Gap Phases Research Articles

Merging in the common envelope and the origin of early R-type stars

Context. Binary systems experiencing one or two common envelope episodes during the red giant branch or the Hertzsprung gap phases can produce a single star, evolving along the Hayashi track, as a final outcome. Even if these objects are expected to be very common in nature, a proper description of their evolution and physical properties is still missing. Moreover, this scenario (red giant merging scenario) has been invoked as the progenitor systems of early-R stars, by assuming that the physical conditions developed as a consequence of the cores merging could produce the mixing into the convective envelope of fresh carbon that was synthesized during the He-flash. Aims. We analyze in detail the red giant merging scenario to verify if the resulting star develops the physical conditions suitable for a dredge-up of C-enriched material from the core to the envelope. Methods. We performed 3D simulations of the merging stars, to check whether He is burnt efficiently during the formation of a self-sustained disk. We therefore did 1D computations of the accretion phase occurring after the merging and of the following evolution up to the settling of quiescent He-burning in the center. We adopted different assumptions on the amount of angular momentum transferred from the disk to the core and on the angular momentum transport. Results. Efficient He-burning does not occur during the merging, because a very high temperature (T > 10 8 K) at the disk/He-core interface develops only for a few minutes. Our computations show that the accretion process is the leading parameter in determining the final properties of the merged object. In particular, the thermal energy delivered by the accreted matter determines the heating of the whole newborn core, thus preventing the developing of highly degenerate physical conditions. This occurrence determines the onset of the He-burning with an He-flash milder and closer to the center, as compared to standard RGB stars. Rotation and different angular momentum transport efficiency plays a secondary role by determining the exact location of the first He-flash. In none of the computed models is material formed in the He-core mixed into the convective envelope, because the H-burning shell, which always active during the He-flashes and later on, acts as a barrier. Conclusions. In the red giant merging scenario, the physical conditions suitable for both a peculiar He-flash and the dredging-up of C-enriched material never occur. Our results speak against the possibility that such an evolutionary scenario could represent the progenitor system of early R-stars.

The progression of the intra-erythrocytic cell cycle of Plasmodium falciparum and the role of the centriolar plaques in asynchronous mitotic division during schizogony

The cell division cycle and mitosis of intra-erythrocytic (IE) Plasmodium falciparum are poorly understood aspects of parasite development which affect malaria molecular pathogenesis. Specifically, the timing of the multiple gap (G), DNA synthesis (S) and chromosome separation (M) phases of parasite mitosis are not well defined, nor whether genome divisions are immediately followed by cleavage of the nuclear envelope. Curiously, daughter merozoite numbers do not follow the geometric expansion expected from equal numbers of binary divisions, an outcome difficult to explain using the standard model of cell cycle regulation. Using controlled synchronisation techniques, confocal microscopy to visualise key organelles and fluorescence in situ hybridization (FISH) to follow the movements and replication of genes and telomeres, we have re-analysed the timing and progression of mitotic events. The asynchronous duplications of the P. falciparum centrosome equivalents, the centriolar plaques, are established and these are correlated with chromosome and nuclear divisions in a new model of P. falciparum schizogony. Our results improve the resolution of the cell cycle and its phases during P. falciparum IE development, showing that asynchronous, independent nuclear division occurs during schizogony, with the centriolar plaques playing a major role in regulating mitotic progression.

The Effect of a DNA Damaging Agent on Embryonic Cell Cycles of the Cnidarian Hydractinia echinata

The onset of gastrulation at the Mid-Blastula Transition can accompany profound changes in embryonic cell cycles including the introduction of gap phases and the transition from maternal to zygotic control. Studies in Xenopus and Drosophila embryos have also found that cell cycles respond to DNA damage differently before and after MBT (or its equivalent, MZT, in Drosophila). DNA checkpoints are absent in Xenopus cleavage cycles but are acquired during MBT. Drosophila cleavage nuclei enter an abortive mitosis in the presence of DNA damage whereas post-MZT cells delay the entry into mitosis. Despite attributes that render them workhorses of embryonic cell cycle studies, Xenopus and Drosophila are hardly representative of diverse animal forms that exist. To investigate developmental changes in DNA damage responses in a distant phylum, I studied the effect of an alkylating agent, Methyl Methanesulfonate (MMS), on embryos of Hydractinia echinata. Hydractinia embryos are found to differ from Xenopus embryos in the ability to respond to a DNA damaging agent in early cleavage but are similar to Xenopus and Drosophila embryos in acquiring stronger DNA damage responses and greater resistance to killing by MMS after the onset of gastrulation. This represents the first study of DNA damage responses in the phylum Cnidaria.

Control of cell cycle progression by phosphorylation of cyclin-dependent kinase (CDK) substrates

The eukaryotic cell cycle is a fundamental evolutionarily conserved process that regulates cell division from simple unicellular organisms, such as yeast, through to higher multicellular organisms, such as humans. The cell cycle comprises several phases, including the S-phase (DNA synthesis phase) and M-phase (mitotic phase). During S-phase, the genetic material is replicated, and is then segregated into two identical daughter cells following mitotic M-phase and cytokinesis. The S- and M-phases are separated by two gap phases (G1 and G2) that govern the readiness of cells to enter S- or M-phase. Genetic and biochemical studies demonstrate that cell division in eukaryotes is mediated by CDKs (cyclin-dependent kinases). Active CDKs comprise a protein kinase subunit whose catalytic activity is dependent on association with a regulatory cyclin subunit. Cell-cycle-stage-dependent accumulation and proteolytic degradation of different cyclin subunits regulates their association with CDKs to control different stages of cell division. CDKs promote cell cycle progression by phosphorylating critical downstream substrates to alter their activity. Here, we will review some of the well-characterized CDK substrates to provide mechanistic insights into how these kinases control different stages of cell division.

Fermionic representation of a symmetrically frustrated SU(3) model: Application to the Haldane-gap antiferromagnets

The one-dimensional spin 1 bilinear–biquadratic model is re-expressed in a symmetrically frustrated SU(3) model, which facilitates us to introduce a fermionic representation and related bond-operator mean-field theory. By analyzing the gap and the static spin susceptibility, we shows that this treatment can easily capture the commensurate and incommensurate Haldane gap phases.

G2 acquisition by transcription-independent mechanism at the zebrafish midblastula transition

Following fertilization of many animal embryos, rapid synchronous cleavage divisions give way to longer, asynchronous cell cycles at the midblastula transition (MBT). The cell cycle changes at the MBT, including the addition of gap phases and checkpoint controls, are accompanied by activation of the zygotic genome and the onset of cell motility. Whereas the biochemical changes accompanying the MBT in the vertebrate embryo have been extensively documented, the cellular events are not well understood. We show that cell cycle remodeling during the zebrafish MBT includes the transcription-independent acquisition of a G2 phase that is essential for preventing entry into mitosis before S-phase completion in cycles 11–13. We provide evidence from high-resolution imaging that inhibition of Cdc25a and Cdk1 activity, but not Cdk2 activity, is essential for cell cycle lengthening and asynchrony between cycles 9 and 12. We demonstrate that lengthening is not required for initiation of zygotic transcription. Our results are consistent with findings from Drosophila and Xenopus that indicate the central importance of G2 addition in checkpoint establishment, and point to similar mechanisms governing the MBT in diverse species.

Wee1 kinase alters cyclin E/Cdk2 and promotes apoptosis during the early embryonic development of Xenopus laevis

BackgroundThe cell cycles of the Xenopus laevis embryo undergo extensive remodeling beginning at the midblastula transition (MBT) of early development. Cell divisions 2–12 consist of rapid cleavages without gap phases or cell cycle checkpoints. Some remodeling events depend upon a critical nucleo-cytoplasmic ratio, whereas others rely on a maternal timer controlled by cyclin E/Cdk2 activity. One key event that occurs at the MBT is the degradation of maternal Wee1, a negative regulator of cyclin-dependent kinase (Cdk) activity.ResultsIn order to assess the effect of Wee1 on embryonic cell cycle remodeling, Wee1 mRNA was injected into one-cell stage embryos. Overexpression of Wee1 caused cell cycle delay and tyrosine phosphorylation of Cdks prior to the MBT. Furthermore, overexpression of Wee1 disrupted key developmental events that normally occur at the MBT such as the degradation of Cdc25A, cyclin E, and Wee1. Overexpression of Wee1 also resulted in post-MBT apoptosis, tyrosine phosphorylation of Cdks and persistence of cyclin E/Cdk2 activity. To determine whether Cdk2 was required specifically for the survival of the embryo, the cyclin E/Cdk2 inhibitor, Δ34-Xic1, was injected in embryos and also shown to induce apoptosis.ConclusionTaken together, these data suggest that Wee1 triggers apoptosis through the disruption of the cyclin E/Cdk2 timer. In contrast to Wee1 and Δ34-Xic1, altering Cdks by expression of Chk1 and Chk2 kinases blocks rather than promotes apoptosis and causes premature degradation of Cdc25A. Collectively, these data implicate Cdc25A as a key player in the developmentally regulated program of apoptosis in X. laevis embryos.

Undamaged DNA Transmits and Enhances DNA Damage Checkpoint Signals in Early Embryos

In Xenopus laevis embryos, the midblastula transition (MBT) at the 12th cell division marks initiation of critical developmental events, including zygotic transcription and the abrupt inclusion of gap phases into the cell cycle. Interestingly, although an ionizing radiation-induced checkpoint response is absent in pre-MBT embryos, introduction of a threshold amount of undamaged plasmid or sperm DNA allows a DNA damage checkpoint response to be activated. We show here that undamaged threshold DNA directly participates in checkpoint signaling, as judged by several dynamic changes, including H2AX phosphorylation, ATM phosphorylation and loading onto chromatin, and Chk1/Chk2 phosphorylation and release from nuclear DNA. These responses on physically separate threshold DNA require gamma-H2AX and are triggered by an ATM-dependent soluble signal initiated by damaged DNA. The signal persists in egg extracts even after damaged DNA is removed from the system, indicating that the absence of damaged DNA is not sufficient to end the checkpoint response. The results identify a novel mechanism by which undamaged DNA enhances checkpoint signaling and provide an example of how the transition to cell cycle checkpoint activation during development is accomplished by maternally programmed increases in the DNA-to-cytoplasm ratio.

Red and near infrared polarized light emissions from polyfluorene copolymer based light emitting diodes

The authors report polarized red, electroluminescence peak at 705nm and near infrared, electroluminescence peak at 950nm, light emission from light emitting diodes based on two polyfluorene copolymers. The copolymers are synthesized from a fluorene monomer combined with donor-acceptor-donor comonomers and designed to have a low band gap and form birefringent liquid crystalline phases. Emission occurs from aligned thin films of polymer layers. The emissive layers are aligned by spin coating on a layer of rubbed conducting polymer poly(3,4-ethylene dioxythiophene)-poly(styrene sulphonate) and thermally converted into glassy nematic liquid crystalline state.

RECOVERY OF A LOWLAND DIPTEROCARP FOREST TWENTY TWO YEARS AFTER SELECTIVE LOGGING AT SEKUNDUR, GUNUNG LEUSER NATIONAL PARK, NORTH SUMATRA, INDONESIA

PRIATNA, D.; KARTAWINATA, K.; ABDULHADI, R. 2004. Recovery of a lowland dipterocarp forest twenty two years after selective logging at Sekundur, Gunung Leuser National Park, North Sumatra, Indonesia. Reinwardtia 12 (3): 237–255. — A permanent 2-ha plot of lowland forest selectively logged in 1978 at Sekundur, Gunung Leuser National Park,which is also a Biosphere Reserve and a World Heritage Site, North Sumatra,was established and investigated in 1982. It was re-examined in 2000, where remeasurement and reidentification of all trees with DBH =10 cm were made.The areas of gap, building and mature phases of the canopy were also measured and mapped. Within this plot, 133 species, 87 genera and 39 families were recorded, with the total number of trees of 1145 or density of 572.5/ha. Euphorbiaceae was the richest family with 18 species (13.5 % of the total) and total number of trees of 248 (21.7 % of the total or density of 124 trees/ha.The most important families were Dipterocarpaceae with IV (Importance Value) = 52.0, followed by Euphorbiaceae with IV = 51.8. The most prevalent species was Shorea kunstleri (Dipterocarpaceae) with IV =24.4, followed by Macaranga diepenhorstii (Euphorbiaceae) with IV = 12.4. They were the species with highest density, 34 trees/ha and 23.5 trees/ha, respectively. During the period of 18 years there has been no shift in the richest families, most importantfamilies and most important species. Euphorbiaceae was the richest family and Dipterocarpaceae was the most important family, with Shorea kunstleri as the most important species with highest importance value throughout the period. The number of species increased from 127 to 133 with increase in density by 36.8% , from 418.5 trees/ha to 572.5 trees/ha. The mortality was 25.57 % or 1.4 % per year. The diameter class distribution indicated that the forest recovery has not been complete. Trees were small, comprising 67.6 % with diameters of 10-20 cm and only two trees had diameters of 100 cm, i.e.Melanochyla caesia and Lithocarpus urceolaris. Based on the basal area of all species, the logged-over forest at Sekundur is estimated to reach the situation similar to undisturbed primary forest in 56 years after logging, but on the basis of basal area of Dipterocarpaceae such condition could be achieved in 172 years.The canopy has not fully recovered and the complete closure of gaps is estimated to take 53 years since the logging started. The canopy consisted of gap phase (24.6 %), building phase (19.7 %) and mature phase (55.7 %). During the period of 18 years the tree mortality was 25.57 % or the rate of 1.4 %/year.Euphorbiaceae experienced the highest mortality, particularly among the trees with diameters of 10-20 cm.Mortality decreased with the increase of diameters.During the same period 520 new trees of 16 species were recruited.The densities of 53 % of the species experienced changes of only one tree or no changes at all.Drastic increase in tree population occurred in light demanding species,such as Baccaurea kunstleri, Endospermum diadenum,Mallotus penangensis,Sapium baccatum and Macaranga diepenhorstii .

Cell cycle-dependent calcium oscillations in mouse embryonic stem cells

During cell cycle progression, somatic cells exhibit different patterns of intracellular Ca(2+) signals during the G(0) phase, the transition from G(1) to S, and from G(2) to M. Because pluripotent embryonic stem (ES) cells progress through cell cycle without the gap phases G(1) and G(2), we aimed to determine whether mouse ES (mES) cells still exhibit characteristic changes of intracellular Ca(2+) concentration during cell cycle progression. With confocal imaging of the Ca(2+)-sensitive dye fluo-4 AM, we identified that undifferentiated mES cells exhibit spontaneous Ca(2+) oscillations. In control cultures where 50.4% of the cells reside in the S phase of the cell cycle, oscillations appeared in 36% of the cells within a colony. Oscillations were not initiated by Ca(2+) influx but depended on inositol 1,4,5-trisphosphate (IP(3))-mediated Ca(2+) release and the refilling of intracellular stores by a store-operated Ca(2+) influx (SOC) mechanism. Using cell cycle synchronization, we determined that Ca(2+) oscillations were confined to the G(1)/S phase ( approximately 70% oscillating cells vs. G(2)/M with approximately 15% oscillating cells) of the cell cycle. ATP induced Ca(2+) oscillations, and activation of SOC could be induced in G(1)/S and G(2)/M synchronized cells. Intracellular Ca(2+) stores were not depleted, and all three IP(3) receptor isoforms were present throughout the cell cycle. Cell cycle analysis after EGTA, BAPTA-AM, 2-aminoethoxydiphenyl borate, thapsigargin, or U-73122 treatment emphasized that IP(3)-mediated Ca(2+) release is necessary for cell cycle progression through G(1)/S. Because the IP(3) receptor sensitizer thimerosal induced Ca(2+) oscillations only in G(1)/S, we propose that changes in IP(3) receptor sensitivity or basal levels of IP(3) could be the basis for the G(1)/S-confined Ca(2+) oscillations.

Cell Cycle and Developmental Regulations of Replication Factors in Mouse Embryonic Stem Cells

Embryonic stem (ES) cells can grow rapidly and permanently while maintaining their differentiation capacity. To gain insight into how the cell cycle progression of undifferentiated murine ES cells is regulated, we have examined the expression patterns of various replication and cell cycle regulators. Most factors including cyclins, Cdc6, and geminin are rather constitutively expressed during the cell cycle of ES cells. Furthermore, the transcript levels of almost all the cell cycle regulators we investigated except for p21 and p27 are higher in undifferentiated ES cells than in murine embryonic fibroblasts (MEFs), and the increased stability of mRNA in ES cells may be partially responsible for this at least with some of the factors. More strikingly, the transcriptional levels of these factors are strongly correlated with the acetylated state of histone H3 at their promoter regions. However, the methylation state of histone or CpG methylation of the promoter region is not generally correlated significantly with the expression pattern of these factors in both cell types. On the protein level, Cdc6, ASK, cyclin A2, and cyclin B1 are extremely abundant in ES cells compared with MEFs. Furthermore, they are rapidly down-regulated upon induction of differentiation of ES cells. The significance of these findings is discussed in relation to the unusual proliferative properties of ES cells in an undifferentiated state.

Spatial relationships between tree species and gap characteristics in broad‐leaved deciduous woodland

AbstractQuestions:1. What are the spatial patterns of all trees, individual tree species, trees within particular height classes, all gaps and gaps with specific properties across the study site in broad‐leaved deciduous forest at a range of scales? 2. Are patterns of the above features spatially associated? 3. Are these patterns indicative of gap creation mechanisms and phases of regeneration?Location:Frame Wood, New Forest, UK.Methods:Ripley's K‐function analysis was applied to spatial information derived from airborne remotely sensed imagery to characterize the patterns of trees and gaps and to test for spatial interactions between these patterns. The patterns of trees and gaps with specific physical and spatial properties were analysed.Results:The pattern of all tree species combined was random for most scales; Quercus robur followed the same random pattern, while Fagus sylvatica and Betula pendula were clustered over most spatial scales. Large gaps (> 250 m2) and larger trees (> 17.5 m) were randomly distributed, while smaller gaps and smaller trees were clustered. Significant spatial relationships were demonstrated between the patterns of different tree species and between trees within different size classes, as well as between the patterns of trees and gaps with specific properties.Conclusions:Small gap patterns and field evidence indicated that progressive gap enlargement is the most likely creation mechanism for large gaps (> 250 m2). Clustered patterns of younger individuals were indicative of patches of past regeneration. As a complement to field‐based data, data derived from remotely sensed imagery provides spatially comprehensive information with which to further investigate woodland stand/community processes and gap dynamics.

Spatial relationships between tree species and gap characteristics in broad-leaved deciduous woodland

Questions: 1. What are the spatial patterns of all trees, individual tree species, trees within particular height classes, all gaps and gaps with specific properties across the study site in broad-leaved deciduous forest at a range of scales? 2. Are patterns of the above features spatially associated? 3. Are these patterns indicative of gap creation mechanisms and phases of regeneration? Location: Frame Wood, New Forest, UK. Methods: Ripley’s K-function analysis was applied to spatial information derived from airborne remotely sensed imagery to characterize the patterns of trees and gaps and to test for spatial interactions between these patterns. The patterns of trees and gaps with specific physical and spatial properties were analysed. Results: The pattern of all tree species combined was random for most scales; Quercus robur followed the same random pattern, while Fagus sylvatica and Betula pendula were clustered over most spatial scales. Large gaps (> 250 m 2 ) and larger trees (> 17.5 m) were randomly distributed, while smaller gaps and smaller trees were clustered. Significant spatial relationships were demonstrated between the patterns of different tree species and between trees within different size classes, as well as between the patterns of trees and gaps with specific properties. Conclusions: Small gap patterns and field evidence indicated that progressive gap enlargement is the most likely creation mechanism for large gaps (> 250 m2). Clustered patterns of younger individuals were indicative of patches of past regeneration. As a complement to field-based data, data derived from remotely sensed imagery provides spatially comprehensive information with which to further investigate woodland stand/community processes and gap dynamics.

Drosophila Wee1 Kinase Regulates Cdk1 and Mitotic Entry during Embryogenesis

Cyclin-dependent kinases (Cdks) are the central regulators of the cell division cycle. Inhibitors of Cdks ensure proper coordination of cell cycle events and help regulate cell proliferation in the context of tissues and organs. Wee1 homologs phosphorylate a conserved tyrosine to inhibit the mitotic cyclin-dependent kinase Cdk1. Loss of Wee1 function in fission or budding yeast causes premature entry into mitosis. The importance of metazoan Wee1 homologs for timing mitosis, however, has been demonstrated only in Xenopus egg extracts and via ectopic Cdk1 activation . Here, we report that Drosophila Wee1 (dWee1) regulates Cdk1 via phosphorylation of tyrosine 15 and times mitotic entry during the cortical nuclear cycles of syncytial blastoderm embryos, which lack gap phases. Loss of maternal dwee1 leads to premature entry into mitosis, mitotic spindle defects, chromosome condensation problems, and a Chk2-dependent block of subsequent development, and then embryonic lethality. These findings modify previous models about cell cycle regulation in syncytial embryos and demonstrate that Wee1 kinases can regulate mitotic entry in vivo during metazoan development even in cycles that lack a G2 phase.

Signalling in stem cells: meeting on signal transduction determining the fate of stem cells.

The meeting “Signal Transduction Determining the Fate of Stem Cells” was held at Montana State University in Bozeman, Montana, between August 9 and 12, 2003. The meeting was sponsored by the American Society for Cell Biology and was organized by G.L. Johnson and N. Terada. ![][1] Many scientific meetings have been organized to present research findings on stem‐cell sources, their pluripotent nature and potential therapeutic applications for treating disease. The theme of this meeting was the signalling pathways that control stem‐cell maintenance and differentiation. In his keynote address, A. Spiegel (Bethesda, MD, USA) emphasized the high therapeutic potential of stem cells, and also the need to understand more about their unique cell and molecular biology to harness their therapeutic application. Although embryonic, haematopoietic and hepatic stem cells from humans are the obvious therapeutics, stem‐cell research in various organisms from flies to humans was presented at this meeting. ### Signalling of stem‐cell proliferation and survival A common feature of stem cells, regardless of origin and type, is their ability to undergo self‐renewal. Cultured stem cells, especially embryonic stem (ES) cells, exhibit a high rate of proliferation and a short cell cycle time (10–12 hours). Studies by S. Dalton (Athens, GA, USA) showed that ES cells have a unique cell cycle that lacks complete G1 and G2 gap phases (Stead et al , 2002). The activity of cyclin‐dependent kinases (Cdks) is constitutively high relative to their activity in somatic cells such as mouse embryo fibroblasts. Genes that are the target of the E2F transcription factor are also constitutively active, consistent with the negligible activity of the retinoblastoma (Rb) protein pathway in these cells. Analysis of Cdk activity in mouse ES cells reveals a novel, constitutively active Cdk6–cyclin D3 complex that is rapidly downregulated following ES cell differentiation. Importantly, this Cdk–cyclin complex is insensitive to the defined Cdk inhibitors such as p16. … [1]: /embed/graphic-1.gif

Isoform switching of Cdc6 contributes to developmental cell cycle remodeling

Xenopus laevis early development is characterized by rapid and synchronous cleavage cycles, which consist of alternating S and M phases. At midblastula transition, zygotic transcription begins and these cleavage cycles are replaced by longer cell division cycles that include gap phases and checkpoints. Herein, we demonstrate developmentally regulated Cdc6 isoform switching that contributes to this developmental cell cycle remodeling. Cdc6 is an essential component of the eukaryotic DNA replication machine that licenses each origin to one round of DNA replication each cell division cycle. The originally characterized Xenopus Cdc6 isoform (here termed Xcdc6A) and a novel isoform (Xcdc6B) have divergent N-terminal regulatory regions and different temporal patterns of expression. Although abundant in the early embryo, Xcdc6A becomes undetectable following midblastula transition. In contrast, while Xcdc6B is present in the early embryo, it is nonfunctional, as judged by lack of chromatin binding. In somatic tissue, however, Xcdc6B binds chromatin and its inhibition blocks entry into S phase. This is the first example of developmental regulation of Cdc6, raising intriguing implications for cell cycle remodeling during embryogenesis.

Synchronization of interphase events depends neither on mitosis nor on cdk1.

Human HT2-19 cells with a conditional cdk1 mutation stop dividing upon cdk1 inactivation and undergo multiple rounds of endoreplication. We show herein that major cell cycle events remain synchronized in these endoreplicating cells. DNA replication alternates with gap phases and cell cycle-specific cyclin E expression is maintained. Centrosomes duplicate in synchrony with chromosome replication, giving rise to polyploid cells with multiple centrosomes. Centrosome migration, a typical prophase event, also takes place in endoreplicating cells. The timing of these events is unaffected by cdk1 inactivation compared with normally dividing cells. Nuclear lamina breakdown, in contrast, previously shown to be dependent on cdk1, does not take place in endoreplicating HT2-19 cells. Moreover, breakdown of all other major components of the nuclear lamina, like the inner nuclear membrane proteins and nuclear pore complexes, seems also to depend on cdk1. Interestingly, the APC/C ubiquitin ligase is activated in these endoreplicating cells by fzr but not by fzy. The oscillations of interphase events are thus independent of cdk1 and of mitosis but may depend on APC/Cfzr activity.

Quantum Phase Transitions of theS=1 Shastry–Sutherland Model

We investigate quantum phase transitions of the two-dimensional S =1 Shastry–Sutherland model, which is characterized by the frustrated orthogonal-dimer structure, by means of the exact diagonalization method and the Ising-type series expansion method. We clarify how distinct spin gap phases realized in the chain system are adiabatically connected to those in the two-dimensional Shastry–Sutherland model. The effect of single-ion anisotropy is also discussed.

Dominant negative E2F inhibits progression of the cell cycle after the midblastula transition in Xenopus.

The cleavage cycle, which is initiated by fertilization, consists of only S and M phases, and the gap phases (G1 and G2) appear after the midblastula transition (MBT) in the African clawed frog, Xenopus laevis. During early development in Xenopus, we examined the E2F activity, which controls transition from the G1 to S phase in the somatic cell cycle. Gel retardation and transactivation assays revealed that, although the E2F protein was constantly present throughout early development, the E2F transactivation activity was induced in a stage-specific manner, that is, low before MBT and rapidly increased after MBT. Introduction of the recombinant dominant negative E2F (dnE2F), but not the control, protein into the 2-cell stage embryos specifically suppressed E2F activation after MBT. Cells in dnE2F-injected embryos appeared normal before MBT, but ceased to proliferate and eventually died at the gastrula. These cells contained decreased cdk activity with enhanced inhibitory phosphorylation of Cdc2 at Tyr15. Thus, E2F activity is required for cell cycle progression and cell viability after MBT, but not essential for MBT transition and developmental progression during the cleavage stage.