Talk:Cell Division - Meiosis: Difference between revisions
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===Meiosis=== | ===Meiosis=== | ||
<pubmed limit=10>Meiosis</pubmed> | <pubmed limit=10>Meiosis</pubmed> | ||
==2013== | |||
===Live births from isolated primary/early secondary follicles following a multi-step culture without organ culture in mice=== | |||
Reproduction. 2013 Apr 23. [Epub ahead of print] | |||
Mochida N, Hasegawa A, Saka K, Ogino M, Hosoda Y, Wada R, Sawai H, Shibahara H. | |||
Source | |||
N Mochida, Department of Obstetrics and Gynecology, Hyogo College of Medicine, Nishinomiya, Japan. | |||
Abstract | |||
Although the ovary has a large store of germ cells, most of them do not reach mature stages. If a culture system could be developed from early growing follicles to mature oocytes, it would be useful for biological research as well as for reproductive medicine. This study was conducted to establish a multi-step culture system from isolated early growing follicles to mature oocytes using a mouse model. Early growing follicles with diameters of 60-95 μm corresponding to primary and early secondary follicles were isolated from 6-day-old mice and classified into three groups by diameter. These follicles contained oocytes with diameters of ~45 μm and one or a few layered granulosa cells on the basal lamina. Embedding in collagen gel was followed by first step culture. After 9-day culture, the growing follicles were transferred to the second step on collagen coated membrane. At day 17 of the culture series, the oocyte-granulosa cell complexes were subjected to in vitro maturation. Around 90 % of the oocytes in follicles surviving at day 17 resumed second meiosis (metaphase II oocytes : 49.0-58.7 %) regardless of the size when the follicle culture started. To assess developmental competence to live birth, the eggs were used for in vitro fertilization and implantation to pseudopregnant mice. We successfully obtained two live offspring that produced next generations after puberty. We thus conclude that the culture system reported here was able to induce growth of small follicles and the resultant mature oocytes were able to develop into normal mice. | |||
PMID 23613617 | |||
==2012== | ==2012== | ||
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Cite this page: Hill, M.A. (2024, April 19) Embryology Cell Division - Meiosis. Retrieved from https://embryology.med.unsw.edu.au/embryology/index.php/Talk:Cell_Division_-_Meiosis |
10 Most Recent Papers
Note - This sub-heading shows an automated computer PubMed search using the listed sub-heading term. References appear in this list based upon the date of the actual page viewing. Therefore the list of references do not reflect any editorial selection of material based on content or relevance. In comparison, references listed on the content page and discussion page (under the publication year sub-headings) do include editorial selection based upon relevance and availability. (More? Pubmed Most Recent)
Meiosis
<pubmed limit=10>Meiosis</pubmed>
2013
Live births from isolated primary/early secondary follicles following a multi-step culture without organ culture in mice
Reproduction. 2013 Apr 23. [Epub ahead of print]
Mochida N, Hasegawa A, Saka K, Ogino M, Hosoda Y, Wada R, Sawai H, Shibahara H. Source N Mochida, Department of Obstetrics and Gynecology, Hyogo College of Medicine, Nishinomiya, Japan.
Abstract
Although the ovary has a large store of germ cells, most of them do not reach mature stages. If a culture system could be developed from early growing follicles to mature oocytes, it would be useful for biological research as well as for reproductive medicine. This study was conducted to establish a multi-step culture system from isolated early growing follicles to mature oocytes using a mouse model. Early growing follicles with diameters of 60-95 μm corresponding to primary and early secondary follicles were isolated from 6-day-old mice and classified into three groups by diameter. These follicles contained oocytes with diameters of ~45 μm and one or a few layered granulosa cells on the basal lamina. Embedding in collagen gel was followed by first step culture. After 9-day culture, the growing follicles were transferred to the second step on collagen coated membrane. At day 17 of the culture series, the oocyte-granulosa cell complexes were subjected to in vitro maturation. Around 90 % of the oocytes in follicles surviving at day 17 resumed second meiosis (metaphase II oocytes : 49.0-58.7 %) regardless of the size when the follicle culture started. To assess developmental competence to live birth, the eggs were used for in vitro fertilization and implantation to pseudopregnant mice. We successfully obtained two live offspring that produced next generations after puberty. We thus conclude that the culture system reported here was able to induce growth of small follicles and the resultant mature oocytes were able to develop into normal mice.
PMID 23613617
2012
Three-dimensional quantitative analysis of chromosomes in the oocytes of aging mice during meiosis I in vitro
Theriogenology. 2012 Nov 19. pii: S0093-691X(12)00467-0. doi: 10.1016/j.theriogenology.2012.08.010. [Epub ahead of print]
Tian N, Zhang L, Zheng JH, Lv DY, Li Y, Ma WY. Source Department of Physics, State Key Laboratory of Low-Dimensional Quantum Physics, Tsinghua University, Beijing, China.
Abstract
The mechanism of senescence is very complicated and can involve formation of chromosome abnormalities and a decline in female fertility. In this study, 3-D visualization of fluorescently labeled chromosomes in oocytes from aging and pubertal mice during in vitro maturation was done with a two-photon laser scanning microscope. Differences between aging and pubertal groups at various maturation stages were analyzed quantitatively in terms of chromosomal morphology, shape, and spatial arrangement. Compared with the pubertal group, the chromosomal morphology of oocytes from aging mice changed: both the mean volume and the mean surface area of chromosomes increased by approximately 20% (P < 0.05) at prometaphase and metaphase of meiosis I (considered to be the weakly condensed folded form of the chromosomes). Furthermore, at these stages, the shape of the chromosomal array became rounder (roundness factor increased by approximately 10%; P < 0.001) and the adhesion among chromosomes became more severe (P < 0.001) at approximately the same stages. Additionally, trends over time for both chromosomal morphology and shape were quite distinct between oocytes from aging and pubertal mice. Interestingly, trends for mean distance were similar; therefore, aging did not seem to influence chromosome movement toward the metaphase plate. These morphologic results should be useful to study age-related degradation of oocyte quality and to interpret results derived from molecular biology. Copyright © 2012 Elsevier Inc. All rights reserved.
PMID 23174780
2010
A review of trisomy X (47,XXX)
Tartaglia NR, Howell S, Sutherland A, Wilson R, Wilson L. Orphanet J Rare Dis. 2010 May 11;5:8. Review. PMID: 20459843 [ Trisomy X - http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2883963/?tool=pubmed
2009
A spindle assembly checkpoint protein functions in prophase I arrest and prometaphase progression
Science. 2009 Nov 13;326(5955):991-4.
Homer H, Gui L, Carroll J.
Oocyte and Embryo Research Laboratory, Department of Cell and Developmental Biology, Division of Biosciences and Institute for Women's Health, University College London, London, UK. h.homer@ucl.ac.uk Abstract Two critical stages of mammalian oocyte regulation are prophase I arrest, which is important for sustaining the oocyte pool, and the progression through meiosis I (MI) to produce fertilizable eggs. We have found that the spindle assembly checkpoint protein BubR1 regulates both stages in mouse oocytes. We show that oocytes depleted of BubR1 cannot sustain prophase I arrest and readily undergo germinal vesicle breakdown, a marker for reentry into MI. BubR1-depleted oocytes then arrest before completing MI, marked by failure of polar body extrusion. Both meiotic defects in BubR1-depleted oocytes are due to reduced activity of the master regulator known as the anaphase-promoting complex (APC), brought about through diminished levels of the APC coactivator Cdh1.
PMID: 19965510
Sperm chromatin-induced ectopic polar body extrusion in mouse eggs after ICSI and delayed egg activation
PLoS One. 2009 Sep 29;4(9):e7171.
Deng M, Li R.
Stowers Institute for Medical Research, Kansas City, Missouri, United States of America. Mdeng3@BICS.BWH.Harvard.edu Abstract Meiotic chromosomes in an oocyte are not only a maternal genome carrier but also provide a positional signal to induce cortical polarization and define asymmetric meiotic division of the oocyte, resulting in polar body extrusion and haploidization of the maternal genome. The meiotic chromosomes play dual function in determination of meiosis: 1) organizing a bipolar spindle formation and 2) inducing cortical polarization and assembly of a distinct cortical cytoskeleton structure in the overlying cortex for polar body extrusion. At fertilization, a sperm brings exogenous paternal chromatin into the egg, which induces ectopic cortical polarization at the sperm entry site and leads to a cone formation, known as fertilization cone. Here we show that the sperm chromatin-induced fertilization cone formation is an abortive polar body extrusion due to lack of spindle induction by the sperm chromatin during fertilization. If experimentally manipulating the fertilization process to allow sperm chromatin to induce both cortical polarization and spindle formation, the fertilization cone can be converted into polar body extrusion. This suggests that sperm chromatin is also able to induce polar body extrusion, like its maternal counterpart. The usually observed cone formation instead of ectopic polar body extrusion induced by sperm chromatin during fertilization is due to special sperm chromatin compaction which restrains it from rapid spindle induction and therefore provides a protective mechanism to prevent a possible paternal genome loss during ectopic polar body extrusion.
PMID: 19787051 http://www.ncbi.nlm.nih.gov/pubmed/19787051
http://www.plosone.org/article/info%3Adoi%2F10.1371%2Fjournal.pone.0007171
2008
Meiotic regulation of TPX2 protein levels governs cell cycle progression in mouse oocytes
PLoS One. 2008 Oct 3;3(10):e3338.
Brunet S, Dumont J, Lee KW, Kinoshita K, Hikal P, Gruss OJ, Maro B, Verlhac MH.
UMR7622, Université Pierre et Marie Curie/CNRS, Bat. C, 5e, 9 quai Saint Bernard, Paris, France. Abstract Formation of female gametes requires acentriolar spindle assembly during meiosis. Mitotic spindles organize from centrosomes and via local activation of the RanGTPase on chromosomes. Vertebrate oocytes present a RanGTP gradient centred on chromatin at all stages of meiotic maturation. However, this gradient is dispensable for assembly of the first meiotic spindle. To understand this meiosis I peculiarity, we studied TPX2, a Ran target, in mouse oocytes. Strikingly, TPX2 activity is controlled at the protein level through its accumulation from meiosis I to II. By RNAi depletion and live imaging, we show that TPX2 is required for spindle assembly via two distinct functions. It controls microtubule assembly and spindle pole integrity via the phosphorylation of TACC3, a regulator of MTOCs activity. We show that meiotic spindle formation in vivo depends on the regulation of at least a target of Ran, TPX2, rather than on the regulation of the RanGTP gradient itself.
PMID: 18833336
http://www.ncbi.nlm.nih.gov/pubmed/18833336
2007
Impact of trisomy on fertility and meiosis in male mice
Hum Reprod. 2007 Feb;22(2):468-76. Epub 2006 Oct 17. Davisson M, Akeson E, Schmidt C, Harris B, Farley J, Handel MA.
The Jackson Laboratory, Bar Harbor, ME 04609, USA. muriel.davisson@jax.org Abstract BACKGROUND: Chromosomal abnormalities frequently are associated with impairment or arrest of spermatogenesis in mammals but are compatible with fertility in female carriers of the same anomaly. In the case of trisomy, mice have extra genomic DNA as well as the chromosomal abnormality, usually present as an extra, unpaired chromosome. Thus, impairment of spermatogenesis in trisomic males could be due to the presence of extra genomic material (i.e. triplicated genes) or due to the chromosomal abnormality and presence of an unpaired chromosome in meiosis.
METHODS: In this study, fertility and chromosomal pairing configurations during meiotic prophase were analysed in male mice trisomic for different segments of the genome. Four have an extra segmental or tertiary trisomic chromosome--Ts(17(16))65Dn, Ts(10(16))232Dn, Ts(12(17))4Rk and Ts(4(17))2Lws--and one has the triplicated segment attached to another chromosome--Ts(16C-tel)1Cje. Ts(17(16))65Dn and Ts(16C-tel)1Cje have similar gene content triplication and differ primarily in whether the extra DNA is in an extra chromosome or not.
RESULTS: The presence of an intact extra chromosome, rather than trisomy per se, is associated with male sterility. Additionally, sterility is correlated with a high frequency of association of the unpaired chromosome with the XY body, which contains the largely unpaired X and Y chromosomes.
CONCLUSIONS: Intact extra chromosomes disrupt spermatogenesis, and unpaired chromosomes establish a unique chromatin territory within meiotic nuclei.
PMID: 17050550
2006
Mouse Emi2 is required to enter meiosis II by reestablishing cyclin B1 during interkinesis
J Cell Biol. 2006 Sep 11;174(6):791-801.
Madgwick S, Hansen DV, Levasseur M, Jackson PK, Jones KT.
Institute for Cell and Molecular Biosciences, The Medical School, University of Newcastle, Newcastle NE2 4HH, England, UK. suzanne.madgwick@ncl.ac.uk Abstract During interkinesis, a metaphase II (MetII) spindle is built immediately after the completion of meiosis I. Oocytes then remain MetII arrested until fertilization. In mouse, we find that early mitotic inhibitor 2 (Emi2), which is an anaphase-promoting complex inhibitor, is involved in both the establishment and the maintenance of MetII arrest. In MetII oocytes, Emi2 needs to be degraded for oocytes to exit meiosis, and such degradation, as visualized by fluorescent protein tagging, occurred tens of minutes ahead of cyclin B1. Emi2 antisense morpholino knockdown during oocyte maturation did not affect polar body (PB) extrusion. However, in interkinesis the central spindle microtubules from meiosis I persisted for a short time, and a MetII spindle failed to assemble. The chromatin in the oocyte quickly decondensed and a nucleus formed. All of these effects were caused by the essential role of Emi2 in stabilizing cyclin B1 after the first PB extrusion because in Emi2 knockdown oocytes a MetII spindle was recovered by Emi2 rescue or by expression of nondegradable cyclin B1 after meiosis I.
PMID: 16966421 http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2064334/?tool=pubmed
2005
How eggs arrest at metaphase II: MPF stabilisation plus APC/C inhibition equals Cytostatic Factor http://www.celldiv.com/content/2/1/4
Mammalian egg activation: from Ca2+ spiking to cell cycle progression. http://www.ncbi.nlm.nih.gov/pubmed/16322541
Mammalian eggs arrest at metaphase of the second meiotic division (MetII). Sperm break this arrest by inducing a series of Ca(2+) spikes that last for several hours. During this time cell cycle resumption is induced, sister chromatids undergo anaphase and the second polar body is extruded. This is followed by decondensation of the chromatin and the formation of pronuclei. Ca(2+) spiking is both the necessary and solely sufficient sperm signal to induce full egg activation. How MetII arrest is established, how the Ca(2+) spiking is induced and how the signal is transduced into cell cycle resumption are the topics of this review. Although the roles of most components of the signal transduction pathway remain to be fully investigated, here I present a model in which a sperm-specific phospholipase C (PLCzeta) generates Ca(2+) spikes to activate calmodulin-dependent protein kinase II and so switch on the Anaphase-Promoting Complex/Cyclosome (APC/C). APC/C activation leads to securin and cyclin B1 degradation and in so doing allows sister chromatids to be segregated and to decondense.
Spindle dynamics during meiosis in Drosophila oocytes
J Cell Biol. 1997 Jun 16;137(6):1321-36. Endow SA, Komma DJ.
Department of Microbiology, Duke University Medical Center, Durham, North Carolina 27710, USA. endow@galactose.mc.duke.edu Abstract Mature oocytes of Drosophila are arrested in metaphase of meiosis I. Upon activation by ovulation or fertilization, oocytes undergo a series of rapid changes that have not been directly visualized previously. We report here the use of the Nonclaret disjunctional (Ncd) microtubule motor protein fused to the green fluorescent protein (GFP) to monitor changes in the meiotic spindle of live oocytes after activation in vitro. Meiotic spindles of metaphase-arrested oocytes are relatively stable, however, meiotic spindles of in vitro-activated oocytes are highly dynamic: the spindles elongate, rotate around their long axis, and undergo an acute pivoting movement to reorient perpendicular to the oocyte surface. Many oocytes spontaneously complete the meiotic divisions, permitting visualization of progression from meiosis I to II. The movements of the spindle after oocyte activation provide new information about the dynamic changes in the spindle that occur upon re-entry into meiosis and completion of the meiotic divisions. Spindles in live oocytes mutant for a loss-of-function ncd allele fused to gfp were also imaged. The genesis of spindle defects in the live mutant oocytes provides new insights into the mechanism of Ncd function in the spindle during the meiotic divisions.
PMID: 9182665
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2132525/?tool=pubmed
