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PubMed1994

Immunocytochemical and ultrastructural characterization of type 1 astrocytes and 0-2A lineage cells in long-term co-cultures.

We examined cultures of purified type 1 astrocytes and mixed glial co-cultures containing type 1 astrocytes and 0-2A lineage cells in media containing fetal calf serum at 5 days in vitro (DIV), 12 DIV, and 30 DIV, using cell-specific immunocytochemical markers and electron microscopy. At all three time points and in both culture systems, the polygonal-shaped type 1 astrocytes were A2B5-, GFAP+, and GalC-(specific markers for 0-2A lineage cells, and mature astrocytes and oligodendrocytes, respectively). From 5 to 30 DIV, the type 1 astrocytes increased markedly in size and the appearance of the cytoskeleton changed dramatically, with the amount of glial filaments increasing and microtubules decreasing. At 5, 12, and 30 DIV, the 0-2A lineage cells were multipolar, A2B5 +, HNK-1 +, GFAP-, and GalC-. The 0-2 lineage cells could not be distinguished as either astrocytes or oligodendrocytes on the basis of immunocytochemical or ultrastructural characteristics. These cells had dense cytoplasm, very few intermediate filaments, and a large number of vacuoles and dense bodies. The general characteristics of the cultured astrocytes at 12 DIV and 30 DIV were similar to mature and aged astrocytes in vivo, respectively. These findings suggest that the culture environment in this study accelerated aging of type 1 astrocytes. 0-2A lineage cells, on the other hand, appeared unable to differentiate into either type 2 astrocytes or oligodendrocytes when cultured in the presence of both type 1 astrocytes and fetal calf serum.

Animals↗

PubMedDate not supplied

Cell lineages generating axial muscle in the zebrafish embryo.

Cell lineage may contribute to determining the numbers, positions and types of cells formed during embryogenesis. In vitro clonal analyses show that vertebrate cells can autonomously maintain lineage commitments to single fates and that terminal development may include an invariant sequence of cell divisions. In addition, in vivo studies with Xenopus led to the proposal that clonal restrictions to spatial 'compartmental' domains arise during early development, analogous to what is observed in insects. In the zebrafish, individual gastrula cells generate clones of progeny that are confined within single tissues, but spatial restrictions have not been described. We now have examined the in vivo terminal cell lineages of zebrafish axial muscles. We obtained no evidence either for strict developmental regulation of division pattern or for spatial compartmentation within muscle lineages.

Animals↗

PubMed1995

p53 gene inactivation in acute lymphoblastic leukemia of B cell lineage associates with chromosomal breakpoints at 11q23 and 8q24.

The clinical heterogeneity of acute lymphoblastic leukemia (ALL) of B cell lineage reflects the presence of distinct molecular pathways leading to well-defined ALL molecular subtypes. These molecular pathways include the formation of the fusion transcripts BCR/ABL and E2A/PBX1, due to t(9;22) and t(1;19), respectively, as well as rearrangements of the MLL gene at 11q23 and of c-MYC at 8q24. Hyperdiploid ALL in the absence of chromosomal structural abnormalities is an additional ALL molecular subtype. Mutations of the RAS family genes and of the p53 tumor suppressor gene represent additional genetic lesions detected in a fraction (10-20%) of ALL cases. RAS activation in ALL may be detected in all molecular subtypes of ALL and denotes poor prognosis. Conversely, little is known regarding the clinical and biological features of ALL cases carrying p53 mutations. In order to help clarify the role of p53 inactivation in ALL development, we have determined the frequency of p53 mutations throughout the molecular spectrum of B cell lineage ALL. We report that p53 inactivation in ALL of B cell lineage is restricted to cases carrying a rearrangement of MLL or c-MYC, whereas it is consistently negative in other molecular subgroups. These data underline the molecular heterogeneity of ALL of B cell lineage and indicate that at least some of the molecular pathways involved in ALL pathogenesis require more than one genetic lesion.

Base Sequence↗

PubMed2003

Essential role for puma in development of postembryonic neural crest-derived cell lineages in zebrafish.

Multipotent neural crest stem cells have been identified in late gestation amniote embryos. Yet, significant questions remain about the mechanisms by which these cells are generated, maintained, and recruited during postembryonic development. The zebrafish, Danio rerio, offers an opportunity to identify genes essential for these processes, by screening for mutants with defects in traits likely to depend on these cells during metamorphosis and adult life. One such trait is the pigment pattern formed by neural crest-derived pigment cells, or chromatophores, which include black melanophores, yellow xanthophores, and iridescent iridophores. Previous analyses have demonstrated that the adult zebrafish pigment pattern depends on the de novo differentiation of latent precursor cells during both early and late phases of pigment pattern metamorphosis. To better understand the development of these cells, in this study, we analyze the zebrafish puma mutant, which ablates most of the adult melanophores that differentiate during metamorphosis, but leaves intact early larval melanophores that differentiate during embryogenesis. We use epistasis analyses to show that puma promotes the development of both early-appearing metamorphic melanophores that depend on the kit receptor tyrosine kinase, as well as late-appearing metamorphic melanophores that depend on both the G-protein-coupled endothelin receptor b1 (ednrb1) and the kit-related fms receptor tyrosine kinase. We further demonstrate that, during pigment pattern metamorphosis, puma mutants have deficiencies in the numbers of cells expressing transcripts for kit, ednrb1, and fms, as well as the HMG domain transcription factor sox10. Because the puma mutant phenotype is temperature-sensitive, we use temperature-shift experiments to identify a critical period for puma activity during pigment pattern metamorphosis. Finally, we use cell transplantations to show that puma acts cell-autonomously to promote the expansion of pigment cell lineages during metamorphosis. These results suggest a model for the lineage diversification of neural crest stem cells during zebrafish postembryonic development.

Animals↗

PubMed1987

A quantitative analysis of the human bone marrow erythroblastic cell lineage using the SAMBA 200 cell image processor. I. The normal maturation sequence.

A quantitative image analysis of the normal maturation sequence for the human bone marrow erythroblastic lineage was performed using the SAMBA 200 cell image processor. The different image analysis steps (image acquisition, preprocessing, segmentation, parametrization and data analysis) are briefly described. Thirty-three parameters related to geometry, color, texture and densitometry were computed on 638 cell images belonging to the five erythroblastic maturation stages. The automated classification of these cells, based upon a stepwise linear discriminant analysis, resulted in 80% correctly classified cells. Acceptance of confusions between successive maturation stages enhanced the rate of correctly classified cells to 100%. Among the ten most discriminating parameters, the nuclear area showed the highest correlation with the changes throughout the maturation process. The projection of the maturation sequence onto the factorial plane resulting from the canonical analysis emphasizes the existence of three phases of the maturation process, a finding that correlates well with the cytologic evolution and the biochemical and functional events during the maturation. The trajectory of cells within this factorial plane is thus regarded as a differentiation path from which a measure of the maturation could be derived.

Bone Marrow Cells↗

PubMed1993

Origin of murine B cell lineages.

Until recently, the hematopoietic stem cells (HSC) that appear early in ontogeny were thought to constitute a homogeneous, self-replenishing population whose developmental potential remains constant throughout the life of the animal. Studies reviewed here, however, demonstrated clear differences in the developmental potential of fetal and adult progenitor populations (including FACS-sorted HSC). These studies, which chart the ability of various progenitor sources to reconstitute functionally distinct B cell populations, define three B cell lineages: B-1a cells (CD5 B cells), derived from progenitors that are present in fetal omentum and fetal liver but are largely absent from adult bone marrow; B-1b cells ("sister" population), derived from progenitors that are present in fetal omentum, fetal liver, and also in adult bone marrow; and conventional B cells, whose progenitors are missing from fetal omentum but are found in fetal liver and adult bone marrow. B-1a and B-1b cells share many properties, including self-replenishment and feedback regulation of development. These B cell studies, in conjunction with evidence for a similar developmental switch for T cells and erythrocytes, suggest that evolution has created a "layered" immune system in which successive progenitors (HSC) reach predominance during development and give rise to differentiated cells (B, T, etc) responsible for progressively more complex immune functions.

Animals↗

PubMed2000

Establishment of the germ cell lineage in mammals.

The germ cell lineage in mice becomes lineage-restricted about 7.2 days postcoitum. Its progenitors have migrated from the proximal region of the epiblast. Cells from the distal region of the epiblast will also give rise to germ cells, if they are transplanted to the proximal region at the appropriate time. Cells in this region are subject to a predisposing signal from the adjacent extra-embryonic ectoderm. It appears that this and other signals determine the emergence of germ cells: unlike in some other organisms, this event is not predetermined.

Animals↗

PubMed2002

Molecular portraits of B cell lineage commitment.

In an attempt to characterize early B cell development including the commitment of progenitor cells to the B cell lineage, we generated and compared genomewide gene expression profiles of human hematopoietic stem cells (HSCs) and pre-B cells (PBCs) by using serial analysis of gene expression. From more than 100,000 serial analysis of gene expression tags collected from human CD34(+) HSCs and CD10(+) CD19(+) PBCs, 42,399 unique transcripts were identified in HSCs but only 16,786 in PBCs, suggesting that more than 60% of transcripts expressed in HSCs were silenced during or after commitment to the B cell lineage. On the other hand, mRNAs of pre-B cell receptor (pre-BCR)-associated genes are virtually missing in HSCs but account for more than 10% of the transcriptome of PBCs, which also show increased expression of apoptosis-related genes. Both concentration of the transcriptional repertoire on pre-BCR-related genes together with marked up-regulation of apoptosis mediators in PBC might reflect selection for the expression of a functional pre-BCR within the bone marrow. Besides known regulator genes of early B cell development such as PAX5, E2A, and EBF, the most abundantly expressed genes in PBCs include ATM, PDGFRA, SIAH1, PIM2, C/EBPB, WNT16, and TCL1, the role of which has not been established yet in early B cell development.

Antigens, CD↗

PubMed1983

Developmental autonomy of muscle fine structure in muscle lineage cells of ascidian embryos.

We have observed ultrastructural features of muscle differentiation in the muscle lineage cells of cleavage-arrested whole embryos and partial embryos of ascidians. Whole embryos of Ciona intestinalis and Ascidia ceratodes were cleavage-arrested with cytochalasin B at the 8-cell stage and reared to an age equivalent to several hours after hatching; these embryos formed extensive myofilaments which were often further organized into myofibrils of different sizes and densities in the peripheral cytoplasm of the two muscle lineage blastomeres (B4.1 pair). Developing myofibrils in cleavage-arrested embryos resembled the muscle elements observed in normal hatched larvae, but were less uniformly organized. A similar development of myofilaments and myofibrils occurred in the muscle lineage cells of multicellular partial embryos reared to "hatching" age. These partial embryos resulted from the isolated muscle lineage pair (B4.1) of blastomeres of the 8-cell stage (Ciona and Ascidia), and from a muscle lineage blastomere pair (B5.2) isolated at the 16-cell stage (Ascidia). Muscle lineage cells in the partial embryos were readily identified by the dense aggregates of mitochondria in their cytoplasm. Taken together, these results from the two kinds of partial embryo effectively eliminate inductive interactions with embryonic tissues other than mesodermal as a necessary factor in the onset of self-differentiation in muscle lineage cells. The relative complexity of muscle phenotype expressed in cleavage-arrested and partial embryos attests to an unusually strong developmental autonomy in the ascidian muscle lineages. This autonomy lends further support to the theory that a localized and segregated egg cytoplasmic determinant is responsible for larval muscle development in ascidian embryos.

Animals↗

PubMed1983

Quantitative regulation of acetylcholinesterase development in the muscle lineage cells of cleavage-arrested ascidian embryos.

Some embryos of Ciona intestinalis which were permanently cleavage-arrested with cytochalasin B at the 1-cell, 4-cell, or 8-cell stages produced, after 12 or 16 h of development time (18 degrees C), a level of muscle acetylcholinesterase activity equal to that found in normal early and later larval stage embryos of the same age. Enzyme activity was measured quantitatively in single whole embryos by a colorimetric procedure using microdensitometry. Quantitative regulation of a differentiation end product indicated that the usual transcriptional and translational control mechanisms for that histospecific protein continued to operate normally in the cleavage-arrested embryos. Acetylcholinesterase expression was apparently regulated independently of the usual cell cytoplasmic volume in the muscle lineage cells and possibly also independently of the normal nuclear number in the lineage. There is an egg cytoplasmic determinant that is segregated into the muscle lineage cells during cleavage and which appears to specify the pathway of larval muscle development. Quantitative control of muscle acetylcholinesterase is possibly one of the consequences of how the agent releases genetic expression in the presumptive muscle cells. Quantitative regulation was not, however, a general functional activity of cleavage-arrested embryos. Mitochondrial cytochrome oxidase, an enzyme whose development is believed to be unaffected by cytoplasmic determinants, was not regulated quantitatively in cleavage-arrested embryos. Cytochrome oxidase activity of cleavage-arrested embryos, measured in single whole embryos by a colorimetric microdensitometry assay, increased only slightly during 16 h of development time whereas the activity in normal control embryos doubled during that time.

Acetylcholinesterase↗

PubMed1994

Malignant lymphomas of B-cell lineage with marked tissue eosinophilia. A report of five cases.

Tissue eosinophilia is commonly seen in Hodgkin's disease and non-Hodgkin's lymphomas of T-cell lineage. In contrast, eosinophilia is infrequent in non-Hodgkin's lymphomas of B-cell origin. We describe five-B-cell lymphomas with exuberant tissue eosinophils. According to the Working Formulation, three were classified as large-cell immunoblastic, one as small lymphocytic lymphoma/chronic lymphocytic leukemia, and one as low-grade, not further subclassified, with features of monocytoid B-cell lymphoma. Immunophenotypic studies in each case revealed B-cell lineage; neoplastic cells expressed monotypic immunoglobulin light chain (four of five cases) or pan-B-cell antigens (five of five cases) and were negative for T-cell antigens. Southern blot hybridization in one case revealed immunoglobulin gene rearrangements, further confirming B-cell lineage. Eosinophilopoiesis is stimulated by interleukin 5 (IL-5), and Epstein-Barr virus (EBV) has been shown to upregulate IL-5 production. Therefore, both EBV infection and IL-5 expression were investigated as possibly pathogenetic mechanisms for the eosinophilia. However, both in situ hybridization studies for EBV mRNA and IL-5 mRNA were negative in the neoplastic cells. In one tumor, IL-5 was abundant in the cytoplasm of the eosinophils, a pattern similar to that seen in five cases of Hodgkin's disease studied with the same technique. Although rare, marked tissue eosinophilia may be associated with B-cell non-Hodgkin's lymphomas. Immunophenotypic or molecular genetic analyses are needed to make the correct diagnosis.

Adult↗

PubMed1999

Cytochemical localization of vanadium(III) in blood cells of ascidian Phallusia mammillata Cuvier, and its relevance to hematic cell lineage determination.

When the blood cells of ascidians Phallusia mammillata are stained with the ligand 2,2'-bipyridine, those cells which contain vanadium(III), in an easily sequestered form, take up the stain producing in situ, a purple complex. This material extracted displays spectral characteristics consistent with the formation of an oxo-bridge vanadium(III) bipyridine dimer. The staining is localized in the signet ring cell, a bivacuolated cell, a cell type with numerous darkly staining compartments, and also by the vacuolated amoebocyte. The possible ramifications of these observation are discussed in relation to the delineation of the signet ring cell lineage.

2,2'-Dipyridyl↗

PubMed2005

Identification of cell lineages involved by t(15;17) in acute promyelocytic leukemia by combined fluorescence activated cell sorting and FISH.

Bone marrow cells from five patients with acute promyelocytic leukemia (APL) with t(15;17) were studied by a combination of fluorescence activated cell sorting and fluorescence in situ hybridization (FISH) to establish the cell lineage involvement of t(15;17). Interphase FISH demonstrated that the fusion gene (PML/RARA) was present in almost all abnormal promyelocytes. In one case, the translocation was demonstrated in both CD34+ and CD34- APL cells. The t(15;17) abnormality was not detectable in erythroblasts nor in T- or B-lymphoid cells. These results suggest that lymphocytes and erythroblasts are not clonally involved in APL, and that malignant transformation in some cases of APL may occur at the level of CD34+ cells.

Adult↗

PubMed1995

Resident CD4+ alpha beta T cells of the murine female genital tract: a phenotypically distinct T cell lineage that rapidly proliferates in response to systemic T cell activation stimuli.

A population of CD4+ cells has been identified in the murine female genital tract (FGT). Phenotypic studies of FGT CD4+ cells demonstrate that they express CD3 and that the majority of these cells are alpha beta TCR+Thy-1+. Most of the Thy-1+CD4+alpha beta TCR+ cells resemble memory T cells based on their expression of CD44, L-selectin and CD45RB antigens. The vast majority of Thy-1+CD4+alpha beta TCR+ FGT cells are CD5+ and all of them are B220-. Systemic stimuli including infection with Trypanosoma brucei brucei, injection with anti-CD3 epsilon, or bacterial superantigens staphylococcal enterotoxin A or B cause a rapid accumulation of CD4+ cells in the FGT exceeding that observed for CD4+ cells in spleen and lymph nodes (LN). Expansion of the FGT CD4+ cells, which are phenotypically distinct from the splenic and LN CD4+ T cells, is due to local proliferation rather than an influx of cells from the circulation. The CD4+ population in the FGT of adult nu/nu mice is dramatically reduced, indicating its thymic dependency. In lpr/lpr mice, FGT CD4 cells do not display changes characteristic of splenic or LN CD4 cells in the same animals. These findings demonstrate that the CD4+ cells of the murine FGT are thymic dependent, but that they constitute a T cell lineage that phenotypically and, probably functionally, is distinct from other peripheral CD4+ T cell populations.

Animals↗

PubMed2005

[Differentiation and function of monocyte/macrophage lineage cells and osteoblasts].

Macrophages, osteoclasts and dendritic cells are derived from hematopoietic stem cells through monocyte/macrophage lineage common precursor cells. Macrophages are induced in the presence of M-CSF alone whereas osteoclasts are induced by M-CSF and RANKL. The cooperation of transcription factors, c-Fos and NFATc1 is essential for osteoclast differentiation. GM-CSF is an inducer of dendritic cells, and in contrast to osteoclast differentiation, M-CSF and c-Fos are inhibitors of dendritic cell differentiation. On the other hand, mesenchymal stem cells(MSCs) give rise to osteoblasts. In embryonic stage, MSCs in perichondrium are marked by ALCAM. Recently, osteoblasts are reported to provide 'Niche' for hematopoietic stem cells in bone marrow. Here we review the differentiation and functions of monocyte/macrophage lineage cells and osteoblasts.

Animals↗

PubMed2006

Matrix elasticity directs stem cell lineage specification.

Microenvironments appear important in stem cell lineage specification but can be difficult to adequately characterize or control with soft tissues. Naive mesenchymal stem cells (MSCs) are shown here to specify lineage and commit to phenotypes with extreme sensitivity to tissue-level elasticity. Soft matrices that mimic brain are neurogenic, stiffer matrices that mimic muscle are myogenic, and comparatively rigid matrices that mimic collagenous bone prove osteogenic. During the initial week in culture, reprogramming of these lineages is possible with addition of soluble induction factors, but after several weeks in culture, the cells commit to the lineage specified by matrix elasticity, consistent with the elasticity-insensitive commitment of differentiated cell types. Inhibition of nonmuscle myosin II blocks all elasticity-directed lineage specification-without strongly perturbing many other aspects of cell function and shape. The results have significant implications for understanding physical effects of the in vivo microenvironment and also for therapeutic uses of stem cells.

Biomarkers↗

PubMed1986

Cell lineage dependent and independent control of Purkinje cell number in the mammalian CNS: further quantitative studies of lurcher chimeric mice.

Recent quantitative studies of lurcher chimeric mice have shown that the adult population of cerebellar Purkinje cells can properly be described as a small number of developmental clones of cells. The clones are not seen as patches of contiguous neurons; rather, the cells of any one clone distribute throughout the half-cerebellum that contains them, intermingling extensively with the Purkinje cells of other linkages. Lurcher----wild-type chimeras were analyzed using the cell autonomous Purkinje-cell-lethal mutant, lurcher (+/Lc), as a cell marker. Cell counts from these chimeras revealed that the number of surviving Purkinje cells was always an integral multiple of a unit clone size. These numerical quanta are the evidence for the existence of Purkinje cell developmental clones. When two different inbred strains of mouse were compared (C3H/HeJ and C57BL/6), the resulting clonal analysis showed that the unit clone size (i.e., the number of Purkinje cells in one quantum) is an autonomous property of the lineage and hence, presumably, intrinsic to the progenitor cell that founded it. The current study uses the lurcher chimeric mouse system to examine the cell lineage relationships among the Purkinje cells of a third inbred strain of mouse, AKR/J. The data both support and extend our previous studies. Quantitative analysis reveals that the Purkinje cells of this strain also exist in clones, and the size of these clones is also strain-specific. The number of cells in a single clone (7850), however, is different from either C3H/HeJ (10,200) or C57BL/6 (9200). The fact that this value is so highly polymorphic among the inbred strains of mouse makes it likely that, rather than being a function of different alleles at a single genetic locus, clone size may well represent a multifactorial (but still cell-autonomous) property of developing Purkinje cells. Additional results from a single chimeric animal suggest strongly that clone number (i.e., the number of progenitors selected to found the population) is not strain-specific but results instead from cell:cell interactions during early nervous system formation.

Animals↗

PubMed2004

Separation of trophoblastic and vascular cell lineages and vascular maturation in early human placental development.

The trophoblast and vascular cell lineages have been studied by immunohistochemistry at 6 and 12-14 weeks of pregnancy. Perivillous and extravillous cytotrophoblasts were specifically stained by anti-cytokeratin 7 whereas endothelial cells were labelled by anti-CD34 at these two stages of pregnancy. Perivillous and extravillous cytotrophoblasts together with erythroblasts showed mitotic figures and anti-Ki67 positive nuclei at the 6th week. In the perivillous cytotrophoblast, the number of Ki67 positive nuclei decreased by 12-14 weeks and the staining was limited to the proximal extravillous trophoblast of cell islands. Some endothelial and perivascular cells were labelled with anti-Ki67 at 12-14 weeks. Erythroblasts did not stain at all at this stage. Endothelial cells bound lectin UEA1 and vessels exhibited a fluorescent signal after anti-myosin staining at 12-14 weeks. These data showed that the cytotrophoblast and endothelial cell lineages are not related from 6 to 12-14 weeks of pregnancy. Because mitotic figures or anti-Ki67 staining were not observed in endothelium or perivascular cells at the 6th week, it seems likely that the endothelial cells committed to vasculogenesis derived from stromal cells. By 12-14 weeks, endothelial cells had nearly achieved their maturation by acquiring 1-fucosyl-binding sites revealed by UEA1-lectin binding and insuring their own renewal by mitosis. The maturation of perivascular cells at 12-14 weeks was shown by the anti-sm-myosin staining. We conclude that placental vasculogenesis involves mesenchymal cells rather than trophoblast. The differenciation of vessels organizing from random plexi to a vascular arborescence may involve paracrine regulatory loops with the trophoblast.

Blood Vessels↗