Evidence for second division restitution as the basis for 2n + n maternal chromosome transmission in a sugarcane cross

Euphytica ◽  
2012 ◽  
Vol 187 (3) ◽  
pp. 359-368 ◽  
Author(s):  
S. R. Hermann ◽  
K. S. Aitken ◽  
P. A. Jackson ◽  
A. W. George ◽  
N. Piperidis ◽  
...  
Keyword(s):  
Maternal Chromosome ◽  
Chromosome Transmission ◽  
Second Division Restitution

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.

Recurrent meiotic nondisjunction of maternal chromosome 15 in a sibship

1998 ◽  
Vol 76 (1) ◽  
pp. 103-104 ◽  
Author(s):  
Jean-Paul Harpey ◽  
Delphine Heron ◽  
Muriel Prudent ◽  
Sylvie Lesourd ◽  
Isabelle Henry ◽  
...  
Keyword(s):  
Chromosome 15 ◽  
Maternal Chromosome ◽  
Meiotic Nondisjunction

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

Use of half-tetrad analysis to discriminate between two types of 2n egg formation in a potato haploid

Genome ◽  
1992 ◽  
Vol 35 (5) ◽  
pp. 741-745 ◽  
Author(s):  
Joanna E. Werner ◽  
David S. Douches ◽  
Rosanna Freyre
Keyword(s):  
Solanum Tuberosum L ◽  
2N Gametes ◽  
Breeding Value ◽  
Tetrad Analysis ◽  
Recombination Rates ◽  
First Division Restitution ◽  
Egg Formation ◽  
Second Division Restitution ◽  
2N Eggs ◽  
Tetraploid Progeny

The ratio of the first division restitution (FDR) to second division restitution (SDR) 2n eggs was estimated in 4182t, a haploid (2n = 2x = 24) of Solanum tuberosum L. that produces 2n eggs by the two modes. The segregation of three genes previously mapped relative to their centromeres, Pgm-2 (2.0 cM), Mdh-1 (33.5 cM), and 6-Pgdh-3 (30.1 cM) was analyzed in the tetraploid offspring of a 2x × 4x cross. Based on the segregation of the Pgm-2 locus, 39.7% of the progeny originated from FDR 2n eggs and 60.3% from SDR. Segregation patterns of the two distal loci within the FDR-derived 4x subpopulation indicated that the gene–centromere recombination rate during megasporogenesis was significantly reduced for Mdh-1 when compared with a previous estimate during microsporogenesis. In the SDR-derived 4x subpopulation, the gene–centromere recombination rates for Mdh-1 and 6-Pgdh-3 were not significantly different from previous estimates. Tetraploid progeny generated from one 2x × 4x cross where the 2x parent produces 2n gametes by two modes can be used to make an unbiased comparison of the potential breeding value of FDR and SDR gametes.Key words: potato, megasporogenesis, first division restitution, second division restitution, isozyme.

Comparison of fetal and maternal chromosome polymorphisms: Applications in prenatal diagnosis

1982 ◽  
Vol 2 (1) ◽  
pp. 25-31 ◽  
Author(s):  
M. Frydman ◽  
D. A. Greenberg ◽  
T. K. Mohandas ◽  
M. M. Kaback
Keyword(s):  
Prenatal Diagnosis ◽  
Maternal Chromosome

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.

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