scholarly journals The Opposing Actions of Arabidopsis CHROMOSOME TRANSMISSION FIDELITY7 and WINGS APART-LIKE1 and 2 Differ in Mitotic and Meiotic Cells

2016 ◽  
Vol 28 (2) ◽  
pp. 521-536 ◽  
Author(s):  
Kuntal De ◽  
Pablo Bolaños-Villegas ◽  
Sayantan Mitra ◽  
Xiaohui Yang ◽  
Garret Homan ◽  
...  
Keyword(s):  
Chromosome Transmission ◽  
Arabidopsis Chromosome

scholarly journals Arabidopsis CHROMOSOME TRANSMISSION FIDELITY 7 ( AtCTF7 / ECO1 ) is required for DNA repair, mitosis and meiosis

2013 ◽  
Vol 75 (6) ◽  
pp. 927-940 ◽  
Author(s):  
Pablo Bolaños‐Villegas ◽  
Xiaohui Yang ◽  
Huei‐Jing Wang ◽  
Chien‐Ta Juan ◽  
Min‐Hsiang Chuang ◽  
...  
Keyword(s):  
Dna Repair ◽  
Chromosome Transmission ◽  
Arabidopsis Chromosome ◽  
Mitosis And Meiosis

Nonrandom Segregation of the Mouse Univalent X Chromosome: Evidence of Spindle-Mediated Meiotic Drive

Genetics ◽  
2000 ◽  
Vol 156 (2) ◽  
pp. 775-783 ◽  
Author(s):  
Renée LeMaire-Adkins ◽  
Patricia A Hunt
Keyword(s):  
X Chromosome ◽  
Chromosome Abnormality ◽  
Three Dimensional ◽  
Fundamental Principle ◽  
Mendelian Inheritance ◽  
Segregation Behavior ◽  
Chromosome Transmission ◽  
Distortion Effect ◽  
Random Segregation ◽  
Transmission Distortion

Abstract A fundamental principle of Mendelian inheritance is random segregation of alleles to progeny; however, examples of distorted transmission either of specific alleles or of whole chromosomes have been described in a variety of species. In humans and mice, a distortion in chromosome transmission is often associated with a chromosome abnormality. One such example is the fertile XO female mouse. A transmission distortion effect that results in an excess of XX over XO daughters among the progeny of XO females has been recognized for nearly four decades. Utilizing contemporary methodology that combines immunofluorescence, FISH, and three-dimensional confocal microscopy, we have readdressed the meiotic segregation behavior of the single X chromosome in oocytes from XO females produced on two different inbred backgrounds. Our studies demonstrate that segregation of the univalent X chromosome at the first meiotic division is nonrandom, with preferential retention of the X chromosome in the oocyte in ∼60% of cells. We propose that this deviation from Mendelian expectations is facilitated by a spindle-mediated mechanism. This mechanism, which appears to be a general feature of the female meiotic process, has implications for the frequency of nondisjunction in our species.

scholarly journals ALTERED FIDELITY OF MITOTIC CHROMOSOME TRANSMISSION IN CELL CYCLE MUTANTS OF S. CEREVISIAE

Genetics ◽  
1985 ◽  
Vol 110 (3) ◽  
pp. 381-395
Author(s):  
Leland H Hartwell ◽  
David Smith
Keyword(s):  
Cell Cycle ◽  
Gene Product ◽  
Mitotic Chromosome ◽  
Mitotic Recombination ◽  
Chromosome Loss ◽  
Temperature Sensitive ◽  
Repair Pathway ◽  
Dna Metabolism ◽  
Temperature Sensitive Mutants ◽  
Chromosome Transmission

ABSTRACT Thirteen of 14 temperature-sensitive mutants deficient in successive steps of mitotic chromosome transmission (cdc2, 4, 5, 6, 7, 8, 9, 13, 14, 15, 16, 17 and 20) from spindle pole body separation to a late stage of nuclear division exhibited a dramatic increase in the frequency of chromosome loss and/or mitotic recombination when they were grown at their maximum permissive temperatures. The increase in chromosome loss and/or recombination is likely to be due to the deficiency of functional gene product rather than to an aberrant function of the mutant gene product since the mutant alleles are, with one exception, recessive to the wild-type allele for this phenotype. The generality of this result suggests that a delay in almost any stage of chromosome replication or segregation leads to a decrease in the fidelity of mitotic chromosome transmission. In contrast, temperature-sensitive mutants defective in the control step of the cell cycle (cdc28), in cytokinesis (cdc3) or in protein synthesis (ils1) did not exhibit increased recombination or chromosome loss.—Based upon previous results with mutants and DNA-damaging agents in a variety of organisms, we suggest that the induction of mitotic recombination in certain mutants is due to the action of a repair pathway upon nicks or gaps left in the DNA. This interpretation is supported by the fact that the induced recombination is dependent upon the RAD52 gene product, an essential component in the recombinogenic DNA repair pathway. Gene products whose deficiency leads to induced recombination are, therefore, strong candidates for proteins that function in DNA metabolism. Among the mutants that induce recombination are those known to be defective in some aspect of DNA replication (cdc2, 6, 8, 9) as well as some mutants defective in the G2 (cdc13 and 17) and M (cdc5 and 14) phases of the mitotic cycle. We suggest that special aspects of DNA metabolism may be occurring in G2 and M in order to prepare the chromosomes for proper segregation.

scholarly journals Distinct Chromosome Segregation Roles for Spindle Checkpoint Proteins

2002 ◽  
Vol 13 (9) ◽  
pp. 3029-3041 ◽  
Author(s):  
Cheryl D. Warren ◽  
D. Michelle Brady ◽  
Raymond C. Johnston ◽  
Joseph S. Hanna ◽  
Kevin G. Hardwick ◽  
...  
Keyword(s):  
Amino Acid ◽  
Chromosome Segregation ◽  
Chromosome Instability ◽  
Spindle Checkpoint ◽  
Adjacent Segment ◽  
Effect Analysis ◽  
Checkpoint Proteins ◽  
Chromosome Transmission ◽  
Acid Fragment ◽  
Molecular Functions

The spindle checkpoint plays a central role in the fidelity of chromosome transmission by ensuring that anaphase is initiated only after kinetochore-microtubule associations of all sister chromatid pairs are complete. In this study, we find that known spindle checkpoint proteins do not contribute equally to chromosome segregation fidelity in Saccharomyces cerevisiae. Loss of Bub1 or Bub3 protein elicits the largest effect. Analysis of Bub1p reveals the presence of two molecular functions. An N-terminal 608-amino acid (nonkinase) portion of the protein supports robust checkpoint activity, and, as expected, contributes to chromosome segregation. A C-terminal kinase-encoding segment independently contributes to chromosome segregation through an unknown mechanism. Both molecular functions depend on association with Bub3p. A 156-amino acid fragment of Bub1p functions in Bub3p binding and in kinetochore localization by one-hybrid assay. An adjacent segment is required for Mad1p binding, detected by deletion analysis and coimmunoprecipitation. Finally, overexpression of wild-type BUB1 or MAD3 genes leads to chromosome instability. Analysis of this activity indicates that the Bub3p-binding domain of Bub1p contributes to this phenotype through disruption of checkpoint activity as well as through introduction of kinetochore or spindle damage.

scholarly journals Maternal imprinting effect on B chromosome transmission in rye

Heredity ◽  
1990 ◽  
Vol 64 (2) ◽  
pp. 197-204 ◽  
Author(s):  
M J Puertas ◽  
M M Jiménez ◽  
F Romera ◽  
J M Vega ◽  
M Díez
Keyword(s):  
B Chromosome ◽  
Chromosome Transmission ◽  
Maternal Imprinting

scholarly journals rough deal: a gene required for proper mitotic segregation in Drosophila.

1989 ◽  
Vol 109 (6) ◽  
pp. 2951-2961 ◽  
Author(s):  
R E Karess ◽  
D M Glover
Keyword(s):  
Cell Death ◽  
Genetic Locus ◽  
Motile Sperm ◽  
High Frequencies ◽  
Morphological Process ◽  
Daughter Cells ◽  
Chromosome Transmission ◽  
Sister Chromatids ◽  
Mitotic Abnormalities ◽  
Homozygous Mutant

We describe a genetic locus rough deal (rod) in Drosophila melanogaster, identified by mutations that interfere with the faithful transmission of chromosomes to daughter cells during mitosis. Five mutant alleles were isolated, each associated with a similar set of mitotic abnormalities in the dividing neuroblasts of homozygous mutant larvae: high frequencies of aneuploid cells and abnormal anaphase figures, in which chromatids may lag, form bridges, or completely fail to separate. Surviving homozygous adults are sterile, and show cuticular defects associated with cell death, i.e., roughened eyes, sparse abdominal bristles, and notched wing margins. The morphological process of spermatogenesis is largely unaffected and motile sperm are produced, but meiocyte aneuploidy is common. The nature of the observed abnormalities in mitotic cells suggests that the reduced fidelity of chromosome transmission to the daughter cells is due to a failure in a mechanism involved in assuring the proper release of sister chromatids.

scholarly journals The Yeast RSC Chromatin-Remodeling Complex Is Required for Kinetochore Function in Chromosome Segregation

2003 ◽  
Vol 23 (9) ◽  
pp. 3202-3215 ◽  
Author(s):  
Jing-mei Hsu ◽  
Jian Huang ◽  
Pamela B. Meluh ◽  
Brehon C. Laurent
Keyword(s):  
Chromatin Remodeling ◽  
Centromeric Chromatin ◽  
Centromeric Dna ◽  
Chromosome Transmission ◽  
Sister Chromatids ◽  
Chromatin Remodeling Complex ◽  
Histone H3 Variant ◽  
Complex Protein ◽  
Genes Encoding ◽  
Kinetochore Function

ABSTRACT The accurate segregation of chromosomes requires the kinetochore, a complex protein machine that assembles onto centromeric DNA to mediate attachment of replicated sister chromatids to the mitotic spindle apparatus. This study reveals an important role for the yeast RSC ATP-dependent chromatin-remodeling complex at the kinetochore in chromosome transmission. Mutations in genes encoding two core subunits of RSC, the ATPase Sth1p and the Snf5p homolog Sfh1p, interact genetically with mutations in genes encoding kinetochore proteins and with a mutation in centromeric DNA. RSC also interacts genetically and physically with the histone and histone variant components of centromeric chromatin. Importantly, RSC is localized to centromeric and centromere-proximal chromosomal regions, and its association with these loci is dependent on Sth1p. Both sth1 and sfh1 mutants exhibit altered centromeric and centromere-proximal chromatin structure and increased missegregation of authentic chromosomes. Finally, RSC is not required for centromeric deposition of the histone H3 variant Cse4p, suggesting that RSC plays a role in reconfiguring centromeric and flanking nucleosomes following Cse4p recruitment for proper chromosome transmission.

scholarly journals CHTF18 ensures the quantity and quality of the ovarian reserve†

2020 ◽  
Vol 103 (1) ◽  
pp. 24-35
Author(s):  
Rebecca A Holton ◽  
Abigail M Harris ◽  
Barenya Mukerji ◽  
Tanu Singh ◽  
Ferdusy Dia ◽  
...  
Keyword(s):  
Ovarian Follicle ◽  
Reproductive Potential ◽  
Oocyte Quality ◽  
Double Strand Breaks ◽  
Dna Double Strand Breaks ◽  
Strand Breaks ◽  
Chromosome Transmission ◽  
Underlying Mechanisms ◽  
Factor C

Abstract The number and quality of oocytes, as well as the decline in both of these parameters with age, determines reproductive potential in women. However, the underlying mechanisms of this diminution are incompletely understood. Previously, we identified novel roles for CHTF18 (Chromosome Transmission Fidelity Factor 18), a component of the conserved Replication Factor C-like complex, in male fertility and gametogenesis. Currently, we reveal crucial roles for CHTF18 in female meiosis and oocyte development. Chtf18−/− female mice are subfertile and have fewer offspring beginning at 6 months of age. Consistent with age-dependent subfertility, Chtf18−/− ovaries contain fewer follicles at all stages of folliculogenesis than wild type ovaries, but the decreases are more significant at 3 and 6 months of age. By 6 months of age, both primordial and growing ovarian follicle pools are markedly reduced to near depletion. Chromosomal synapsis in Chtf18−/− oocytes is complete, but meiotic recombination is impaired resulting in persistent DNA double-strand breaks, fewer crossovers, and early homolog disjunction during meiosis I. Consistent with poor oocyte quality, the majority of Chtf18−/− oocytes fail to progress to metaphase II following meiotic resumption and a significant percentage of those that do progress are aneuploid. Collectively, our findings indicate critical functions for CHTF18 in ensuring both the quantity and quality of the mammalian oocyte pool.

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