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PubMed2001

HMG-17 is an early marker of inductive interactions in the developing mouse kidney.

We studied the relationship between proliferation, differentiation, and the expression of high-mobility-group protein 17 (HMG-17) during metanephric kidney development. Proliferating cells were found homogenously throughout the early kidney rudiment. The expression pattern of HMG-17 mRNA, on the other hand, was distinctly uneven: In the undifferentiated mesenchyme, the cells in the cranial "tail" part of the mesenchyme showed only a weak signal, whereas a group of cells lying close to the tip of the ureteric bud showed strong HMG-17 expression. The region distinctly positive for HMG-17 is known to contain the first cells to undergo mesenchyme-to-epithelium transition. Using the transfilter model system, strong expression of HMG-17 mRNA, followed by mesenchyme-to-epithelium transition, could be induced also in the "tail" part of the mesenchyme. The upregulation of HMG-17 in the metanephrogenic mesenchyme thus results from interaction with an inductor tissue. Throughout the renal development, the HMG-17 mRNA was also abundant in those epithelial and mesenchymal cells that were undergoing active cell differentiation, and the transcript was downregulated in mature cells. HMG-17 expression thus correlated with the processes of induction and differentiation rather than with proliferation. The present results suggest that HMG-17 could have a role in the activation of the genes regulating kidney organogenesis.

Animals↗
PubMed2003

Cellular and molecular mechanisms of development of the external genitalia.

The limb and external genitalia are appendages of the body wall. Development of these structures differs fundamentally in that masculine development of the external genitalia is androgen dependent, whereas development of the limb is not. Despite this fundamental difference in developmental regulation, epithelial-mesenchymal interactions play key roles in the development of both structures, and similar regulatory molecules are utilized as mediators of morphogenetic cell-cell interactions during development of both the limb and external genitalia. Given the relatively high incidence of hypospadias, a malformation of penile development, it is appropriate and timely to review the morphological, endocrine, and molecular mechanisms of development of the genital tubercle (GT), the precursor of the penis in males and the clitoris in females. Morphological observations comparing development of the GT in humans and mouse emphasize the validity of the mouse as an animal model of GT development and validate the results of experimental studies. Accordingly, the use of mutant mice provides important insights into the roles of specific regulatory molecules in development of the external genitalia. While our current understanding of the morphological and molecular mechanisms of mammalian external genitalia development is still rudimentary, this review summarizes the current state of our knowledge and whenever possible draws from the rich experimental embryology literature on other relevant organs such as the developing limb. Future research on the hormonal and molecular mechanisms of GT development may yield strategies to prevent or reduce the incidence of hypospadias and to elucidate the molecular genetic mechanisms of GT morphogenesis, especially in relation to common organogenetic pathways utilized in other organ systems.

Animals↗
PubMed2002

Epithelial cell proliferation and apoptosis in the developing murine palatal rugae.

Epithelial cell proliferation and apoptosis during morphogenesis of the murine palatal rugae (PR) were examined histochemically by using anti-bromodeoxyuridine (BrdU) and the terminal deoxynucleotidyl transferase-mediated UTP nick-end-labelling (TUNEL) technique. Formation of the PR rudiment was observed as an epithelial placode in fetuses at 12.5 days post-coitus (dpc). During the PR formation, BrdU-positive cells were detected mainly in the epithelium of the interplacode and interprotruding areas in fetuses administered BrdU maternally at 2 h before killing. TUNEL-positive cells were detected only at the epithelial placode area in 12.5-14.5 dpc. At 16.5-18.5 dpc, the BrdU-positive cells were decreased in number in the epithelial cells at the interprotruding area of the PR. Only a few TUNEL-positive cells were observed in the protruding area of the PR at 16.5 dpc. These results suggest that cell proliferation and apoptosis in the palatal epithelium are involved spatiotemporally in the murine PR morphogenesis.

Animals↗
PubMed2003

Müller cells express the neuronal progenitor cell marker nestin in both differentiated and undifferentiated human foetal retina.

Tritiated thymidine studies suggest that Müller cells are the last cells born in the retina, although several authors describe Müller cells throughout the retina from very early ages. In this study immunohistochemistry was used to identify progenitor and Müller cells in human foetal retina. Antibodies to nestin (an intermediate filament protein expressed by neural progenitor cells), vimentin, cellular retinaldehyde binding protein (CRALBP) and glutamate and aspartate transporter (GLAST), which are each expressed by Müller cells, were used in combination with anti-Ki67 to identify proliferating cells. By definition, Ki67-positive proliferating cells were present in undifferentiated retina, but not in differentiated retina. Nestin-immunoreactive (IR) cells colocalized with vimentin throughout the retina. CRALBP-IR was detected in differentiated retina and in some proliferating cells. GLAST-IR cells were present only within the differentiated region. Nestin, vimentin and CRALBP each colocalized with mitotic Ki67-IR cells, suggesting that in foetal retina Müller cells and retinal progenitor cells are overlapping populations and that Müller cells are end-stage progenitor cells.

Amino Acid Transport System X-AG↗
PubMed2001

Effects of the curly tail genotype on neuroepithelial integrity and cell proliferation during late stages of primary neurulation.

The curly tail (ct/ct) mouse mutant shows a high frequency of delay or failure of neural tube closure, and is a good model for human neural tube defects, particularly spina bifida. In a previous study we defined distinct domains of gene expression in the caudal region of non-mutant embryos during posterior (caudal) neuropore closure (Gofflot et al. Developmental Dynamics 210, 431-445, 1997). Here we use BrdU incorporation into S-phase nuclei to investigate the relationship between cell proliferation and the previously described gene expression domains in ct/ct mutant embryos. The BrdU-immunostained sections were also examined for abnormalities of tissue structure; immunohistochemical detection of perlecan (an extracellular heparan sulphate proteoglycan) was used as an indicator of neuroepithelial basement membrane structure and function. Quantitation of BrdU uptake revealed that at early stages of neurulation, cell proliferation was specifically reduced in the paraxial mesoderm of all ct/ct embryos compared with wild type controls, but at later stages (more cranial levels) it was increased. Those ct/ct embryos with enlarged posterior neuropore (indicating delay of closure) additionally showed an increased BrdU labelling index within the open neuroepithelium at all axial levels; however, this tissue was highly abnormal with respect to cell and nuclear morphology. It showed cell death and loss of cells from the apical surface, basement membrane defects including increased perlecan immunoreactivity, and increased separation from the underlying mesenchyme and notochord. These observations suggest that the mechanism of delay or failure of neuroepithelial curvature that leads to neural tube defects in curly tail embryos involves abnormalities of neuroepithelial-mesenchymal interactions that may be initiated by abnormal cellular function within the neuroepithelium. Minor histological and proliferation abnormalities are present in all ct/ct embryos, regardless of phenotype.

Animals↗
PubMedDate not supplied

[Olfactory bulb neurogenesis and its neurological impact].

Contrary to the long-held dogma according to which the adult mammalian brain does not produce neurons anymore, neuronal turnover has been reported in two discrete areas of the adult brain: the hippocampus and the olfactory bulb. Adult-generated neurons are produced from neural stem cells located in the hippocampal subgranular zone and the subventricular zone of the lateral ventricles. Recently, number of genetic and epigenetic factors that modulate proliferation of stem cells, migration, differentiation and survival of newborn neurons have been characterized. We know that neurogenesis increases in the diseased brain, after stroke or after traumatic brain injury. Importantly, progenitors from the subventricular zone, but not from the subgranular zone, are incorporated at the sites of injury, where they replace some of the degenerated neurons. Thus, the central nervous system has the capacity to regenerate itself after injury and, today, researchers develop strategies aimed at promoting neurogenesis in diseased areas. This basic research is attracting a lot of attention because of the hope that it will lead to regeneration and reconstruction therapy for the damaged brain. In this review, we discuss major findings concerning the organization of the neurogenic niche located in the subventricular zone and examine both intrinsic and extrinsic factors that regulate adult neurogenesis. Then, we present evidences for the intrinsic capability of the adult brain for cell replacement, and shed light on recent works demonstrating that one can greatly enhance appropriate brain cell replacement by using molecular cues known to endogenously control proliferation, migration, differentiation and/or survival of subventricular zone progenitors. Finally, we review some of the advantages and limits of strategies aimed at using endogenous progenitors and their relevance to human clinics.

Aging↗
PubMed2006

The chromosomes of Rodentolepis nana (Siebold, 1852) Spasskii, 1954 obtained from naturally infected mice conventionally maintained in a Braziuan laboratory animal house.

The karyotype of Rodentolepis nana obtained from mice in Rio de Janeiro, Brazil, was described. The diploid chromosome number obtained by the division of embryonic cells was 2n = 12. The first and the third pairs presented subterminal centromeres and the other pairs were all acrocentric. The studied species differed in chromosome morphology when compared to previous description by Mutafova and Gergova (1994) in Bulgaria, suggesting an intraspecific variation.

Animals↗
PubMed1992

Antisense c-myc effects on preimplantation mouse embryo development.

Antisense DNA inhibition of gene expression was explored as an approach toward elucidating mechanisms regulating development of preimplantation mammalian embryos. Specifically, a role for the c-myc protooncogene was examined. Detection of c-myc mRNA and immunoreactive nuclear c-myc protein in preimplantation mouse embryos at the eight-cell/morula and blastocyst stages suggested that this DNA-binding protein could be important during early embryo-genesis. The effects of c-myc oligodeoxyribonucleotides (oligos) on the in vitro development of two-cell mouse embryos were examined. Embryos cultured in medium containing an unmodified (phosphodiester) antisense c-myc oligo complementary to the translation initiation codon and spanning the first seven codons exhibited a dose-dependent arrest at the eight-cell/morula stage. At lower concentrations (7.5 microM) this inhibitory effect was specific to the antisense oligo and did not occur with the sense-strand complement or with duplexes of the antisense and sense oligos. However, at 4-fold higher concentrations of DNA (30 microM), all unmodified c-myc oligos were embryotoxic, causing embryos to arrest at the two-cell to four-cell stages. In contrast, almost all (98%) two-cell embryos cultured with a modified (chimeric phosphorothioate/phosphodiester) antisense c-myc oligo (7.5 microM) exhibited developmental arrest at the eight-cell/morula stage, whereas no developmental arrest occurred following incubation with high concentrations of the modified sense complement (30 microM). Culture of freshly recovered eight-cell embryos with antisense c-myc led to the absence of c-myc protein but no change in epidermal growth factor receptor in those embryos that developed a blastocoel. These effects on c-myc were specific for the antisense oligo. These results suggest that c-myc function becomes particularly critical for preimplantation mouse embryos at the eight-cell/morula stage of development and establish that antisense DNA can be successfully applied as an approach toward elucidating the roles of specific genes in preimplantation mammalian embryo development.

Animals↗
PubMed2002

FGF10 maintains stem cell population during mouse incisor development.

Mouse incisors have a cervical loop that gives rise to dental epithelium in the apical region of the tooth germ, in contrast to molars. In a study of formation of the stem-cell compartment, we focused on expression patterns of fibroblast growth factor (Fgf) 10 and Fgf3 in developing mice incisors. At E14, Fgf10 and Fgf3 were coexpressed in the dental papilla. After E16 mesenchymal cells underlying cervical loop expressed Fgf10 but not Fgf3. To illustrate the role of FGF10, we analyzed incisor development of Fgf10-deficient mice. The germs of FGF10-null mice proceeded to cap stage normally. However, at a later stage, the cervical loop was not formed. Functional disorder of FGF10 by a neutralizing anti-FGF10 antibody induced apoptosis in the cervical loop of incisor explants. Recombinant FGF10 rescued the cervical loop from apoptosis. These results show that FGF10 maintains the stem-cell compartment in the developing incisor tooth germ.

Animals↗
PubMed1987

An unusual radiation-induced G2 arrest in the zygote of the BALB/c mouse strain.

Female mice of the BALB/c strain were superovulated, mated with males of the same strain, and irradiated with 1 Gy of X-rays at hourly intervals during the first cell cycle of the embryos. Two types of effects were found in the embryos, depending on the time of X-irradiation. When irradiation was delivered between 14 and 21 h after human chorionic gonadotrophin (hCG) injection, cultured two-cell embryos developed normally up to the morula stage, where a high mortality occurred. On the other hand, when irradiation was given between 17 and 24 h after hCG injection, a high proportion of the eggs was unable to cleave and remained blocked at the one-cell stage. Cytofluorometric analysis of the pronuclear DNA content of uncleaved zygotes showed that DNA synthesis was unaffected by X-irradiation, and that they were blocked in G2 phase of the first cell cycle. Similar studies on other strains, as well as reciprocal crosses between BALB/c and F1(female BALB/c X male C57 BLACK) mice showed that the 'one-cell block' is determined by the maternal genotype and results most probably from a direct action of X-rays on a radiosensitive cytoplasmic factor necessary for the first embryonic cell division, and appearing 17 h after hCG injection. A high proportion of blocked zygotes (30-40 per cent) recovered partially, cleaved with a delay of about 20 h, and died soon after, almost none of them being able to reach the blastocyst stage. At the time of maximum radiosensitivity, the LD50 for development up to the blastocyst stage was 0.95 Gy.

Animals↗
PubMed2002

Inhibitory effect of murine kidney extracts on mast cells derived from human umbilical cord blood.

We examined the effect of aqueous murine kidney extract (MKE) on the growth of mast cells prepared from the liquid culture of human umbilical cord blood CD34+ cells in the presence of a combination of recombinant human stem cell factor (SCF) and interleukin-6 (IL-6). Cultured cells were mature mast cells that expressed CD117 antigen on their surface, a specific marker for human mast cell, and they contained 6.53 pg histamine per cell. Adding MKE resulted in a 53% inhibition of mast cell growth and a 40% decrease in histamine content in mast cells in a serum-free liquid culture stimulated by SCF and IL-6. The inhibitory molecule for the growth of human mature mast cells was estimated at about 30 kDa of protein from gel-filtration HPLC. This fraction also inhibited the growth of murine peritoneal cells-derived mast cells. These results suggest that MKE contains regulator(s) that suppress the growth of mast cells and histamine synthesis. and that act beyond species specificity.

Animals↗
PubMed1999

Optimization strategies for production of mammalian embryos by nuclear transfer.

In order to optimize each of the individual steps in the nuclear transfer procedure, we report alternative protocols useful for producing recipient cytoplasts and for improving the success rate of nuclear transfer embryos in cattle, rhesus monkey, and hamster. Vital labeling of maternal chromatin/spindle is accomplished by long wavelength fluorochromes Sybr14 and rhodamine labeled tubulin allowing constant monitoring and verification during enucleation. The use of Chinese hamster ovary (CHO) donor cells expressing the viral influenza hemagglutinin fusion protein (HA-300a+), to adhere and induce fusion between the donor cells and enucleated cow, rhesus and hamster oocytes was examined. Cell surface hemagglutinin was activated with trypsin prior to nuclear transfer and fusion was induced by a short incubation of a newly created nuclear transfer couplet at pH 5.2 at room temperature. Donor cell cytoplasm was dynamically labeled with CMFDA, or further transfected with the green fluorescence protein (GFP) gene, so that fusion could be directly monitored using live imaging. High rates of fusion were observed between CHO donor cells and hamster (100%), rhesus (100%), and cow recipient cytoplasts (81.6%). Live imaging during fusion revealed rapid intermixing of cytoplasmic components between a recipient and a donor cell. Prelabeled donor cytoplasmic components were uniformly distributed throughout the recipient cytoplast, within minutes of fusion, while the newly introduced nucleus remained at the periphery. The fusion process did not induce activation as evidenced by unchanged distribution and density of cortical granules in the recipient cytoplasts. After artificial activation, the nuclear transfer embryos created in this manner were capable of completing several embryonic cell divisions. These procedures hold promise for enhancing the efficiency of nuclear transfer in mammals of importance for biomedical research, agriculture, biotechnology, and preserving unique, rare, and endangered species.

Animals↗
PubMed1991

Pathways of degradation and mechanism of action of antisense oligonucleotides in Xenopus laevis embryos.

Recently, we described a new class of antisense oligonucleotides that can be used to direct the cleavage of mRNAs in Xenopus laevis embryos by RNase H (Dagle et al., Nucleic Acids Res. 18, 4751-4757). In this study, we have examined several factors that determine the activity of these derivatives. In embryos, oligodeoxyribonucleotides were found to be rapidly degraded by a 3' exonuclease. Modification of 3'-terminal phosphodiester linkages as phosphoramidates blocks this activity. The predominant sites of endonucleolytic cleavage within the embryo are localized close to the 5' termini demonstrating the necessity of multiply modifying phosphodiester linkages at each end of the molecule. A stretch of at least six consecutive phosphodiester linkages is required to form an effective substrate for Xenopus RNase H; mRNA degradation with an oligonucleotide containing fewer than six contiguous unmodified internucleoside linkages is greatly diminished. Injection of an anti-cyclin B oligonucleotide containing eight unmodified residues results in degradation of cyclin B mRNAs and subsequent inhibition of embryonic cell division. An oligonucleotide with the same sequence but containing four consecutive phosphodiesters has no observable effect on the cell cycle. This last observation suggests that, in Xenopus embryos, hybridization alone has a limited role, if any, in oligonucleotide-mediated inhibition of gene expression.

Animals↗
PubMed2006

Chromokinesin Xklp1 contributes to the regulation of microtubule density and organization during spindle assembly.

Xklp1 is a chromosome-associated kinesin required for Xenopus early embryonic cell division. Function blocking experiments in Xenopus egg extracts suggested that it is required for spindle assembly. We have reinvestigated Xklp1 function(s) by monitoring spindle assembly and microtubule behavior under a range of Xklp1 concentrations in egg extracts. We found that in the absence of Xklp1, bipolar spindles form with a reduced efficiency and display abnormalities associated with an increased microtubule mass. Likewise, centrosomal asters assembled in Xklp1-depleted extract show an increased microtubule mass. Conversely, addition of recombinant Xklp1 to the extract reduces the microtubule mass associated with spindles and asters. Our data suggest that Xklp1 affects microtubule polymerization during M-phase. We propose that these attributes, combined with Xklp1 plus-end directed motility, contribute to the assembly of a functional bipolar spindle.

Animals↗
PubMed2005

The terminal phase of cytokinesis in the Caenorhabditis elegans early embryo requires protein glycosylation.

RNA interference (RNAi) was used to characterize the requirement of protein glycosylation for cell membrane stability during cytokinesis in the early embryo. This screen targeted 13 enzymes or components of polypeptide sugar transferases that initiate either N-glycosylation or three different pathways of O-glycosylation. RNAi of genes in the mucin-type and epidermal growth factor-fringe glycosylation pathways did not affect cytokinesis. However, embryos deficient in N-glycosylation exhibited a variable inability to complete cytokinesis. The most potent block in early embryonic cell division was obtained by RNAi of the polypeptide xylose transferase (ppXyl-T), which is required to initiate the proteoglycan modification pathway. Two generations of ppXyl-T RNAi-feeding treatment reduced the body size, mobility, brood size, and life span of adult animals. Embryos escaping ppXyl-T and Gal-T2 RNAi lethality develop to adulthood but have cytokinesis-deficient offspring, suggesting that glycosyltransferases in the proteoglycan pathway are maternal proteins in the early embryo. Gal-T2::GFP fusions and anti-Gal-T2 antibodies revealed a perinuclear staining pattern, consistent with the localization of the Golgi apparatus. RNAi in green fluorescent protein (GFP)-tagged strains to follow tubulin, PIE-1, and chromatin showed that deficient proteoglycan biosynthesis uncouples the stability of newly formed cell membranes from cytokinesis, whereas cleavage furrow initiation, mitotic spindle function, karyokinesis, and partitioning of intrinsic components are intact.

Amino Acid Sequence↗
PubMed1999

Identification of XDRP1; a Xenopus protein related to yeast Dsk2p binds to the N-terminus of cyclin A and inhibits its degradation.

Using the N-terminus of cyclin A1 in a two-hybrid screen as a bait, we identified a Xenopus protein, XDRP1, that contains a ubiquitin-like domain in its N-terminus and shows significant homology in its C-terminal 50 residues to Saccharomyces cerevisiae Dsk2 and Schizosaccharomyces pombe dph1. XDRP1 is a nuclear phosphoprotein in Xenopus cells, and its phosphorylation is mediated by cyclin A-dependent kinase. XDRP1 binds to both embryonic and somatic forms of cyclin A (A1 and A2) in Xenopus cells, but not to B-type cyclins. The N-terminal ubiquitin-like domain of XDRP1, but not the C-terminal Dsk2-like domain, is required for interaction with cyclin A. XDRP1 requires residues 130-160 of cyclin A1 for efficient binding, which do not include the destruction box of cyclin A. The addition of bacterially expressed XDRP1 protein to frog egg extract inhibited the Ca(2+)-induced degradation of cyclin A, but not that of cyclin B. The injection of XDRP1 protein into fertilized Xenopus eggs blocked embryonic cell division.

Amino Acid Sequence↗
PubMed1995

Genetic characterization of ms (3) K81, a paternal effect gene of Drosophila melanogaster.

The vast majority of known male sterile mutants of Drosophila melanogaster fail to produce mature sperm or mate properly. The ms(3) K81(1) mutation is one of a rare class of male sterile mutations in which sterility is caused by developmental arrest after sperm entry into the egg. Previous studies showed that males homozygous for the K81(1) mutation produce progeny that arrest at either of two developmental stages. Most embryos arrest during early nuclear cycles, whereas the remainder are haploid embryos that arrest at a later stage. This description of the mutant phenotype was based on the analysis of a single allele isolated from a natural population. It was therefore unclear whether this unique paternal effect phenotype reflected the normal function of the gene. The genetic analysis and initial molecular characterization of five new K81 mutations are described here. Hemizygous conditions and heteroallelic combinations of the alleles were associated with male sterility caused by defects in embryogenesis. No other mutant phenotypes were observed. Thus, the K81 gene acted as a strict paternal effect gene. Moreover, the biphasic pattern of developmental arrest was common to all the alleles. These findings strongly suggested that the unusual embryonic phenotype caused by all five new alleles was due to loss of function of the K81+ gene. The K81 gene is therefore the first clear example of a strict paternal effect gene in Drosophila. Based on the embryonic lethal phenotypes, we suggest that the K81+ gene encodes a sperm-specific product that is essential for the male pronucleus to participate in the first few embryonic nuclear divisions.

Alleles↗
PubMed1997

Calmodulin point mutations affect Drosophila development and behavior.

Calmodulin (CAM) is recognized as a major intermediary in intracellular calcium signaling, but as yet little is known of its role in developmental and behavioral processes. We have generated and studied mutations to the endogenous Cam gene of Drosophila melanogaster that change single amino acids within the protein coding region. One of these mutations produces a striking pupal lethal phenotype involving failure of head eversion. Various mutant combinations produce specific patterns of ectopic wing vein formation or melanotic scabs on the cuticle. Anaphase chromosome bridging is also seen as a maternal effect during the early embryonic nuclear divisions. In addition, specific behavioral defects such as poor climbing and flightlessness are detected among these mutants. Comparisons with other Drosophila mutant phenotypes suggests potential CAM targets that may mediate these developmental and behavioral effects, and analysis of the CAM crystal structure suggests the structural consequences of the individual mutations.

Alleles↗