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PubMed1994

Effect of 3H decays on DNA partition during cell division.

Normal human embryonic lung fibroblasts were grown in the presence of different concentrations of tritium-labeled thymidine ([3H]dThd) for various periods of time, and the flow of cells from metaphase to anaphase was followed. Mitotic indices were evaluated as a function of the percentage of cells in metaphase and anaphase. They revealed that the presence of [3H]dThd induces a disturbance of the metaphase-anaphase transition. The DNA content of cells in metaphase and anaphase was measured with cytophotometry after the cells were grown in the presence of the radioactive precursor. It was found that the latter interfered with the flow of cells from metaphase to anaphase, impairing the symmetric distribution of DNA between daughter cells.

Anaphase↗
PubMed2000

Disruption of the murine calpain small subunit gene, Capn4: calpain is essential for embryonic development but not for cell growth and division.

Calpains are a family of Ca(2+)-dependent intracellular cysteine proteases, including the ubiquitously expressed micro- and m-calpains. Both mu- and m-calpains are heterodimers, consisting of a distinct large 80-kDa catalytic subunit, encoded by the genes Capn1 and Capn2, and a common small 28-kDa regulatory subunit (Capn4). The physiological roles and possible functional distinctions of mu- and m-calpains remain unclear, but suggested functions include participation in cell division and migration, integrin-mediated signal transduction, apoptosis, and regulation of cellular control proteins such as cyclin D1 and p53. Homozygous disruption of murine Capn4 eliminated both mu- and m-calpain activities, but this did not affect survival and proliferation of cultured embryonic stem cells or embryonic fibroblasts, or the early stages of organogenesis. However, mutant embryos died at midgestation and displayed defects in the cardiovascular system, hemorrhaging, and accumulation of erythroid progenitors.

Animals↗
PubMed1986

C-myc expression is dissociated from DNA synthesis and cell division in Xenopus oocyte and early embryonic development.

The combined use of a human c-myc probe and of an antibody raised against the human c-myc gene product demonstrated that the Xenopus cells contained a 2.5-kb c-myc transcript and synthesized a c-myc immunoreactive 65-kd polypeptide. In full-grown oocytes, p65c-myc was predominantly located in the nucleus. In non-dividing Xenopus oocytes c-myc mRNA was present at a steady-state level 10(4) times higher than that of growing somatic A6 cells. This very high level of c-myc transcript was reached early in oogenesis and remained constant thereafter. The rate of p65c-myc synthesis also reached high levels, but only in vitellogenic oocytes, suggesting a post-transcriptional control. Although the cell cycle is resumed at a very fast pace in developing embryos, no further increase in total embryonic content of c-myc RNA could be demonstrated up to the swimming tadpole stage. Furthermore, in embryos the rate of synthesis of p65c-myc decreased to a level markedly lower than that of cell cycle-arrested vitellogenic oocytes. This observation suggests that the function of the c-myc gene in the cell cycle may not be implicated directly in sustaining DNA synthesis or mitosis.

Animals↗
PubMed1986

Development of cell and fiber lamination in the mouse superior colliculus.

The emergence of laminar organization in the superior colliculus was investigated in the mouse with several anatomical methods, including tritiated-thymidine autoradiography, Golgi impregnation, and general stains for cell bodies and for fibers. The sequence of neurogenesis, cell migration, and early morphological differentiation of neurons was shown to exhibit a discontinuity between the lower and upper divisions (i.e., between the deep and intermediate "gray" and "white" layers and the superficial "gray" and "white" layers). These events proceed in an inside-out order within the lower division, but the same events within the upper division commence in advance of the completion of this progression. Thus, peak generation times for layers of the lower division proceed from (embryonic day) E11 to E13 and for the upper division from E12 to E13. Cell migration, as monitored with tritiated-thymidine labelling, reflects closely the pattern of cytogenesis. This is most clearly evident on E15 when a population of E11-labelled cells is divided into superficial and deep layers (the strata superficiale and profundum--SS and SP) by the interposition of E13-labelled cells at an intermediate level (stratum intermedium--SI). A contingent of the latter cells continue their migration and join their predecessors within the SS on E17, a time point when cell migrations are largely complete. Paralleling this sequence of arrival of neurons and the formation of three primary layers, both the time course of accumulation of fiber fascicles and the early morphological differentiation of neurons in the interval from E13 to E17 tends to proceed from SP to SS and from SS to SI. Thus, the transverse fiber system and large multipolar neurons of SP develop in advance of the longitudinal fiber system and vertically oriented neurons of SS, which in turn develop precociously with respect to the longitudinal fibers and medium-sized multipolar neurons of SI. In contrast, later events of differentiation that underly a major radial growth and an architectonic sublamination of the primary strata proceed in a simpler inside-out sequence from E17 to (postnatal day) P6. The major morphogenetic events underlying the establishment of statification in the colliculus appear to involve the operation of relatively independent programs of assembly for the two basic subdivisions. It is probable that selective cell-cell interactions contribute to the delivery of concurrently generated neurons to different laminae as well as to the deployment of axons in a manner that respects laminar boundaries.

Animals↗
PubMed2000

DNA replication defects delay cell division and disrupt cell polarity in early Caenorhabditis elegans embryos.

In early Caenorhabditis elegans embryos, asymmetric cell divisions produce descendants with asynchronous cell cycle times. To investigate the relationship between cell cycle regulation and pattern formation, we have identified a collection of embryonic-lethal mutants in which cell divisions are delayed and cell fate patterns are abnormal. In div (for division delayed) mutant embryos, embryonic cell divisions are delayed but remain asynchronous. Some div mutants produce well-differentiated cell types, but they frequently lack the endodermal and mesodermal cell fates normally specified by a transcriptional activator called SKN-1. We show that mislocalization of PIE-1, a negative regulator of SKN-1, prevents the specification of endoderm and mesoderm in div-1 mutant embryos. In addition to defects in the normally asymmetric distribution of PIE-1, div mutants also exhibit other losses of asymmetry during early embryonic cleavages. The daughters of normally asymmetric divisions are nearly equal in size, and cytoplasmic P-granules are not properly localized to germline precursors in div mutant embryos. Thus the proper timing of cell division appears to be important for multiple aspects of asymmetric cell division. One div gene, div-1, encodes the B subunit of the DNA polymerase alpha-primase complex. Reducing the function of other DNA replication genes also results in a delayed division phenotype and embryonic lethality. Thus the other div genes we have identified are likely to encode additional components of the DNA replication machinery in C. elegans.

Amino Acid Sequence↗
PubMed1996

A non-muscle myosin required for embryonic polarity in Caenorhabditis elegans.

Daughter cells with distinct fates can arise through intrinsically asymmetrical divisions. Before such divisions, factors crucial for determining cell fates become asymmetrically localized in the mother cell. In Caenorhabditis elegans, PAR proteins are required for the early asymmetrical divisions that establish embryonic polarity, and are asymmetrically localized in early blastomeres, although the mechanism of their distribution is not known. Here we report the identification in C. elegans of nonmuscle myosin II heavy chain (designated NMY-2) by means of its interaction with the PAR-1 protein, a putative Ser/Thr protein kinase. Furthermore, injections of nmy-2 antisense RNA into ovaries of adult worms cause embryonic partitioning defects and lead to mislocalization of PAR proteins. We therefore conclude the NMY-2 is required for establishing cellular polarity in C. elegans embryos.

Animals↗
PubMed2005

Drosophila neural progenitor polarity and asymmetric division.

In the Drosophila embryonic central nervous system, the neural precursor cells called neuroblasts undergo a number of asymmetric divisions along the apical-basal axis to give rise to different daughter cells of distinct fates. This review summarizes recent progress in understanding the mechanisms of these asymmetric cell divisions. We discuss proteins that are localized at distinct domains of cortex in the neuroblasts and their role in generating asymmetry. We also review uniformly cortical localized factors and actin cytoskeleton-associated motor proteins with regard to their potential role to serve as a link between distinct cortical domains in the neuroblasts. In this review, asymmetric divisions of sensory organ precursor and larval neuroblasts are also briefly discussed.

Animals↗
PubMed2000

Regulation of proliferation of the fetal myocardium.

Growth of the myocardium involves the completion of a fixed number of rounds of cell division during the embryonic and fetal stages followed by entry into a postmitotic state and hypertrophy of the postmitotic cardiomyocytes during the later stages of heart growth. It has been suggested that at the time of its determination in the early embryo, the embryonic myocardium is programmed for a fixed and limited number of cell divisions, after which the transition to the postmitotic state occurs autonomously. The proliferative response of cultured myocardium of the fetal chick was explored in four culture settings: monolayer cell culture, collagen lattice culture, organ culture of reaggregated cardiomyocyte tissue (cardiomyocyte spheroid culture), and organ culture of pieces of the ventricle wall. Several growth factors were identified by their ability to stimulate DNA synthesis in cardiomyocytes, identified by the incorporation of 5-bromodeoxyuridine (BrdU). The serine proteases thrombin and trypsin, fibroblast growth factor-2 (FGF-2), transforming growth factor-alpha (TGF-alpha), and insulin-like growth factor-II (IGF-II) all show growth factor activity but only for cardiomyocytes cultured in three-dimensional myocardial tissue, and not for cardiomyocytes maintained in monolayer cell culture. Thus, during its proliferation phase, the growth of the fetal myocardium is not controlled solely by internal, cell-autonomous programs, but is subject to external regulation by a family of peptide growth factors. The unconventional setting of three-dimensional culture of the myocardium is required to demonstrate its responsiveness to growth factor challenge.

Animals↗
PubMed2003

Chondroitin proteoglycans are involved in cell division of Caenorhabditis elegans.

Glycosaminoglycans such as heparan sulphate and chondroitin sulphate are extracellular sugar chains involved in intercellular signalling. Disruptions of genes encoding enzymes that mediate glycosaminoglycan biosynthesis have severe consequences in Drosophila and mice. Mutations in the Drosophila gene sugarless, which encodes a UDP-glucose dehydrogenase, impairs developmental signalling through the Wnt family member Wingless, and signalling by the fibroblast growth factor and Hedgehog pathways. Heparan sulphate is involved in these pathways, but little is known about the involvement of chondroitin. Undersulphated and oversulphated chondroitin sulphate chains have been implicated in other biological processes, however, including adhesion of erythrocytes infected with malaria parasite to human placenta and regulation of neural development. To investigate chondroitin functions, we cloned a chondroitin synthase homologue of Caenorhabditis elegans and depleted expression of its product by RNA-mediated interference and deletion mutagenesis. Here we report that blocking chondroitin synthesis results in cytokinesis defects in early embryogenesis. Reversion of cytokinesis is often observed in chondroitin-depleted embryos, and cell division eventually stops, resulting in early embryonic death. Our findings show that chondroitin is required for embryonic cytokinesis and cell division.

Animals↗
PubMed2000

Embryonic polarity: protein stability in asymmetric cell division.

Recent work on pattern formation in Caenorhabditis elegans has uncovered a new mechanism of asymmetric cell division: the cytoplasm is polarized by cortical proteins, and this polarization then influences the stability of other maternally expressed proteins that in turn determine early embryonic cell fates.

Animals↗
PubMed1976

Changes in type of collagen synthesized as clones of chick chondrocytes grow and eventually lose division capacity.

Clones of embryonic chick chondrocytes have been isolated and collagen biosynthesis has been followed as the clones grow and eventually lose division capacity. Analysis of collagen type at each successive subculture until the time of cellular senescence has shown that a change in synthesis occurs from the cartilage-specific Type II collagen (chain composition [alpha1(II)]3) to a mixture of Type I collagen (chain composition [alpha1(I)2alpha2) and the Type I trimer (chain composition[alpha1(I)]3). The results demonstrate unequivocally that the expression of the chick chondrocyte phenotype is unstable in vitro, and that previous experiments with mass cultures of chondrocytes cannot be accounted for by overgrowth of fibroblasts. Since similar morphological changes and a similar "switching" in collagen biosynthesis have been observed after growth of chondrocytes for a few days in 5-bromo-2'-deoxyuridine, it is proposed that growth in this analog accelerates those changes that eventually lead to cellular senescence.

Aging↗
PubMed2003

Cystic partially differentiated nephroblastoma, embryonal rhabdomyosarcoma, and multiple congenital anomalies associated with variegated mosaic aneuploidy and premature centromere division: a case report.

A rare association of embryonal genitourinary tumor(s) with cerebral malformations has been reported in eight infants with variegated mosaic aneuploidy (VMA) and premature centromere division. The authors report a new case of cystic partially differentiated nephroblastoma and embryonal rhabdomyosarcoma associated with VMA, premature centromere division, microcephalus, Dandy-Walker malformation, and cataracts. Nonrandom involvement of the chromosomes was found in VMA of the lymphocytes and the skin fibroblasts. In the cultured nephroblastoma cells, hyperdiploidy involving the same group of chromosomes involved in VMA of the somatic cells was observed, suggesting their derivation from the aneuploid population of the somatic cells.

Abnormalities, Multiple↗
PubMed1987

The establishment of the embryonic-abembryonic axis in the mouse embryo.

The influence of cell division order on the establishment of the embryonic-abembryonic axis (EA axis) of the mouse embryo was investigated. Aggregate embryos were constructed in which a labelled cell (or pair of cells) was combined with a group of unlabelled cells all of which were up to one cell cycle earlier or later in their progress through development to the blastocyst stage. The aggregates were cultured first to the nascent blastocyst stage and then to the expanded blastocyst stage. The positions of the progeny of the labelled cells in relation to the nascent blastocoel and to the orientation of the embryonic-abembryonic axis were recorded. It was concluded that cell division order does influence the establishment of the EA axis, early dividing cells tending to be associated with the nascent blastocoel and the site of the nascent blastocoel tending to mark the site of the abembryonic pole. However, the influence of division order was diminished by a requirement for intercellular cooperation during blastocoel formation and by a counteracting influence of division order arising from its effects on the allocation of cells to the inner cell mass.

Animals↗
PubMed1984

Analysis of cell division by time-lapse cinematographic studies of hydrocortisone-treated embryonic lung fibroblasts.

Hydrocortisone is a modulator of cell division and has been shown to prolong the replicative in vitro life span of human embryonic lung fibroblasts. Time lapse cinematography was used to analyze the proliferative behavior of individual cells in populations of fibroblasts exposed to hydrocortisone in young cultures during a single growth cycle and in aged cultures that had been continuously exposed to hydrocortisone. Results indicate that hydrocortisone causes a decrease in the interdivision time (IDT) of a portion of the cells in the population and this effect is augmented after continuous exposure to hydrocortisone. Hydrocortisone does not appear to increase the number of initial dividers in the population but increases growth rate in the early stages of the culture period. Analysis of mother-daughter IDT pairs further suggests that hydrocortisone exerts its effects on IDT independently for a given cell.

Cell Cycle↗
PubMed1981

Evidence for regulation of growth, size and pattern in the developing chick limb bud.

This paper examines the hypothesis that the developing chick limb bud has mechanisms for regulating the control of growth, size and pattern. The tests included: surgical removal of selected parts of the limb field, X-irradiation, temperature shock and the manipulation of known limb organizer regions (removal of the apical ectodermal ridge, or the addition of an extra zone of polarizing activity). The results strongly support the idea that there are regulatory mechanisms controlling both the pattern and the size of the limb and suggest that they involve regulation of the growth rate via control of cell division throughout the embryonic period. Possible mechanisms are discussed.

Animals↗
PubMed1998

The time-pattern of rises and falls in proliferation fades with senescence of mortal lines and is perpetuated in immortal rat hepatoma Fao cell line.

Immortal cells perpetuate the rises and falls of proliferation that are progressively damped in mortal long-term cultured cells. For immortal rat hepatoma Fao cells, similar waves of proliferation occurred about every 3-4 wk. Under the same conditions, embryonic human fibroblasts and transformed but not immortalized embryonic fibroblasts display similarly recurring proliferation waves that progressively decrease in amplitude until senescence of the lines. In addition, strains of diploid normal human skin fibroblasts cultured under different culture conditions display a similar time-pattern of proliferation. Although the amplitude and baseline of these fluctuations are characteristic for each cell line, a common point was marked slow down in proliferation after every sequence of about 25 population doublings for all cells. Renewed proliferation waves of Fao cells allow about 22-23 additional population doublings each. Normal embryonic fibroblast culture and its transformed counterpart accumulate about 30 and 60 population doublings, respectively, before senescence. Normal fibroblast strains accumulate about 25 population doublings over their entire life spans. This halt in proliferation after every stretch of about 25 population doublings may correspond to a structural or functional stop following attrition of telomeric DNA. This putative stop may be bypassed once in transformed embryonic cells and repetitively in immortal cells. In support of this hypothesis, we observed rapid telomere shortening, in two steps, during divisions of mortal embryonic cells, and maintenance of long telomeres in immortal Fao cells, which may indicate episodic repair of telomeres. Alternatively, such maintenance of long telomeres may reflect survival and successive clonal growth of rare cells with long telomeres. We suggest that the balance between telomere attrition and repair processes regulates the waves of proliferation.

Animals↗