scholarly journals Malorientation in half-bivalents at anaphase: analysis of autosomal laggards in untreated, cold-treated, and cold-recovering crane fly spermatocytes.

1984 ◽  
Vol 98 (3) ◽  
pp. 859-869 ◽  
Author(s):  
M A Janicke ◽  
J R LaFountain

Exposing crane fly larvae to 6 degrees C or returning them to 22 degrees C after exposure to 6, 2, or 0.2 degrees C can induce any number of autosomes in their primary spermatocytes to lag near the spindle equator at anaphase. Autosomal laggards in cold-recovering cells are contained in bivalents until anaphase (Janicke, M. A., and J. R. LaFountain, 1982, Chromosoma, 85:619-631). We report here documentation that lagging autosomes in cold-treated and cold-recovering cells are maloriented. During meiosis I, half-bivalents usually associate with only one pole via kinetochore fibers, with sister chromatids being oriented to the same pole. In contrast, laggards had kinetochore microtubules (kMTs) extending from them toward both poles: one sister was oriented to one pole and the other had some or all of its kMTs extending toward the opposite pole. Bipolar malorientation of autosomal laggards also was observed in one untreated cell. The number of kMTs per half-bivalent was similar in lagging and non-lagging autosomes, and those kMTs were contained in long birefringent kinetochore fibers. The overall spindle structure in cold-recovering cells was similar to that observed in untreated anaphase cells. Giemsa-stained centromeric dots of sister chromatids were contiguous in non-laggards and separated in laggards at anaphase. We conclude that bipolar malorientations can exist at anaphase in chromosomes that remain paired until anaphase, that cold recovery increases the frequency of that anomaly, and that such malorientations may be one cause of anaphase lag.

2000 ◽  
Vol 150 (6) ◽  
pp. 1223-1232 ◽  
Author(s):  
Leocadia V. Paliulis ◽  
R. Bruce Nicklas

In meiosis I, two chromatids move to each spindle pole. Then, in meiosis II, the two are distributed, one to each future gamete. This requires that meiosis I chromosomes attach to the spindle differently than meiosis II chromosomes and that they regulate chromosome cohesion differently. We investigated whether the information that dictates the division type of the chromosome comes from the whole cell, the spindle, or the chromosome itself. Also, we determined when chromosomes can switch from meiosis I behavior to meiosis II behavior. We used a micromanipulation needle to fuse grasshopper spermatocytes in meiosis I to spermatocytes in meiosis II, and to move chromosomes from one spindle to the other. Chromosomes placed on spindles of a different meiotic division always behaved as they would have on their native spindle; e.g., a meiosis I chromosome attached to a meiosis II spindle in its normal fashion and sister chromatids moved together to the same spindle pole. We also showed that meiosis I chromosomes become competent meiosis II chromosomes in anaphase of meiosis I, but not before. The patterns for attachment to the spindle and regulation of cohesion are built into the chromosome itself. These results suggest that regulation of chromosome cohesion may be linked to differences in the arrangement of kinetochores in the two meiotic divisions.


Genetics ◽  
1986 ◽  
Vol 113 (3) ◽  
pp. 517-529
Author(s):  
Jules O'Rear ◽  
Jasper Rine

ABSTRACT In Saccharomyces cerevisiae, a reciprocal translocation between chromosome II and a linear plasmid carrying a centromere (CEN6) has split chromosome II into two fragments: one, approximately 530 kilobase pairs (kbp) in size, has the left arm and part of the right arm of chromosome II; the other, a telocentric fragment approximately 350 kbp in size, has CEN6 and the rest of the right arm of chromosome II. A cross of this yeast strain with a strain containing a complete chromosome II exhibits a high frequency of precocious centromere separation (separation of sister chromatids during meiosis I) of the telocentric fragment. Precocious centromere separation is not due to the position of the centromere per se, since diploids that are homozygous for both fragments of chromosome II segregate the telocentric fragment with normal meiotic behavior. The precocious centromere separation described here differs from previously described examples in that pairing and synapsis of this telocentric chromosome seem to be normal. One model of how centromeres function in meiosis is that replication of the centromere is delayed until the second meiotic division. Data presented in this paper indicate that replication of the centromere is complete before the first meiotic division. The precocious separation of the centromere described here may be due to improper synapsis of sequences flanking the centromere.


2010 ◽  
Vol 188 (3) ◽  
pp. 335-349 ◽  
Author(s):  
Rihui Yan ◽  
Sharon E. Thomas ◽  
Jui-He Tsai ◽  
Yukihiro Yamada ◽  
Bruce D. McKee

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.


2000 ◽  
Vol 10 (19) ◽  
pp. 1182-1190 ◽  
Author(s):  
Rebecca J Kamieniecki ◽  
Robert M.Q Shanks ◽  
Dean S Dawson
Keyword(s):  

Genetics ◽  
1987 ◽  
Vol 115 (3) ◽  
pp. 579-579

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.


1992 ◽  
Vol 101 (3) ◽  
pp. 547-559 ◽  
Author(s):  
M. Hatsumi ◽  
S.A. Endow

The Drosophila microtubule motor protein, nonclaret disjunctional (ncd), is required for proper chromosome distribution in meiosis and mitosis. We have examined the meiotic and mitotic divisions in wild-type Drosophila oocytes and early embryos, and the effects of three ncd mutants (cand, ncd and ncdD) on spindle structure and chromosome movement. The ncd mutants cause abnormalities in spindle structure early in meiosis I, and abnormal chromosome configurations throughout meiosis I and II. Defective divisions continue in early embryos of the motor null mutant, cand, with abnormal early mitotic spindles. The effects of mutants on spindle structure suggest that ncd is required for proper meiotic spindle assembly, and may play a role in forming or maintaining spindle poles in meiosis. The disruption of normal meiotic and mitotic chromosome distribution by ncd mutants can be attributed to its role as a spindle motor, although a role for ncd as a chromosome-associated motor protein is not excluded. The ncd motor protein functions not only in meiosis, but also performs an active role in the early mitotic divisions of the embryo.


2015 ◽  
Vol 211 (2) ◽  
pp. 295-308 ◽  
Author(s):  
Hui-Ju Yang ◽  
Haruhiko Asakawa ◽  
Tokuko Haraguchi ◽  
Yasushi Hiraoka

During meiosis, the kinetochore undergoes substantial reorganization to establish monopolar spindle attachment. In the fission yeast Schizosaccharomyces pombe, the KNL1–Spc7-Mis12-Nuf2 (KMN) complex, which constitutes the outer kinetochore, is disassembled during meiotic prophase and is reassembled before meiosis I. Here, we show that the nucleoporin Nup132 is required for timely assembly of the KMN proteins: In the absence of Nup132, Mis12 and Spc7 are precociously assembled at the centromeres during meiotic prophase. In contrast, Nuf2 shows timely dissociation and reappearance at the meiotic centromeres. We further demonstrate that depletion of Nup132 activates the spindle assembly checkpoint in meiosis I, possibly because of the increased incidence of erroneous spindle attachment at sister chromatids. These results suggest that precocious assembly of the kinetochores leads to the meiosis I defects observed in the nup132-disrupted mutant. Thus, we propose that Nup132 plays an important role in establishing monopolar spindle attachment at meiosis I through outer kinetochore reorganization at meiotic prophase.


1981 ◽  
Vol 59 (9) ◽  
pp. 770-776 ◽  
Author(s):  
Peggy J. Sillers ◽  
Arthur Forer

Single chromosomal spindle fibres in anaphase Nephrotoma ferruginea (crane fly) spermatocytes were irradiated with monochromatic ultraviolet light focussed to a 4-μm spot by means of an ultraviolet microbeam apparatus. The movement of the half-bivalent associated with the irradiated spindle fibre was either unaffected or the half-bivalent stopped moving; i.e., the effect was all-or-none. When the half-bivalent associated with the irradiated spindle fibre did stop moving, the partner half-bivalent moving towards the opposite pole (i.e., the half-bivalent with which the first half-bivalent was previously paired) also stopped moving: all other half-bivalents moved normally. In over 90% of the 69 cases the movements of the two half-bivalents were only temporarily blocked; when movement resumed both half-bivalents resumed movement at the same time, after stoppage times ranging from 2 min to more than 15 min. In a few cases the half-bivalents never resumed poleward motion.When half-bivalents that had stopped movement finally resumed movement they often did not reach the poles; i.e., they "lagged" and remained separate from the other chromosomes. This result occurred only in spermatocytes of N. ferruginea. In spermatocytes of N. suturalis or N. abbreviata, on the other hand, the stopped half-bivalents did not lag but always reached the poles.Half-bivalent pairs that stopped moving in N. ferruginea spermatocytes did so for shorter times than did those previously reported (after irradiation of chromosomal spindle fibres) in N. suturalis spermatocytes. We suggest that the difference is due to our use of monochromatic ultraviolet light as opposed to the previous use of heterochromatic ultraviolet light. We assume that different wavelengths of monochromatic light produce different effects, that any given monochromatic irradiation produces only one effect (albeit different effects at different wavelengths), but that heterochromatic irradiations can produce multiple effects.Irradiation of the interzone (between separating half-bivalents) had no effect on the chromosome-to-pole movements of the half-bivalents. Therefore the stoppage of movement of half-bivalent pairs is specific for irradiation of chromosomal spindle fibres. On the other hand, irradiation of the interzone often blocked pole-to-pole elongation.


Author(s):  
David H. Myszka ◽  
Andrew P. Murray

The fixed pivots of a planar 4R linkage that can achieve four design positions are constrained to a center-point curve. The curve is a circular cubic function and plots can take one of five different forms. The center-point curve can be generated with a compatibility linkage obtained from an opposite pole quadrilateral of the four design positions. This paper presents a method to identify design positions that generate distinctive shapes of the center-point curves. The form of the center-point curve is dependent on whether the shape of the opposite pole quadrilateral is an open or closed form of a rhombus, kite, parallelogram, or when the sum of two sides equals the other two. Interesting cases of three and five position synthesis are also explored. Four and five position cases are generated that have center points at infinity allowing a PR dyad with line of slide in any direction to achieve the design positions. Further, a center-point curve for five specific design positions is revealed.


2011 ◽  
Vol 22 (16) ◽  
pp. 2848-2861 ◽  
Author(s):  
Dai Tsuchiya ◽  
Claire Gonzalez ◽  
Soni Lacefield

In many eukaryotes, disruption of the spindle checkpoint protein Mad2 results in an increase in meiosis I nondisjunction, suggesting that Mad2 has a conserved role in ensuring faithful chromosome segregation in meiosis. To characterize the meiotic function of Mad2, we analyzed individual budding yeast cells undergoing meiosis. We find that Mad2 sets the duration of meiosis I by regulating the activity of APCCdc20. In the absence of Mad2, most cells undergo both meiotic divisions, but securin, a substrate of the APC/C, is degraded prematurely, and prometaphase I/metaphase I is accelerated. Some mad2Δ cells have a misregulation of meiotic cell cycle events and undergo a single aberrant division in which sister chromatids separate. In these cells, both APCCdc20 and APCAma1 are prematurely active, and meiosis I and meiosis II events occur in a single meiotic division. We show that Mad2 indirectly regulates APCAma1 activity by decreasing APCCdc20 activity. We propose that Mad2 is an important meiotic cell cycle regulator that ensures the timely degradation of APC/C substrates and the proper orchestration of the meiotic divisions.


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