scholarly journals Condensin restructures chromosomes in preparation for meiotic divisions

2004 ◽  
Vol 167 (4) ◽  
pp. 613-625 ◽  
Author(s):  
Raymond C. Chan ◽  
Aaron F. Severson ◽  
Barbara J. Meyer
Keyword(s):  
Caenorhabditis Elegans ◽  
Chromosome Segregation ◽  
Germ Cells ◽  
Protein Complex ◽  
Mitotic Chromosome ◽  
Meiotic Chromosome ◽  
Ordered Structure ◽  
Homologous Chromosomes ◽  
Sister Chromatids ◽  
Chromosome Resolution

The production of haploid gametes from diploid germ cells requires two rounds of meiotic chromosome segregation after one round of replication. Accurate meiotic chromosome segregation involves the remodeling of each pair of homologous chromosomes around the site of crossover into a highly condensed and ordered structure. We showed that condensin, the protein complex needed for mitotic chromosome compaction, restructures chromosomes during meiosis in Caenorhabditis elegans. In particular, condensin promotes both meiotic chromosome condensation after crossover recombination and the remodeling of sister chromatids. Condensin helps resolve cohesin-independent linkages between sister chromatids and alleviates recombination-independent linkages between homologues. The safeguarding of chromosome resolution by condensin permits chromosome segregation and is crucial for the formation of discrete, individualized bivalent chromosomes.

scholarly journals Excess crossovers impede faithful meiotic chromosome segregation in C. elegans

2020 ◽  
Author(s):  
Jeremy A. Hollis ◽  
Marissa L. Glover ◽  
Aleesa Schlientz ◽  
Cori K. Cahoon ◽  
Bruce Bowerman ◽  
...  
Keyword(s):  
Caenorhabditis Elegans ◽  
Chromosome Segregation ◽  
High Frequency ◽  
Meiotic Chromosome ◽  
Dependent Manner ◽  
Homologous Chromosomes ◽  
Crossover Interference ◽  
C Elegans ◽  
Functional Consequences ◽  
Chromosome Bridges

AbstractDuring meiosis, at least one crossover must form between each pair of homologous chromosomes to ensure their proper partitioning. However, most organisms limit the number of crossovers by a phenomenon called crossover interference; why this occurs is not well understood. Here we investigate the functional consequences of extra crossovers in Caenorhabditis elegans. Using a fusion chromosome that exhibits a high frequency of supernumerary crossovers, we find that essential chromosomal structures are mispatterned, subjecting chromosomes to improper spindle forces and leading to congression and segregation defects. Moreover, we uncover mechanisms that counteract these errors; anaphase I chromosome bridges were often able to resolve in a LEM-3 nuclease dependent manner, and tethers between homologs that persisted were frequently resolved during Meiosis II by a second mechanism. This study thus provides evidence that excess crossovers impact chromosome patterning and segregation, and also sheds light on how these errors are corrected.

scholarly journals The Essentiality of the Fungus-Specific Dam1 Complex Is Correlated with a One-Kinetochore-One-Microtubule Interaction Present throughout the Cell Cycle, Independent of the Nature of a Centromere

2011 ◽  
Vol 10 (10) ◽  
pp. 1295-1305 ◽  
Author(s):  
Jitendra Thakur ◽  
Kaustuv Sanyal
Keyword(s):  
Saccharomyces Cerevisiae ◽  
Cell Cycle ◽  
Candida Albicans ◽  
Fission Yeast ◽  
Chromosome Segregation ◽  
Spindle Assembly Checkpoint ◽  
Mitotic Chromosome ◽  
Content Type ◽  
Spindle Elongation ◽  
Dam1 Complex

ABSTRACTA fungus-specific outer kinetochore complex, the Dam1 complex, is essential inSaccharomyces cerevisiae, nonessential in fission yeast, and absent from metazoans. The reason for the reductive evolution of the functionality of this complex remains unknown. BothCandida albicansandSchizosaccharomyces pombehave regional centromeres as opposed to the short-point centromeres ofS. cerevisiae. The interaction of one microtubule per kinetochore is established both inS. cerevisiaeandC. albicansearly during the cell cycle, which is in contrast to the multiple microtubules that bind to a kinetochore only during mitosis inS. pombe. Moreover, the Dam1 complex is associated with the kinetochore throughout the cell cycle inS. cerevisiaeandC. albicansbut only during mitosis inS. pombe. Here, we show that the Dam1 complex is essential for viability and indispensable for proper mitotic chromosome segregation inC. albicans. The kinetochore localization of the Dam1 complex is independent of the kinetochore-microtubule interaction, but the function of this complex is monitored by a spindle assembly checkpoint. Strikingly, the Dam1 complex is required to prevent precocious spindle elongation in premitotic phases. Thus, constitutive kinetochore localization associated with a one-microtubule-one kinetochore type of interaction, but not the length of a centromere, is correlated with the essentiality of the Dam1 complex.

scholarly journals Distinct Developmental Function of Two Caenorhabditis elegans Homologs of the Cohesin Subunit Scc1/Rad21

2003 ◽  
Vol 14 (6) ◽  
pp. 2399-2409 ◽  
Author(s):  
Yoshiko Mito ◽  
Asako Sugimoto ◽  
Masayuki Yamamoto
Keyword(s):  
Cell Cycle ◽  
Caenorhabditis Elegans ◽  
Chromosome Segregation ◽  
Mitotic Chromosome ◽  
Dependent Manner ◽  
C Elegans ◽  
Late Embryogenesis ◽  
A Cell ◽  
Cohesin Subunit ◽  
Cycle Dependent

Cohesin, which mediates sister chromatid cohesion, is composed of four subunits, named Scc1/Rad21, Scc3, Smc1, and Smc3 in yeast. Caenorhabditis elegans has a single homolog for each of Scc3, Smc1, and Smc3, but as many as four for Scc1/Rad21 (COH-1, SCC-1/COH-2, COH-3, and REC-8). Except for REC-8 required for meiosis, function of these C. elegans proteins remains largely unknown. Herein, we examined their possible involvement in mitosis and development. Embryos depleted of the homolog of either Scc3, or Smc1, or Smc3 by RNA interference revealed a defect in mitotic chromosome segregation but not in chromosome condensation and cytokinesis. Depletion of SCC-1/COH-2 caused similar phenotypes. SCC-1/COH-2 was present in cells destined to divide. It localized to chromosomes in a cell cycle-dependent manner. Worms depleted of COH-1 arrested at either the late embryonic or the larval stage, with no indication of mitotic dysfunction. COH-1 associated chromosomes throughout the cell cycle in all somatic cells undergoing late embryogenesis or larval development. Thus, SCC-1/COH-2 and the homologs of Scc3, Smc1, and Smc3 facilitate mitotic chromosome segregation during the development, presumably by forming a cohesin complex, whereas COH-1 seems to play a role important for development but unrelated to mitosis.

scholarly journals Regulation of mating in the cell cycle of Saccharomyces cerevisiae.

1977 ◽  
Vol 75 (2) ◽  
pp. 355-365 ◽  
Author(s):  
B J Reid ◽  
L H Hartwell
Keyword(s):  
Cell Cycle ◽  
Dna Synthesis ◽  
High Frequency ◽  
Nuclear Division ◽  
Diploid Cell ◽  
Yeast Cells ◽  
Temperature Sensitive ◽  
Restrictive Temperature ◽  
Haploid Strain ◽  
Cdc 2

The capacity of haploid a yeast cells to mate (fuse with a haploid strain of alpha mating type followed by nuclear fusion to produce a diploid cell) was assessed for a variety of temperature-sensitive cell division cycle (cdc) mutants at the permissive and restrictive temperatures. Asynchronous populations of some mutants do not mate at the restrictive temperature, and these mutants define genes (cdc 1, 4, 24, and 33) that are essential both for the cell cycle and for mating. For most cdc mutants, asynchronous populations mate well at the restrictive temperature while populations synchronized at the cdc block do not. Populations of a mutant carrying the cdc 28 mutation mate well at the restrictive temperature after synchronization at the cdc 28 step. These results suggest that mating can occur from the cdc 28 step, the same step at which mating factors arrest cell cycle progress. The cell cycle interval in which mating can occur may or may not extend to the immediately succeeding and diverging steps (cdc 4 and cdc 24). High frequency mating does not occur in the interval of the cell cycle extending from the step before the initiation of DNA synthesis (cdc 7) through DNA synthesis (cdc 2, 8, and 21), medial nuclear division (cdc 13), and late nuclear division (cdc 14 and 15).

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