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At least 469 records · Page 26Linked to original sources

PubMed2005

A role for the anaphase-promoting complex inhibitor Emi2/XErp1, a homolog of early mitotic inhibitor 1, in cytostatic factor arrest of Xenopus eggs.

Unfertilized vertebrate eggs are arrested in metaphase of meiosis II with high cyclin B/Cdc2 activity to prevent parthenogenesis. Until fertilization, exit from metaphase is blocked by an activity called cytostatic factor (CSF), which stabilizes cyclin B by inhibiting the anaphase-promoting complex (APC) ubiquitin ligase. The APC inhibitor early mitotic inhibitor 1 (Emi1) was recently found to be required for maintenance of CSF arrest. We show here that exogenous Emi1 is unstable in CSF-arrested Xenopus eggs and is destroyed by the SCF(betaTrCP) ubiquitin ligase, suggesting that endogenous Emi1, an apparent 44-kDa protein, requires a stabilizing factor. However, anti-Emi1 antibodies crossreact with native Emi2/Erp1/FBXO43, a homolog of Emi1 and conserved APC inhibitor. Emi2 is stable in CSF-arrested eggs, is sufficient to prevent CSF release, and is rapidly degraded in a Polo-like kinase 1-dependent manner in response to calcium-mediated egg activation. These results identify Emi2 as a candidate CSF maintenance protein.

Anaphase↗

PubMed2006

Deletion mapping of genetic regions associated with apomixis in Hieracium.

Although apomixis has been quoted as a technology with the potential to deliver benefits similar in scale to those achieved with the Green Revolution, very little is currently known of the genetic mechanisms that control this trait in plants. To address this issue, we developed Hieracium, a genus of daisies native to Eurasia and North America, as a genetic model to study apomixis. In a molecular mapping study, we defined the number of genetic loci involved in apomixis, and we explored dominance and linkage relationships between these loci. To avoid difficulties often encountered with inheritance studies of apomicts, we based our mapping effort on the use of deletion mutagenesis, coupled with amplified fragment length polymorphism (AFLP) as a genomic fingerprinting tool. The results indicate that apomixis in Hieracium caespitosum is controlled at two principal loci, one of which regulates events associated with the avoidance of meiosis (apomeiosis) and the other, an unlinked locus that controls events associated with the avoidance of fertilization (parthenogenesis). AFLP bands identified as central to both loci were isolated, sequenced, and used to develop sequence-characterized amplified region (SCAR) markers. The validity of the AFLP markers was verified by using a segregating population generated by hybridization. The validity of the SCAR markers was verified by their pattern of presence/absence in specific mutants. The mutants, markers, and genetic data derived from this work are now being used to isolate genes controlling apomixis in this system.

Asteraceae↗

PubMed1976

Selective cannibalism in the rotifer asplanchna sieboldi: contact recognition of morphotype and clone.

Populations of A. sieboldi reproduce primarily by diploid femal parthenogenesis. Females may exhibit a pronounced, nongenetic polymorphism which is controlled by the diet. The cruciform and especially the campanulate morphotypes are larger than the saccate morphotype and are cannibalistic. Direct observations of various predator-prey interactions between the different morphotypes of two taxonomically distinct clones show that the feeding responses of cannibals after actual prey contact are predictable and extremely selective. Companulates from clone B respond regularly to saccate but only rarely to cruciform or campanulate clonemates; the same predators typically respond to cruciforms and campanulates from clone C. Cruciforms from clone C rarely respond to saccate and cruciform clonemates but readily attack all morphotypes from clone B. In contrast, campanulates from clone C show no selectivity. Morphotype- and clone-specific recognition responses, which are mediated by coronal contact chemoreceptors, permit efficient prey discrimination and protection withotu involving prey handling or development of energy-demanding, defensive structures, such as the body-wall outgrowths of the cruciform morphotype. Selective feeding of cannibals may increase the fitness of a clone, both by effecting a more adaptive distribution of its morphotypes and by enhancing its ability to compete directly and indirectly with cooccurring clones. The magnitude of cannibalism in this rotifer may be dependent upon a complex suite of heterogeneous predator-prey interactions and greatly affected by shifting densities and distributions of different clones and female morphotypes.

Age Factors↗

PubMed1978

Somatic cell origin of teratocarcinomas.

Malignant teratocarcinomas arise from developmentally totipotent normal stem cells. Whether the targets are embryonal somatic cells or germinal cells has long been a matter of controversy. Past experiments on teratocarcinoma induction by ectopic grafting of early rodent embryos or fetal germinal ridges have remained ambiguous because embryos ordinarily soon form germ cells, and parthenogenetic germ cells form "embryos." In order to interrupt the developmental cycle at its most telling point, day 6 (egg-cylinder stage) mouse embryos of genetically sterile types were grafted; in such grafts, only a terminal residue of totipotent embryonal somatic ("ectoderm") cells is available, and subsequent germ cell development is severely impaired. One graft series, from S1(J)/+ matings, comprised 25% S1(J)/S1(J) presumptive sterile embryos; these grafts formed tumors containing embryonal carcinoma cells as often (47%) as did control +/+ grafts (41%) on the same genetic background. In another series, from W/+ matings, tumors of the sterile W/W genotype were individually identified by means of a closely linked marker, phosphoglucomutase (PGM, EC 2.7.5.1; Pgm-1 locus), coding for electrophoretic enzyme variants and incorporated into the stock. Four tumors were obtained (out of 16) that had the PGM-1D phenotype diagnostic for W/W, and that also contained embryonal carcinoma cells. Therefore, the malignancy arises here in susceptible somatic embryonal stem cells at the terminal stage of their capacity for totipotency. Other teratocarcinomas-whether induced or spontaneous-of ostensible germ-cell origin by parthenogenesis may also depend upon development of the same somatic target cells before neoplastic conversion can occur. A general model based on these experiments is proposed for all malignancies: Malignant transformation of a particular kind of normal stem cell may be possible only when that stem cell has progressed to the threshold of further differentiation.

Animals↗

PubMed1990

Antibiotics cause parthenogenetic Trichogramma (Hymenoptera/Trichogrammatidae) to revert to sex.

Completely parthenogenetic Trichogramma wasps can be rendered permanently bisexual by treatment with three different antibiotics or high temperatures. The evidence strongly suggests that maternally inherited microorganisms cause parthenogenesis in these wasps. Theories predict female-biased sex ratio in offspring under the influence of maternally inherited symbionts, but extreme sex ratios of 100% females were never considered because the lack of males would prevent the host's reproduction.

Journal Article↗

PubMed1990

Sexual reproduction as an adaptation to resist parasites (a review).

Darwinian theory has yet to explain adequately the fact of sex. If males provide little or no aid to offspring, a high (up to 2-fold) extra average fitness has to emerge as a property of a sexual parentage if sex is to be stable. The advantage must presumably come from recombination but has been hard to identify. It may well lie in the necessity to recombine defenses to defeat numerous parasites. A model demonstrating this works best for contesting hosts whose defense polymorphisms are constrained to low mutation rates. A review of the literature shows that the predictions of parasite coevolution fit well with the known ecology of sex. Moreover, parasite coevolution is superior to previous models of the evolution of sex by supporting the stability of sex under the following challenging conditions: very low fecundity, realistic patterns of genotype fitness and changing environment, and frequent mutation to parthenogenesis, even while sex pays the full 2-fold cost.

Adaptation, Biological↗

PubMed1996

The Mos/mitogen-activated protein kinase (MAPK) pathway regulates the size and degradation of the first polar body in maturing mouse oocytes.

Mos is an upstream activator of mitogen-activated protein kinase (MAPK) and, in mouse oocytes, is responsible for metaphase II arrest. This activity has been likened to its function in Xenopus oocytes as a component of cytostatic factor. Thus, Mos-deficient female mice (MOS-/-) are less fertile and oocytes derived from these animals fail to arrest at metaphase II and undergo parthenogenetic activation [Colledge, W. H., Carlton, M. B. L., Udy, C. B. & Evans, M. J. (1994) Nature (London) 370, 65-68 and Hashimoto, N., Watanabe, N., Furuta. Y., Tamemoto, B., Sagata, N., Yokoyama, M., Okazaki, K., Nagayoshi, M., Takeda, N., Ikawa, Y. & Aizawa, S. (1994) Nature (London) 370, 68-71]. Here we show that maturing MOS-/- oocytes fail to activate MAPK throughout meiosis, while p34cdc2 kinase activity is normal until late in metaphase II when it decreases prematurely. Phenotypically, the first meiotic division of MOS-/- oocytes frequently resembles mitotic cleavage or produces an abnormally large polar body. In these oocytes, the spindle shape is altered and the spindle fails to translocate to the cortex, leading to the establishment of an altered cleavage plane. Moreover, the first polar body persists instead of degrading and sometimes undergoes an additional cleavage, thereby providing conditions for parthenogenesis. These studies identify meiotic spindle formation and programmed degradation of the first polar body as new and important roles for the Mos/MAPK pathway.

Animals↗

PubMed1997

Wolbachia, normally a symbiont of Drosophila, can be virulent, causing degeneration and early death.

Wolbachia, a maternally transmitted microorganism of the Rickettsial family, is known to cause cytoplasmic incompatibility, parthenogenesis, or feminization in various insect species. The bacterium-host relationship is usually symbiotic: incompatibility between infected males and uninfected females can enhance reproductive isolation and evolution, whereas the other mechanisms enhance progeny production. We have discovered a variant Wolbachia carried by Drosophila melanogaster in which this cozy relationship is abrogated. Although quiescent during the fly's development, it begins massive proliferation in the adult, causing widespread degeneration of tissues, including brain, retina, and muscle, culminating in early death. Tetracycline treatment of carrier flies eliminates both the bacteria and the degeneration, restoring normal life-span. The 16s rDNA sequence is over 98% identical to Wolbachia known from other insects. Examination of laboratory strains of D. melanogaster commonly used in genetic experiments reveals that a large proportion actually carry Wolbachia in a nonvirulent form, which might affect their longevity and behavior.

Animals↗

PubMed1995

Biological and biochemical comparative studies on Schistosoma mansoni from two localities in Egypt where S. haematobium is endemic.

The changing pattern of Schistosoma mansoni and S. haematobium distribution in Egypt is generally attributed to ecological changes caused by the construction of the Aswan High Dam. Although S. mansoni was previously restricted to Lower Egypt, it is now found at certain foci in Upper Egypt. In areas of Lower Egypt where S. mansoni and S. haematobium are sympatric, S. mansoni eggs are shed almost exclusively in the stools of patients, whereas in Upper Egypt they are more frequently shed in the urine. In spite of this difference, the eggs and adult worms obtained from hamsters infected with S. mansoni strains from each of these areas proved to be morphologically identical. Protein patterns and isoenzyme profiles of male or female adult worms of each of the two isolates, obtained from infected hamsters, also proved virtually identical. In hamsters with mixed infections of S. mansoni and S. haematobium, some S. mansoni females cross-mated with S. haematobium males and they then developed ovaries and laid eggs which were typical of S. mansoni and which were excreted from the urinary bladder. In Upper Egypt, which is predominantly a S. haematobium area, patients with established infections may have a preponderance of S. haematobium males associated with S. mansoni females. These females may then migrate to the vesicular plexus and deposit S. mansoni eggs in the urinary bladder, to be shed subsequently in the urine. The observations appear to be better explained by the phenomenon of parthenogenesis than by the production of true genetic hybrids.

Animals↗

PubMedDate not supplied

Molecular biology of male infertility.

About 15% of couples have reduced fertility and in approximately one-half of all cases the reason is male infertility, usually of genetic origin. Thus, in the context of research in genes involved in reproduction and sex determination, genetic anomalies in gametogenesis are being extensively studied. The most frequent pathogenic causes of male infertility are Y-chromosomal microdeletions (8-15%) in the long arm of the Y chromosome, which, by loss of specific DNA segments, leads to loss of vital genes for sperm production. Infertile men, who attend infertility clinics, rise to 15% among those with azoospermia or spermatogenesis problem. The new technique of intracytoplasmic sperm injection has allowed many infertile men to achieve their dreams of fatherhood. However, the spermatogenic defect is genetic anomalies, which might be a potential risk of transmitting this defect to future offspring. Therefore, genetic counseling of all couples with the diagnosis of male infertility is recommended before their enrolment in intrauterine insemination, in vitro fertilization, and intracytoplasmic sperm injection. The important role of genetic abnormalities in the causation of human male infertility is increasingly recognized. While much remains to be learned in this fast-moving field, considerable progress has been made in the clinical delineation of genetic forms of male infertility and in the characterization of the responsible genes and their mutations or deletions. This review should provide insight into the understanding of parthenogenesis of male infertility in the human.

Female↗

PubMed2002

Cloning and characterization of a gene encoding glutathione-regulated potassium-efflux system protein KefKL from the endosymbiont Wolbachia.

The maternally inherited intracellular symbiont Wolbachia is well known for inducing a variety of reproductive and developmental abnormalities in the diverse arthropod hosts it infects. It has been implicated in causing cytoplasmic incompatibility (CI), parthenogenesis, feminization of genetic males and male killing in different hosts. However, the molecular mechanisms by which this fastidious bacterium causes these abnormalities have not yet been determined. In our study, representational difference analysis (RDA) was used to analyze the genomic difference between different Wolbachia strains. A gene encoding glutathione-regulated potassium-efflux system protein KefKL from Wolbachia in Drosophila simulans Riverside (w Ri) was isolated. The homologous genes from Wolbachia in Drosophila melanogaster yw67c23 (wMel) and Wolbachia in Drosophila melanogaster CantonS (wMelCS) were also cloned and sequenced. Sequence analysis showed that these deduced amino acid sequences contained two important motifs: Na+/H+ antiportor and NAD binding domain, which shared conserved sequences among different strains. Considering the crucial function of KefKL for ionic homeostasis, this gene might play an important role in Wolbachia physiology. Further study indicated that there was no homologue detected from Wolbachia in Drosophila simulans DSW/Mau (wMa) and Wolbachia in Drosophila simulans Noumea (wNo). Whether Wolbachia contained KefKL (or the homologous gene) was consistent with the phylogenetic studies using wsp sequences, which showed that wMa and wNo were grouped into one branch, while w Ri, wMel and wMelCS were more closely related.

Amino Acid Sequence↗

PubMed1975

Aster formation in eggs of Xenopus laevis. Induction by isolated basal bodies.

We have assayed various materials for their ability to induce aster formation by microinjection into unfertilized eggs of Xenopus laevis. We have found that purified basal bodies from Chlamydomonas reinhardtii and Tetrahymena pyriformis induce the formation of asters and irregular cleavage furrows within 1 h after injection. Other microtubule structures such as flagella, flagellar axonemes, cilia, and brain microtubules are completely ineffective at inducing asters or cleavage furrows in unfertilized eggs. When known amounts of sonicated Tetrahymena and Chlamydomonas preparations are injected into unfertilized eggs, 50% of the injected eggs show a furrowing response at approximately 3 cell equvalents for Chlamydomonas and 0.1 cell equivalent for Tetrahymena. These results are close to those expected if basal bodies were the effective astral-inducing agent in these cells. Other materials effective at inducing asters in unfertilized eggs, such as crude brain nuclei, sperm, and a particulate fraction from brain known to induce parthenogenesis in eggs of Rana pipiens, probably contain centrioles as the effective agent. Our experiments provide the first functional assay to indicate that centrioles play an active role in aster initiation. None of the injected materials effective in unfertilized eggs produced any observable response in fully grown oocytes. Oocytes and eggs were found to have equal tubulin pools as judged by colchicine-binding activity. Therefore, the inability of oocytes to form asters cannot be due to a lack of an organizing center or to a lack of tubulin. Experiments in which D2O was found to stimulate aster-like fibrous areas in eggs but not oocytes suggest that the inability of oocytes to form asters may be due to an inability of tubulin in oocytes to assemble.

Animals↗

PubMed2003

Genetic conflicts over sex ratio: mite-endosymbiont interactions.

Nucleocytoplasmic genetic conflicts arise as a result of asymmetric transmission of cytoplasmic and nuclear genes. Spread of a cytoplasmic element promoting female-biased sex ratios creates selection on nuclear genes for mechanisms that decrease the bias. Here we investigate the conflict over sex ratio between the cytoplasmic bacterium Wolbachia and the two-spotted spider mite Tetranychus urticae Koch. We show that, first, infected females produce significantly more female-biased sex ratios than uninfected (cured) females. Second, this effect is not due to parthenogenesis, male killing, or feminization, phenotypes commonly associated with infection by Wolbachia. Third, sex ratio is a trait with a heritable component in this species; thus, it can evolve under selection. Fourth, the sex ratio produced by uninfected (cured) females changes over time, approaching the sex ratio produced by females from the infected culture. On the basis of these results, we suggest that after sex ratio manipulation by Wolbachia, a host compensatory mechanism evolved that allows infected females to produce the sex ratio favored by nuclear genes. We discuss the evolution of "mutualism" with respect to the evolution of host mechanisms that compensate for effects induced by vertically transmitted "parasites."

Animals↗

PubMed2003

The evolution of androgenesis.

It is well known that some species produce offspring carrying only female chromosomes by processes such as apomixis and parthenogenesis (generically termed "gynogenesis"). There are also several cases of natural reproduction by androgenesis in which diploid offspring carry nuclear chromosomes from only the male parent. We used population genetics models to investigate the conditions for invasion of rare androgenesis alleles and the consequences of their spread. Our models predict that androgenesis alleles often spread to fixation. If fixation causes the loss of females or female function in the population, population extinction occurs. Therefore, androgenesis alleles represent a new class of selfish genetic elements. Extinction is more likely in dioecious species than in hermaphrodites. Within dioecious species, extinction is more likely when androgenesis occurs via paternal apomixis (vs. fusion or doubling of haploid nuclei) and when females are the heterogametic sex (vs. male heterogamety). The apparent rarity of androgenesis compared to gynogenesis could be because androgenesis is harder to detect and more often leads to population extinction. Also, there could be greater evolutionary constraints on the origin of mutations for androgenesis. We suggest characteristics of groups in which further cases of androgenesis are more likely to be found.

Alleles↗

PubMed2004

Derivation and comparative assessment of retinal pigment epithelium from human embryonic stem cells using transcriptomics.

Human stem-cell derivatives are likely to play an important role in the future of regenerative medicine. Evaluation and comparison to their in vivo counterparts is critical for assessment of their therapeutic potential. Transcriptomics was used to compare a new differentiation derivative of human embryonic stem (hES) cells--retinal pigment epithelium (RPE)--to human fetal RPE. Several hES cell lines were differentiated into putative RPE, which expressed RPEspecific molecular markers and was capable of phagocytosis, an important RPE function. Isolated hES cell-derived RPE was able to transdifferentiate into cells of neuronal lineage and redifferentiate into RPE-like cells through multiple passages (>30 Population doublings). Gene expression profiling demonstrated their higher similarity to primary RPE tissue than of existing human RPE cell lines D407 and ARPE-19, which has been shown to attenuate loss of visual function in animals. This is the first report of the isolation and characterization of putative RPE cells from hES cells, as well as the first application of transcriptomics to assess embryonic stem-cell derivatives and their in vivo counterparts--a "differentiomics" outlook. We describe for the first time, a differentiation system that does not require coculture with animal cells or factors, thus allowing the production of zoonoses-free RPE cells suitable for subretinal transplantation in patients with retinal degenerative diseases. With the further development of therapeutic cloning, or the creation of the banks of homozygous human leucocyte antigen (HLA) hES cells using parthenogenesis, RPE lines could be generated to overcome the problem of immune rejection and could be one of the nearest term applications of stem-cell technology.

Cell Differentiation↗

PubMed1992

Enhanced production of monoclonal antibodies against zona pellucida-free, unfertilized mouse oocytes by intrasplenic immunization.

Monoclonal antibodies were obtained by intrasplenic insertion of a total of 40-50 zona pellucida-free, unfertilized mouse oocytes into each mouse. The oocytes were prepared by a combined enzyme-mechanical method without impairing the fertility of the oocyte or inducing parthenogenesis. Of a total of 1063 hybrids obtained, 15 yielded supernatants with positive reactions to unfertilized oocytes. Tests for preimplantation stage specificity demonstrated that 9 of the supernatants detected antigen epitopes in unfertilized oocytes only. The other supernatants showed positive reaction patterns to various embryonal stages of the preimplantation period. Two supernatants recognized materials in the culture medium shedded by zona pellucida-free oocytes. Thus, by applying intrasplenic immunization, the production of antibodies against zona pellucida-free mouse oocytes is enhanced. The procedures described outline a rational way of selecting antibodies of interest for research in the mechanism of fertilization.

Animals↗

PubMed2003

Induction of apoptosis in starfish eggs requires spontaneous inactivation of MAPK (extracellular signal-regulated kinase) followed by activation of p38MAPK.

Mitogen-activated protein kinase (MAPK) (extracellular signal-regulated kinase) prevents DNA replication and parthenogenesis in maturing oocytes. After the meiotic cell cycle in starfish eggs, MAPK activity is maintained until fertilization. When eggs are fertilized, inactivation of MAPK occurs, allowing development to proceed. Without fertilization, highly synchronous apoptosis of starfish eggs starts 10 h after germinal vesicle breakdown, which varies according to season and individual animals. For induction of the apoptosis, MAPK should be activated for a definite period, called the MAPK-dependent period, during which eggs develop competence to die, although the exact duration of the period was unclear. In this study, we show that the duration of the MAPK-dependent period was approximately 8 h. Membrane blebbing occurred approximately 2 h after the MAPK-dependent period. Surprisingly, when MAPK was inhibited by U0126 after the MAPK-dependent period, activation of caspase-3 occurred earlier than in the control eggs. Thus, inactivation of MAPK is a prerequisite for apoptosis. Also, even in the absence of the inhibitor, MAPK was inactivated spontaneously when eggs began to bleb, indicating that inactivation of MAPK after the MAPK-dependent period acts upstream of caspase-3. Inactivation of MAPK also resulted in the activation of p38MAPK, which may contribute to apoptotic body formation.

Animals↗

PubMed2025

The ecology, evolution, and physiology of Cardinium: a widespread heritable endosymbiont of invertebrates.

Candidatus Cardinium hertigii (Cardinium) are maternally transmitted obligate intracellular bacteria found in a wide range of invertebrate hosts, including arthropods and nematodes. Infection with Cardinium has substantial consequences for host biology, with many strains manipulating host reproduction to favor symbiont transmission by (i) feminizing male hosts, (ii) altering host sex allocation, (iii) inducing parthenogenesis, or (iv) causing cytoplasmic incompatibility. Other Cardinium strains can confer benefits to their host or alter host behavior. Cardinium-modified host phenotypes can result in selective sweeps of cytological elements through host populations and potentially reinforce host speciation. Cardinium has potential for applications in controlling arthropod pest species and arthropod-vectored disease transmission, although much remains to be explored regarding Cardinium physiology and host interactions. In this review, we provide an overview of Cardinium evolution and host distribution. We describe the various host phenotypes associated with Cardinium and how biological and environmental factors influence these symbioses. We also provide an overview of Cardinium metabolism, physiology, and potential mechanisms for interactions with hosts based on recent studies using genomics and transcriptomics. Finally, we discuss new methodologies and directions for Cardinium research, including improving our understanding of Cardinium physiology, response to environmental stress, and potential for controlling arthropod pest populations.

Symbiosis↗