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Meiosis I (meiosis + i)
Selected AbstractsMyosin localization during meiosis I of crane-fly spermatocytes gives indications about its role in divisionCYTOSKELETON, Issue 2 2003Rosalind V. Silverman-Gavrila Abstract We showed previously that in crane-fly spermatocytes myosin is required for tubulin flux [Silverman-Gavrila and Forer, 2000a: J Cell Sci 113:597,609], and for normal anaphase chromosome movement and contractile ring contraction [Silverman-Gavrila and Forer, 2001: Cell Motil Cytoskeleton 50:180,197]. Neither the identity nor the distribution of myosin(s) were known. In the present work, we used immunofluorescence and confocal microscopy to study myosin during meiosis-I of crane-fly spermatocytes compared to tubulin, actin, and skeletor, a spindle matrix protein, in order to further understand how myosin might function during cell division. Antibodies to myosin II regulatory light chain and myosin II heavy chain gave similar staining patterns, both dependent on stage: myosin is associated with nuclei, asters, centrosomes, chromosomes, spindle microtubules, midbody microtubules, and contractile rings. Myosin and actin colocalization along kinetochore fibers from prometaphase to anaphase are consistent with suggestions that acto-myosin forces in these stages propel kinetochore fibres poleward and trigger tubulin flux in kinetochore fibres, contributing in this way to poleward chromosome movement. Myosin and actin colocalization at the cell equator in cytokinesis, similar to studies in other cells [e.g., Fujiwara and Pollard, 1978: J Cell Biol 77:182,195], supports a role of actin-myosin interactions in contractile ring function. Myosin and skeletor colocalization in prometaphase spindles is consistent with a role of these proteins in spindle formation. After microtubules or actin were disrupted, myosin remained in spindles and contractile rings, suggesting that the presence of myosin in these structures does not require the continued presence of microtubules or actin. BDM (2,3 butanedione, 2 monoxime) treatment that inhibits chromosome movement and cytokinesis also altered myosin distributions in anaphase spindles and contractile rings, consistent with the physiological effects, suggesting also that myosin needs to be active in order to be properly distributed. Cell Motil. Cytoskeleton 55:97,113, 2003. © 2003 Wiley-Liss, Inc. [source] The A-type cyclins and the meiotic cell cycle in mammalian male germ cellsINTERNATIONAL JOURNAL OF ANDROLOGY, Issue 4 2004Debra J. Wolgemuth Summary There are two mammalian A-type cyclins, cyclin Al and A2. While cyclin A1 is limited to male germ cells, cyclin A2 is widely expressed. Cyclin A2 promotes both Gl/S and G2/M transitions in somatic cells and cyclin A2-deficient mice are early embryonic lethal. We have shown that cyclin Al is essential for passage of spermatocytes into meiosis I (MI) by generating mice null for the cyclin A1 gene Ccna1. Both Ccna1,/, males and females were healthy but the males were sterile because of a cell cycle arrest before MI. This arrest was associated with desynapsis abnormalities, low M-phase promoting factor activity, and apoptosis. We have now determined that human cyclin A1 is expressed in similar stages of spermatogenesis and are exploring its role in human male infertility and whether it may be a novel target for new approaches for male contraception. [source] Transitions in the evolution of meiosisJOURNAL OF EVOLUTIONARY BIOLOGY, Issue 3 2000Hurst Meiosis may have evolved gradually within the eukaryotes with the earliest forms having a one-step meiosis. It has been speculated that the putative transition from a one-step meiosis without recombination to one with recombination may have been stimulated by the invasion of Killer alleles. These imaginary selfish elements are considered to act prior to recombination. They prime for destruction (which occurs after cell division) the half of the cell on the opposite side of the meiotic spindle. Likewise the transition from one-step to two-step meiosis might have been stimulated by a subtly different sort of imaginary distorter allele, a SisterKiller. These are proposed to act after recombination. It has yet to be established that the presence of such distorter alleles could induce the transitions in question. To investigate these issues we have analysed the dynamics of a modifier (1) of recombination and (2) of the number of steps of meiosis, as they enter a population with one-step meiosis. For the modifier of recombination, we find that invasion conditions are very broad and that persistence of Killer and modifier is likely through most parameter space, even when the recombination rate is low. However, if we allow a Killer element to mutate into one that is self-tolerant, the modifier and the nonself-tolerant alleles are typically both lost from the population. The modifier of the number of steps can invade if the SisterKiller acts at meiosis II. However, a SisterKiller acting at meiosis I, far from promoting the modifier's spread, actually impedes it. In the former case the invasion is easiest if there is no recombination. The SisterKiller hypothesis therefore fails to provide a reasonable account of the evolution of two-step meiosis with recombination. As before, the evolution of self-tolerance on the part of the selfish element destroys the process. We conclude that the conditions under which SisterKillers promote the evolution of two-step meiosis are very much more limited than originally considered. We also conclude that there is no universal agreement between ESS and modifier analyses of the same transitions. [source] The cell cycle control protein cdc25C is present, and phosphorylated on serine 214 in the transition from germinal vesicle to metaphase II in human oocyte meiosis,MOLECULAR REPRODUCTION & DEVELOPMENT, Issue 7 2008S. Cunat Abstract Cdc25C is a dual specificity phosphatase essential for dephosphorylation and activation of cyclin-dependent kinase 1 (cdk1), a prerequisite step for mitosis in all eucaryotes. Cdc25C activation requires phosphorylation on at least six sites including serine 214 (S214) which is essential for metaphase/anaphase transit. Here, we have investigated S214 phosphorylation during human meiosis with the objectives of determining if this mitotic phosphatase cdc25C participates in final meiotic divisions in human oocytes. One hundred forty-eight human oocytes from controlled ovarian stimulation protocols were stained for immunofluorescence: 33 germinal vesicle (GV), 37 metaphase stage I (MI), and 78 unfertilized metaphase stage II (MII). Results were stage dependent, identical, independent of infertility type, or stimulation protocol. During GV stages, phospho-cdc25C is localized at the oocyte periphery. During early meiosis I (MI), phosphorylated cdc25C is no longer detected until onset of meiosis I. Here, phospho-cdc25C localizes on interstitial microtubules and at the cell periphery corresponding to the point of polar body expulsion. As the first polar body reaches the periphery, phosphorylated cdc25C is localized at the junction corresponding to the mid body position. On polar body expulsion, the interior signal for phospho-cdc25C is lost, but remains clearly visible in the extruded polar body. In atresic or damaged oocytes, the polar body no longer stains for phospho-cdc25C. Human cdc25C is both present and phosphorylated during meiosis I and localizes in a fashion similar to that seen during human mitotic divisions implying that the involvement of cdc25C is conserved and functional in meiotic cells. Mol. Reprod. Dev. 75: 1176,1184, 2008. © 2007 Wiley-Liss, Inc. [source] Asymmetric division of spindle microtubules and microfilaments during bovine meiosis from metaphase I to metaphase IIIMOLECULAR REPRODUCTION & DEVELOPMENT, Issue 2 2005Guang-Peng Li Abstract The kinetics of spindle and chromosomes during bovine oocyte meiosis from meiosis I to meiosis III is described. The results of this study showed that (1) oocytes began to extrude the first polar body (Pb1) at the early anaphase I stage and the Pb1 totally separated from the mother cell only when oocytes reach the MII stage; (2) the morphology of the spindle changed from barrel-shaped at the metaphase stage to cylinder-shaped at early anaphase, and then to a thin, long triangle-shaped cone at late anaphase and telophase stages; (3) chromosome morphology went from an individual visible stage at metaphase to a less defined chromatin state during anaphase and telophase stages, and then back to visible individual chromosomes at the next metaphase; (4) chromatin that connected with the floor of the cone became the polar bodies and expelled, and almost all of the microtubules (MTs) and microfilaments (MFs) composing the spindles moved towards and contributed to the polar bodies; and (5) the size of the metaphase I (MI) spindle was larger than the metaphase II (MII) and metaphase III (MIII) spindles. The MII spindle, however, is more barrel-shaped than the MI spindle. This study suggests that spindle MTs and MFs during bovine oocyte meiosis are asymmetrically divided into the polar bodies. Mol. Reprod. Dev. 71: 220,226, 2005. © 2005 Wiley-Liss, Inc. [source] Sexual devolution in plants: apomixis uncloaked?BIOESSAYS, Issue 9 2008Richard D. Noyes There are a growing number of examples where naturally occurring mutations disrupt an established physiological or developmental pathway to yield a new condition that is evolutionary favored. Asexual reproduction by seed in plants, or apomixis, occurs in a diversity of taxa and has evolved from sexual ancestors. One form of apomixis, diplospory, is a multi-step development process that is initiated when meiosis is altered to produce an unreduced rather than a reduced egg cell. Subsequent parthenogenetic development of the unreduced egg yields genetically maternal progeny. While it has long been apparent from cytological data that meiosis in apomicts was malfunctional or completely bypassed, the genetic basis of the phenomenon has been a long-standing mystery. New data from genetic analysis of Arabidopsis mutants1 in combination with more sophisticated molecular understanding of meiosis in plants indicate that a weak mutation of the gene SWI, called DYAD, interferes with sister chromatid cohesion in meiosis I, causes synapsis to fail in female meiosis and yields two unreduced cells. The new work shows that a low percentage of DYAD ovules produce functional unreduced egg cells (2n) that can be fertilized by haploid pollen (1n) to give rise to triploid (3n) progeny. While the DYAD mutants differ in some aspects from naturally occurring apomicts, the work establishes that mutation to a single gene can effectively initiate apomictic development and, furthermore, focuses efforts to isolate apomixis genes on a narrowed set of developmental events. Profitable manipulation of meiosis and recombination in agronomically important crops may be on the horizon. BioEssays 30:798,801, 2008. © 2008 Wiley Periodicals, Inc. [source] |