scholarly journals Prolonged mitosis causes separase deregulation and chromosome nondisjunction

Cell Reports ◽  
2021 ◽  
Vol 34 (3) ◽  
pp. 108652
Author(s):  
Norihisa Shindo ◽  
Makoto Otsuki ◽  
Kazuhiko S.K. Uchida ◽  
Toru Hirota
Keyword(s):  
Chromosome Nondisjunction

scholarly journals Nonrecombinant meiosis I nondisjunction in Saccharomyces cerevisiae induced by tRNA ochre suppressors.

Genetics ◽  
1989 ◽  
Vol 123 (1) ◽  
pp. 81-95 ◽  
Author(s):  
E J Louis ◽  
J E Haber
Keyword(s):  
Saccharomyces Cerevisiae ◽  
Mitotic Chromosome ◽  
Stop Codon ◽  
Fold Increase ◽  
Wild Type ◽  
Yeast Saccharomyces Cerevisiae ◽  
Nonsense Mutations ◽  
Chromosome Iii ◽  
Meiosis I ◽  
Chromosome Nondisjunction

Abstract The presence of the tRNA ochre suppressors SUP11 and SUP5 is found to induce meiosis I nondisjunction in the yeast Saccharomyces cerevisiae. The induction increases with increasing dosage of the suppressor and decreases in the presence of an antisuppressor. The effect is independent of the chromosomal location of SUP11. Each of five different chromosomes monitored exhibited nondisjunction at frequencies of 0.1%-1.1% of random spores, which is a 16-160-fold increase over wild-type levels. Increased nondisjunction is reflected by a marked increase in tetrads with two and zero viable spores. In the case of chromosome III, for which a 50-cM map interval was monitored, the resulting disomes are all in the parental nonrecombinant configuration. Recombination along chromosome III appears normal both in meioses that have no nondisjunction and in meioses for which there was nondisjunction of another chromosome. We propose that a proportion of one or more proteins involved in chromosome pairing, recombination or segregation are aberrant due to translational read-through of the normal ochre stop codon. Hygromycin B, an antibiotic that can suppress nonsense mutations via translational read-through, also induces nonrecombinant meiosis I nondisjunction. Increases in mistranslation, therefore, increase the production of aneuploids during meiosis. There was no observable effect of SUP11 on mitotic chromosome nondisjunction; however some disomes caused SUP11 ade2-ochre strains to appear white or red, instead of pink.

Dosage dependence of maternal contribution to somatic cell division in Drosophila melanogaster

Development ◽  
1991 ◽  
Vol 113 (4) ◽  
pp. 1357-1364 ◽  
Author(s):  
M. Carmena ◽  
C. Gonzalez ◽  
J. Casal ◽  
P. Ripoll
Keyword(s):  
Drosophila Melanogaster ◽  
Cell Division ◽  
Somatic Cell ◽  
Early Development ◽  
Normal Cell ◽  
Chromosome Behaviour ◽  
Wild Type ◽  
Maternal Contribution ◽  
Different Doses ◽  
Chromosome Nondisjunction

Most mitotic mutants in Drosophila do not lead to lethality in early development despite the highly abnormal chromosome behaviour that they elicit. This has been explained as being the effect of maternally provided wild-type products. We have tested this hypothesis by studying cuticular clones derived from cells in which there has been loss of a marked Y chromosome due to chromosome nondisjunction in individuals homozygous for the mutation abnormal spindle who are progeny of heterozygous mothers. We have found that the size and frequency of these clones are higher than in control flies. Furthermore, by analysing flies whose female parents have different doses of the asp+ gene, we have found that there is a correlation between the amount of maternally contributed asp+ product and the frequency and size of cuticular clones. We have also estimated the time in development when the first mitotic mistakes take place, i.e. the time when maternal products are no longer sufficient to carry out normal cell division.

The genetic analysis of distributive segregation in Drosophila melanogaster. I. Isolation and characterization of Aberrant X segregation (Axs), a mutation defective in chromosome partner choice.

Genetics ◽  
1989 ◽  
Vol 122 (4) ◽  
pp. 801-821 ◽  
Author(s):  
A E Zitron ◽  
R S Hawley
Keyword(s):  
X Chromosome ◽  
Partner Choice ◽  
Fourth Chromosome ◽  
X Chromosomes ◽  
Isolation And Characterization ◽  
Dominant Female ◽  
Chromosome Associations ◽  
Female Specific ◽  
Chromosome Nondisjunction

Abstract We describe the isolation and characterization of Aberrant X segregation (Axs), a dominant female-specific meiotic mutation. Although Axs has little or no effect on the frequency or distribution of exchange, or on the disjunction of exchange bivalents, nonexchange X chromosomes undergo nondisjunction at high frequencies in Axs/+ and Axs/Axs females. This increased X chromosome nondisjunction is shown to be a consequence of an Axs-induced defect in distributive segregation. In Axs-bearing females, fourth chromosome nondisjunction is observed only in the presence of nonexchange X chromosomes and is argued to be the result of improper X and fourth chromosome associations within the distributive system. In XX females bearing a compound fourth chromosome, the frequency of nonhomologous disjunction of the X chromosomes from the compound fourth chromosome is shown to account for at least 80% of the total X nondisjunction observed. In addition, Axs diminishes or ablates the capacity of nonexchange X chromosomes to form trivalents in females bearing either a Y chromosome or a small free duplication for the X. Axs also impairs compound X from Y segregation. The effect of Axs on these segregations parallels the defects observed for homologous nonexchange X chromosome disjunction in Axs females. In addition to its dramatic effects on the X chromosome, Axs exerts a similar effect on the segregation of a major autosome. We conclude that Axs defines a locus required for proper homolog disjunction within the distributive system.

scholarly journals Chromosome errors in human eggs shape natural fertility over reproductive life span

Science ◽  
2019 ◽  
Vol 365 (6460) ◽  
pp. 1466-1469 ◽  
Author(s):  
Jennifer R. Gruhn ◽  
Agata P. Zielinska ◽  
Vallari Shukla ◽  
Robert Blanshard ◽  
Antonio Capalbo ◽  
...  
Keyword(s):  
Life Span ◽  
Chromosome Segregation ◽  
Pregnancy Loss ◽  
Natural Fertility ◽  
Congenital Disorders ◽  
Human Oocytes ◽  
Reproductive Life ◽  
Reproductive Life Span ◽  
Quantitative Explanation ◽  
Chromosome Nondisjunction

Chromosome errors, or aneuploidy, affect an exceptionally high number of human conceptions, causing pregnancy loss and congenital disorders. Here, we have followed chromosome segregation in human oocytes from females aged 9 to 43 years and report that aneuploidy follows a U-curve. Specific segregation error types show different age dependencies, providing a quantitative explanation for the U-curve. Whole-chromosome nondisjunction events are preferentially associated with increased aneuploidy in young girls, whereas centromeric and more extensive cohesion loss limit fertility as women age. Our findings suggest that chromosomal errors originating in oocytes determine the curve of natural fertility in humans.

scholarly journals B CHROMOSOME NONDISJUNCTION IN CORN: CONTROL BY FACTORS NEAR THE CENTROMERE

Genetics ◽  
1981 ◽  
Vol 97 (2) ◽  
pp. 379-389
Author(s):  
Wayne R Carlson ◽  
Tau-San Chou
Keyword(s):  
B Chromosome ◽  
B Chromosomes ◽  
Translocation Chromosome ◽  
Pollen Mitosis ◽  
Second Pollen Mitosis ◽  
Chromosome Nondisjunction

ABSTRACT B chromosomes of corn are stable at all mitotic and meiotic divisions of the plant except the second pollen mitosis. In the latter division, B chromosomes undego mitotic nondisjunction at rates as high as 98%. Studies by several workers on B-A translocation chromosomes have provided evidence for the existence of four factors on the B chromosome that control nondisjunction and are separable from the centromere. Two of these factors, referred to here as factors 3 and 4, flank the B chromosome centromere. Factor 3 is the centromere-adjacent heterochromatin in the long arm of the B chromosome; factor 4 is located in the minute short arm. Evidence is presented here supporting the existence of factors 3 and 4. Deficiencies that include each factor were identified following centromeric misdivision events, with breaks at or near the centromere of a B-translocation chromosome. B chromosomes lacking factors 3 or 4 show much less nondisjunction than do chromosomes containing them. The possible function of factor 4 in nondisjuntion is also discussed.

scholarly journals THE EFFECT OF TEMPERATURE AND PARENTAL AGE ON RECOMBINATION AND NONDISJUNCTION IN CAENORHABDITIS ELEGANS

Genetics ◽  
1979 ◽  
Vol 92 (2) ◽  
pp. 409-418 ◽  
Author(s):  
A M Rose ◽  
D L Baillie
Keyword(s):  
Recombination Event ◽  
Egg Production ◽  
Recombination Frequency ◽  
Temperature Shift ◽  
Effect Of Temperature ◽  
Temperature Sensitive ◽  
Parental Age ◽  
Linkage Groups ◽  
C Elegans ◽  
Chromosome Nondisjunction

ABSTRACT The effect of temperature and parental age on recombination frequency in C. elegans was studied between pairs of closely linked markers on linkage groups I and V. In the regions studied, recombination frequency vaned three-fold over the temperature range 13.5° to 26°. Temperature-shift experiments indicated that a temperature-sensitive recombination event occurs approximately 50 oocytes prior to fertilization. Recombination frequency was observed to decrease with maternal age. The greatest decrease was observed in the first 24 hours of egg production. The frequency of male progeny, a measure of X-chromosome nondisjunction was also studied. This frequency increased with elevated temperature and age of the parent.

Tetraploid embryos rescue embryonic lethality caused by an additional maternally inherited X chromosome in the mouse

Development ◽  
1998 ◽  
Vol 125 (17) ◽  
pp. 3353-3363 ◽  
Author(s):  
Y. Goto ◽  
N. Takagi
Keyword(s):  
X Chromosome ◽  
High Frequency ◽  
Cell Lineage ◽  
Mouse Embryos ◽  
Primitive Endoderm ◽  
Parietal Endoderm ◽  
Maternal Imprinting ◽  
Early Lethality ◽  
Ectoplacental Cone ◽  
Chromosome Nondisjunction

Mouse embryos with an additional maternally inherited X chromosome, i.e., disomic for XM (DsXM), cease to grow early in development and have a deficient extraembryonic region. We hypothesized that the underdeveloped extraembryonic region is attributed to two copies of XM that escape inactivation due to maternal imprinting. To examine the validity of this hypothesis and throw more light on the significance of X chromosome dosage on cell differentiation, we generated DsXM(XMXMXP and XMXMY) embryos at a high frequency taking advantage of the elevated incidence of X chromosome nondisjunction in female mice heterozygous for two Robertsonian X-autosome translocations, Rb(X.2)2Ad and Rb(X.9)6H. Although two XM chromosomes seem to remain active in both trophectoderm and primitive endoderm, detailed histological examination showed that the polar trophectoderm derivatives (ectoplacental cone and extraembryonic ectoderm) are severely affected, but the primitive endoderm derivatives (visceral and parietal endoderm) are relatively unaffected. Successful rescue of DsXM embryos by aggregation with tetraploid embryos show that X chromosome inactivation occurred normally leaving one X active in epiblast derivatives. Thus, two copies of active XM chromosome in cells of the polar trophectoderm cell lineage seem to be the main cause of early lethality shown by DsXM embryos as a result of failure in formation of ectoplacental cone and extraembryonic ectoderm.

scholarly journals Meiotic mutants that cause a polar decrease in recombination on the X chromosome in Caenorhabditis elegans.

Genetics ◽  
1994 ◽  
Vol 136 (1) ◽  
pp. 119-127
Author(s):  
S A Broverman ◽  
P M Meneely
Keyword(s):  
Caenorhabditis Elegans ◽  
Genetic Map ◽  
X Chromosome ◽  
Recessive Mutations ◽  
Feature Characteristic ◽  
Comparable Effect ◽  
Chromosome Recombination ◽  
The Right ◽  
Chromosome Nondisjunction ◽  
Pairing Region

Abstract Recessive mutations in three autosomal genes, him-1, him-5 and him-8, cause high levels of X chromosome nondisjunction in hermaphrodites of Caenorhabditis elegans, with no comparable effect on autosomal disjunction. Each of the mutants has reduced levels of X chromosome recombination, correlating with the increase in nondisjunction. However, normal or elevated levels of recombination occur at the end of the X chromosome hypothesized to contain the pairing region (the left end), with recombination levels decreasing in regions approaching the right end. Thus, both the number and the distribution of X chromosome exchange events are altered in these mutants. As a result, the genetic map of the X chromosome in the him mutants exhibits a clustering of genes due to reduced recombination, a feature characteristic of the genetic map of the autosomes in non-mutant animals. We hypothesize that these him genes are needed for some processive event that initiates near the left end of the X chromosome.

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