Phosphorylated proteins are involved in sister-chromatid arm cohesion during meiosis I

1999 ◽  
Vol 112 (17) ◽  
pp. 2957-2969 ◽  
Author(s):  
J.A. Suja ◽  
C. Antonio ◽  
A. Debec ◽  
J.S. Rufas
Keyword(s):  
Sister Chromatid ◽  
Chromosome Structure ◽  
Metaphase Plate ◽  
Mitotic Chromosomes ◽  
Phosphorylated Proteins ◽  
Sister Chromatids ◽  
Sequential Release ◽  
Sister Kinetochore ◽  
Meiosis I ◽  
Metaphase I

Sister-chromatid arm cohesion is lost during the metaphase I/anaphase I transition to allow homologue separation. To obtain needed information on this process we have analysed in grasshopper bivalents the sequential release of arm cohesion in relation to the behaviour of chromatid axes. Results show that sister axes are associated during early metaphase I but separate during late metaphase I leading to a concomitant change of chromosome structure that implies the loss of sister-kinetochore cohesion. Afterwards, homologues initiate their separation asynchronously depending on their size, and number and position of chiasmata. In all bivalents thin chromatin strands at the telomeres appeared as the last point of contact between sister chromatids. Additionally, we have analysed the participation of phosphoproteins recognised by the MPM-2 monoclonal antibody against mitotic phosphoproteins in arm cohesion in bivalents and two different kinds of univalents. Results show the absence of MPM-2 phosphoproteins at the interchromatid domain in mitotic chromosomes and meiotic univalents, but their presence in metaphase I bivalents. These phosphoproteins are lost at the onset of anaphase I. Taken together, these data have prompted us to propose a ‘working’ model for the release of arm cohesion during meiosis I. The model suggests that MPM-2 phosphoproteins may act as cohesive proteins associating sister axes. Their modification, once all bivalents are correctly aligned at the metaphase plate, would trigger a change of chromosome structure and the sequential release of sister-kinetochore, arm, and telomere cohesions.

scholarly journals Dynamic bonds and polar ejection force distribution explain kinetochore oscillations in PtK1 cells

2013 ◽  
Vol 201 (4) ◽  
pp. 577-593 ◽  
Author(s):  
Gul Civelekoglu-Scholey ◽  
Bin He ◽  
Muyao Shen ◽  
Xiaohu Wan ◽  
Emanuele Roscioli ◽  
...  
Keyword(s):  
Metaphase Plate ◽  
Quantitative Model ◽  
Force Distribution ◽  
Mitotic Chromosomes ◽  
Chromosome Behavior ◽  
Sister Chromatids ◽  
Ejection Force ◽  
Sister Kinetochore ◽  
Spindle Microtubules ◽  
Key Features

Duplicated mitotic chromosomes aligned at the metaphase plate maintain dynamic attachments to spindle microtubules via their kinetochores, and multiple motor and nonmotor proteins cooperate to regulate their behavior. Depending on the system, sister chromatids may display either of two distinct behaviors, namely (1) the presence or (2) the absence of oscillations about the metaphase plate. Significantly, in PtK1 cells, in which chromosome behavior appears to be dependent on the position along the metaphase plate, both types of behavior are observed within the same spindle, but how and why these distinct behaviors are manifested is unclear. Here, we developed a new quantitative model to describe metaphase chromosome dynamics via kinetochore–microtubule interactions mediated by nonmotor viscoelastic linkages. Our model reproduces all the key features of metaphase sister kinetochore dynamics in PtK1 cells and suggests that differences in the distribution of polar ejection forces at the periphery and in the middle of PtK1 cell spindles underlie the observed dichotomy of chromosome behavior.

scholarly journals Loss of Sister Kinetochore Co-orientation and Peri-centromeric Cohesin Protection after Meiosis I Depends on Cleavage of Centromeric REC8

2020 ◽  
Author(s):  
Sugako Ogushi ◽  
Ahmed Rattani ◽  
Jonathan Godwin ◽  
Jean Metson ◽  
Lothar Schermelleh ◽  
...  
Keyword(s):  
Catalytic Activity ◽  
Sister Chromatid ◽  
Spindle Pole ◽  
Sister Chromatids ◽  
Sister Kinetochore ◽  
Meiosis I

SummaryProtection of peri-centromeric REC8 cohesin from separase and sister kinetochore attachment to microtubules emanating from the same spindle pole (co-orientation) ensure that sister chromatids remain associated after meiosis I. Both features are lost during meiosis II, when sister kinetochores bi-orient and lose peri-centromeric REC8 protection, resulting in sister chromatid disjunction and the production of haploid gametes. By transferring spindle-chromosome complexes (SCCs) between meiosis I and II cells, we have discovered that both sister kinetochore co-orientation and peri-centromeric cohesin protection depend on the SCC and not the cytoplasm. Moreover, the catalytic activity of separase at meiosis I is necessary not only for converting kinetochores from a co-to a bi-oriented state but also for deprotection of peri-centromeric cohesin and that cleavage of REC8 may be the key event. Crucially, we show that selective cleavage of REC8 in the vicinity of kinetochores is sufficient to destroy co-orientation in univalent chromosomes, albeit not in bivalents where resolution of chiasmata through cleavage of Rec8 along chromosome arms may also be required.

scholarly journals Direct evaluation of cohesin-mediated sister kinetochore associations at meiosis I in fission yeast

2021 ◽  
Author(s):  
Masashi Nambu ◽  
Atsuki Kishikawa ◽  
Takatomi Yamada ◽  
Kento Ichikawa ◽  
Yunosuke Kira ◽  
...  
Keyword(s):  
Fission Yeast ◽  
Chromosome Segregation ◽  
Mitotic Chromosomes ◽  
Direct Evaluation ◽  
Homologous Chromosomes ◽  
Sister Chromatids ◽  
Pheromone Signaling ◽  
Sister Kinetochore ◽  
Novel Method ◽  
Meiosis I

Kinetochores drive chromosome segregation by mediating chromosome interactions with the spindle. In higher eukaryotes, sister kinetochores are separately positioned on opposite sides of sister centromeres during mitosis, but associate with each other during meiosis I. Kinetochore association facilitates the attachment of sister chromatids to the same pole, enabling the segregation of homologous chromosomes toward opposite poles. In the fission yeast, Schizosaccharomyces pombe, Rec8-containing meiotic cohesin is suggested to establish kinetochore associations by mediating cohesion of the centromere cores. However, cohesin-mediated kinetochore associations on intact chromosomes have never been demonstrated directly. Here, we describe a novel method for the direct evaluation of kinetochore associations on intact chromosomes in live S. pombe cells, and demonstrate that sister kinetochores and the centromere cores are positioned separately on mitotic chromosomes but associate with each other on meiosis I chromosomes. Furthermore, we demonstrate that kinetochore association depends on meiotic cohesin and the cohesin regulators, Moa1 and Mrc1, and requires mating-pheromone signaling for its establishment. These results confirm cohesin-mediated kinetochore association and its regulatory mechanisms, along with the usefulness of the developed method for its analysis.

Phosphorylation of histone H3 is correlated with changes in the maintenance of sister chromatid cohesion during meiosis in maize, rather than the condensation of the chromatin

2000 ◽  
Vol 113 (18) ◽  
pp. 3217-3226 ◽  
Author(s):  
E. Kaszas ◽  
W.Z. Cande
Keyword(s):  
Sister Chromatid ◽  
Meiotic Chromosome ◽  
Histone H3 ◽  
Sister Chromatid Cohesion ◽  
Chromosome Condensation ◽  
Mitotic Chromosomes ◽  
Sister Chromatids ◽  
H3 Phosphorylation ◽  
Chromatid Cohesion ◽  
Metaphase I

Meiotic chromosome condensation is a unique process, characterized by dramatic changes in chromosome morphology that are required for the correct progression of pairing, synapsis, recombination and segregation of sister chromatids. We used an antibody that recognizes a ser 10 phosphoepitope on histone H3 to monitor H3 phosphorylation during meiosis in maize meiocytes. H3 phosphorylation has been reported to be an excellent marker for chromosome condensation during mitotic prophase in animal cells. In this study, we find that on maize mitotic chromosomes only pericentromeric regions are stained; there is little staining on the arms. During meiosis, chromosome condensation from leptotene through diplotene occurs in the absence of H3 phosphorylation. Instead, the changes in H3 phosphorylation at different stages of meiosis correlate with the differences in requirements for sister chromatid cohesion at different stages. Just before nuclear envelope breakdown, histone H3 phosphorylation is seen first in the pericentromeric regions and then extends through the arms at metaphase I; at metaphase II only the pericentromeric regions are stained. In afd1 (absence of first division), a mutant that is defective in many aspects of meiosis including sister chromatid cohesion and has equational separation at metaphase I, staining is restricted to the pericentromeric regions during metaphase I and anaphase I; there is no staining at metaphase II or anaphase II. We conclude that changes in the level of phosphorylation of ser10 in H3 correspond to changes in the cohesion of sister chromatids rather than the extent of chromosome condensation at different stages of meiosis.

scholarly journals SOLO: a meiotic protein required for centromere cohesion, coorientation, and SMC1 localization in Drosophila melanogaster

2010 ◽  
Vol 188 (3) ◽  
pp. 335-349 ◽  
Author(s):  
Rihui Yan ◽  
Sharon E. Thomas ◽  
Jui-He Tsai ◽  
Yukihiro Yamada ◽  
Bruce D. McKee
Keyword(s):  
Drosophila Melanogaster ◽  
Sister Chromatid ◽  
Sister Chromatid Cohesion ◽  
Early Prophase ◽  
Wild Type ◽  
Sister Chromatids ◽  
Chromatid Cohesion ◽  
Mutant Phenotypes ◽  
Meiosis I ◽  
Novel Protein

Sister chromatid cohesion is essential to maintain stable connections between homologues and sister chromatids during meiosis and to establish correct centromere orientation patterns on the meiosis I and II spindles. However, the meiotic cohesion apparatus in Drosophila melanogaster remains largely uncharacterized. We describe a novel protein, sisters on the loose (SOLO), which is essential for meiotic cohesion in Drosophila. In solo mutants, sister centromeres separate before prometaphase I, disrupting meiosis I centromere orientation and causing nondisjunction of both homologous and sister chromatids. Centromeric foci of the cohesin protein SMC1 are absent in solo mutants at all meiotic stages. SOLO and SMC1 colocalize to meiotic centromeres from early prophase I until anaphase II in wild-type males, but both proteins disappear prematurely at anaphase I in mutants for mei-S332, which encodes the Drosophila homologue of the cohesin protector protein shugoshin. The solo mutant phenotypes and the localization patterns of SOLO and SMC1 indicate that they function together to maintain sister chromatid cohesion in Drosophila meiosis.

The influence of fixation on the morphology of mitotic chromosomes

1986 ◽  
Vol 28 (4) ◽  
pp. 536-539 ◽  
Author(s):  
Axel J. J. Dietrich
Keyword(s):  
Acetic Acid ◽  
Chemical Composition ◽  
Strong Influence ◽  
Chromosome Structure ◽  
Human Lymphocytes ◽  
Chromosome Morphology ◽  
Mitotic Chromosomes ◽  
Specific Chemical ◽  
C Banding ◽  
Sister Chromatids

It is well known that there is a strong influence of fixation, i.e., acetic methanol versus formaldehyde, on the chromosome morphology at stages of the first meiotic division. In this study the influence of both these types of fixation on the morphology of mitotic chromosomes was examined in human lymphocytes. After methanol – acetic acid (3:1) fixation, the chromosomes show the "classical" condensed shape in which it is not always possible to recognize the two sister chromatids. These chromosomes are accessible to the conventional G-, R-, and C-banding techniques. After formaldehyde fixation at a relatively high pH, the chromosomes are thinner and longer (two to six times) when compared with chromosomes following methanol – acetic acid fixation. They show a scaffold-like morphology, sometimes with a halo of thin material around it. In all cases the two sister chromatids could be recognized. This chromosome structure could be easily stained with silver, Giemsa, 4,6-diamino-2-phenyl-indole (DAPI), and fluorescein isocyanate isomere 1 (FITC). The results obtained following these stainings gave no indication to any specific chemical composition of a probable central scaffold. The scaffold-like structures were not accessible to G-, R-, or C-banding techniques. The only effect observed following these banding techniques was the disappearance of the halo of thin material around the central scaffold-like structure.Key words: chromosome structure, fixation influence, human lymphocytes.

scholarly journals CORRIGENDUM

Genetics ◽  
1987 ◽  
Vol 115 (3) ◽  
pp. 579-579
Keyword(s):  
Sister Chromatid ◽  
Recombination Event ◽  
Linear Plasmid ◽  
Wild Type ◽  
Spore Viability ◽  
Yeast Plasmid ◽  
Type Locus ◽  
Sister Chromatids ◽  
Chromosome Ii ◽  
Meiosis I

ABSTRACT In the paper by Jules O'Rear and Jasper Rine (Genetics  113: 517-529; July, 1986) entitled "Precocious meiotic centromere separation of a novel yeast chromosome," the authors described a gene conversion event between a linear yeast plasmid carrying a LYS2 gene and a mutant lys2 gene at the wild-type locus on chromosome II. When these yeasts were mated to wild-type yeast and the resulting diploids sporulated, linked markers on the linear plasmid showed unusual segregation and poor spore viability was observed. On the basis of these observations, we proposed that the recombination event between the linear plasmid and chromosome II had split chromosome II into two fragments, one of which carried the normal centromere of chromosome II (fragment IIa) and the other, a telocentric fragment (fragment IIb), carried the centromere present on the linear plasmid. Separation of the chromosomes from these cells on OFAGE gels verified that chromosome II had been split into two fragments. Furthermore, we proposed that the sister chromatids of the telocentric fragment (fragment IIb) separated precociously in meiosis I when complete chromosome II and fragment IIa were present. In discussions with colleagues, an alternative explanation arose in which a recombination event between a sister chromatid of fragment IIa and a sister chromatid of chromosome II would result in each chromosome II chromatid being joined to a fragment IIa chromatid at CEN2. The two daughter cells of meiosis I would therefore each receive one chromatid of fragment IIa and one chromatid of chromosome II. Segregation of the two sister chromatids of fragment IIb to one pole in meiosis I without precocious centromere separation would result in the observed tetrad classes. To distinguish between these two mechanisms, a centromere-linked marker was introduced into the cross between the strain containing the two fragments of chromosome II and a wild-type strain. Tetrad analysis of the resulting diploid is consistent with the recombination model for the poor spore viability and inconsistent with precocious centromere separation. We thank Drs. Eric Lambie, Michael Lichten and Tom Petes for helpful discussions.

scholarly journals Mouse satellite DNA, centromere structure, and sister chromatid pairing.

1986 ◽  
Vol 103 (4) ◽  
pp. 1145-1151 ◽  
Author(s):  
L M Lica ◽  
S Narayanswami ◽  
B A Hamkalo
Keyword(s):  
Electron Microscopy ◽  
Sister Chromatid ◽  
Satellite Dna ◽  
Marker Chromosome ◽  
Restriction Enzymes ◽  
Centromeric Heterochromatin ◽  
Mitotic Chromosomes ◽  
Metaphase Chromosomes ◽  
Sister Chromatids ◽  
Mouse Satellite Dna

The experiments described were directed toward understanding relationships between mouse satellite DNA, sister chromatid pairing, and centromere function. Electron microscopy of a large mouse L929 marker chromosome shows that each of its multiple constrictions is coincident with a site of sister chromatid contact and the presence of mouse satellite DNA. However, only one of these sites, the central one, possesses kinetochores. This observation suggests either that satellite DNA alone is not sufficient for kinetochore formation or that when one kinetochore forms, other potential sites are suppressed. In the second set of experiments, we show that highly extended chromosomes from Hoechst 33258-treated cells (Hilwig, I., and A. Gropp, 1973, Exp. Cell Res., 81:474-477) lack kinetochores. Kinetochores are not seen in Miller spreads of these chromosomes, and at least one kinetochore antigen is not associated with these chromosomes when they were subjected to immunofluorescent analysis using anti-kinetochore scleroderma serum. These data suggest that kinetochore formation at centromeric heterochromatin may require a higher order chromatin structure which is altered by Hoechst binding. Finally, when metaphase chromosomes are subjected to digestion by restriction enzymes that degrade the bulk of mouse satellite DNA, contact between sister chromatids appears to be disrupted. Electron microscopy of digested chromosomes shows that there is a significant loss of heterochromatin between the sister chromatids at paired sites. In addition, fluorescence microscopy using anti-kinetochore serum reveals a greater inter-kinetochore distance than in controls or chromosomes digested with enzymes that spare satellite. We conclude that the presence of mouse satellite DNA in these regions is necessary for maintenance of contact between the sister chromatids of mouse mitotic chromosomes.

scholarly journals Meiotic cohesin REC8 marks the axial elements of rat synaptonemal complexes before cohesins SMC1β and SMC3

2003 ◽  
Vol 160 (5) ◽  
pp. 657-670 ◽  
Author(s):  
Maureen Eijpe ◽  
Hildo Offenberg ◽  
Rolf Jessberger ◽  
Ekaterina Revenkova ◽  
Christa Heyting
Keyword(s):  
Synaptonemal Complex ◽  
Sister Chromatid ◽  
Meiotic Prophase ◽  
S Phase ◽  
Synaptonemal Complexes ◽  
Sister Chromatids ◽  
Chromatid Cohesion ◽  
Axial Element ◽  
Striking Contrast ◽  
Metaphase I

In meiotic prophase, the sister chromatids of each chromosome develop a common axial element (AE) that is integrated into the synaptonemal complex (SC). We analyzed the incorporation of sister chromatid cohesion proteins (cohesins) and other AE components into AEs. Meiotic cohesin REC8 appeared shortly before premeiotic S phase in the nucleus and formed AE-like structures (REC8-AEs) from premeiotic S phase on. Subsequently, meiotic cohesin SMC1β, cohesin SMC3, and AE proteins SCP2 and SCP3 formed dots along REC8-AEs, which extended and fused until they lined REC8-AEs along their length. In metaphase I, SMC1β, SMC3, SCP2, and SCP3 disappeared from the chromosome arms and accumulated around the centromeres, where they stayed until anaphase II. In striking contrast, REC8 persisted along the chromosome arms until anaphase I and near the centromeres until anaphase II. We propose that REC8 provides a basis for AE formation and that the first steps in AE assembly do not require SMC1β, SMC3, SCP2, and SCP3. Furthermore, SMC1β, SMC3, SCP2, and SCP3 cannot provide arm cohesion during metaphase I. We propose that REC8 then provides cohesion. RAD51 and/or DMC1 coimmunoprecipitates with REC8, suggesting that REC8 may also provide a basis for assembly of recombination complexes.

THE ULTRASTRUCTURE OF KINETOCHORES OF UNPAIRED CHROMOSOMES IN A WHEAT HYBRID

1973 ◽  
Vol 15 (4) ◽  
pp. 801-806 ◽  
Author(s):  
E. B. Wagenaar ◽  
D. F. Bray
Keyword(s):  
Sister Chromatid ◽  
Metaphase Plate ◽  
Polar Regions ◽  
Equatorial Plate ◽  
Univalent Chromosome ◽  
Wheat Hybrid ◽  
Opposite Pole ◽  
Kinetochore Region ◽  
Metaphase I

The kinetochore region of unpaired chromosomes (univalents) consists of two kinetochores, each belonging to a sister chromatid, that are located adjacent to one another on the surface of the univalent chromosome. This condition results in a movement by the univalent towards one of the polar regions at the onset of metaphase I. Once arrived in this region, one of the sister kinetochores obtains attachments of microtubules from the opposite pole. This results in a gradual return of the univalent to the equatorial plate, where it reaches an equilibrium. The sister kinetochores remain adjacent during the movement, but once arrived at the metaphase plate they develop a typical mitotic appearance, in which the sister kinetochores have opposite positions on the chromosomes.

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