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Andrew Chess – One of the best experts on this subject based on the ideXlab platform.
Asynchronous Replication and autosome pair non equivalence in human embryonic stem cellsPLOS ONE, 2009Co-Authors: Devkanya Dutta, Alexande W Ensminge, Jacob Zucke, Andrew ChessAbstract:
A number of mammalian genes exhibit the unusual properties of random monoallelic expression and random Asynchronous Replication. Such exceptional genes include genes subject to X inactivation and autosomal genes including odorant receptors, immunoglobulins, interleukins, pheromone receptors, and p120 catenin. In differentiated cells, random Asynchronous Replication of interspersed autosomal genes is coordinated at the whole chromosome level, indicative of chromosome-pair non-equivalence. Here we have investigated the Replication pattern of the random Asynchronously replicating genes in undifferentiated human embryonic stem cells, using fluorescence in situ hybridization based assay. We show that allele-specific Replication of X-linked genes and random monoallelic autosomal genes occur in human embryonic stem cells. The direction of Replication is coordinated at the whole chromosome level and can cross the centromere, indicating the existence of autosome-pair non-equivalence in human embryonic stem cells. These results suggest that epigenetic mechanism(s) that randomly distinguish between two parental alleles are emerging in the cells of the inner cell mass, the source of human embryonic stem cells.
monoallelic expression and Asynchronous Replication of p120 catenin in mouse and human cellsJournal of Biological Chemistry, 2005Co-Authors: Alexande A Gimelbra, Alexande W Ensminge, Jacob Zucke, Andrew ChessAbstract:
The number of autosomal mammalian genes subject to random monoallelic expression has been limited to genes highly specific to the function of chemosensory neurons or lymphocytes, making this phenomenon difficult to address systematically. Here we demonstrate that Asynchronous DNA Replication can be used as a marker for the identification of novel genes with monoallelic expression and identify p120 catenin, a gene involved in cell adhesion, as belonging to this class. p120 is widely expressed; its presence in available cell lines allowed us to address quantitative aspects of monoallelic expression. We show that the epigenetic choice of active allele is clonally stable and that biallelic clones express p120 at twice the level of monoallelic clones. Unlike previous reports about genes of this type, we found that expression of p120 can be monoallelic in one cell type and strictly biallelic in another. We show that in human lymphoblasts, the silencing of one allele is incomplete. These unexpected properties are likely to be wide-spread, as we show that the Tlr4 gene shares them. Identification of monoallelic expression of a nearly ubiquitous gene indicates that this type of gene regulation is more common than previously thought. This has important implications for carcinogenesis and definition of cell identity.
coordination of the random Asynchronous Replication of autosomal lociNature Genetics, 2003Co-Authors: Nandita Singh, Joos Gribnau, Farah A W Ebrahimi, Alexande A Gimelbra, Alexande W Ensminge, Michael Tacke, Andrew ChessAbstract:
Random monoallelic expression and Asynchronous Replication define an unusual class of autosomal mammalian genes. We show that every cell has randomly chosen either the maternal or paternal copy of each given autosome pair, such that alleles of these genes scattered across the chosen chromosome replicate earlier than the alleles on the homologous chromosome. Thus, chromosome-pair non-equivalence, rather than being limited to X-chromosome inactivation, is a fundamental property of mouse chromosomes.
Howard Ceda – One of the best experts on this subject based on the ideXlab platform.
programming Asynchronous Replication in stem cellsNature Structural & Molecular Biology, 2017Co-Authors: Hagi Masika, Margani Farago, Merav Hech, Reba Condiotti, Kirill Makedonski, Yosef Uganim, Tal Urstyncohe, Yehudi Ergma, Howard CedaAbstract:
Asynchronous Replication-timing patterns undergo programmed switching between maternal and paternal alleles in embryonic and adult stem cells.
Asynchronous Replication and allelic exclusion in the immune systemNature, 2001Co-Authors: Raul Mostoslavsky, Nandita Singh, Andrew Chess, Toyoaki Tenze, Enjami Reubinoff, Maya Goldmi, Chana Gabay, Sharo Elizu, Howard CedaAbstract:
The development of mature B cells involves a series of molecular decisions which culminate in the expression of a single light-chain and heavy-chain antigen receptor on the cell surface1,2. There are two alleles for each receptor locus, so the ultimate choice of one receptor type must involve a process of allelic exclusion. One way to do this is with a feedback mechanism that downregulates rearrangement after the generation of a productive receptor molecule3, but recent work suggests that monoallelic epigenetic changes may also take place even before rearrangement4. To better understand the basis for distinguishing between alleles, we have analysed DNA Replication timing. Here we show that all of the B-cell-receptor loci (μ, κ and λ) and the TCRβ locus replicate Asynchronously. This pattern, which is established randomly in each cell early in development and maintained by cloning, represents an epigenetic mark for allelic exclusion, because it is almost always the early-replicating allele which is initially selected to undergo rearrangement in B cells. These results indicate that allelic exclusion in the immune system may be very similar to the process of X chromosome inactivation.
Asynchronous Replication of imprinted genes is established in the gametes and maintained during developmentNature, 1999Co-Authors: Itama Simo, Toyoaki Tenze, Enjami Reubinoff, Dahlia Hillma, Joh R Mccarrey, Howard CedaAbstract:
Genomic imprinting is characterized by allele-specific expression of multiple genes within large chromosomal domains1 that undergo DNA Replication Asynchronously during S phase2,3. Here we show, using both fluorescence in situ hybridization analysis and S-phase fractionation techniques, that differential Replication timing is associated with imprinted genes in a variety of cell types, and is already present in the pre-implantation embryo soon after fertilization. This pattern is erased before meiosis in the germ line, and parent-specific Replication timing is then reset in late gametogenesis in both the male and female. Thus, Asynchronous Replication timing is established in the gametes and maintained throughout development, indicating that it may function as a primary epigenetic marker for distinguishing between the parental alleles.
Lydia Avivi – One of the best experts on this subject based on the ideXlab platform.
the aberrant Asynchronous Replication characterizing lymphocytes of cancer patients is erased following stem cell transplantationBMC Cancer, 2010Co-Authors: Arno Nagle, Samuel Cytro, Maya Mashevich, Avital Korensteinila, Lydia AviviAbstract:
Aberrations of allelic Replication timing are epigenetic markers observed in peripheral blood cells of cancer patients. The aberrant markers are non-cancer-type-specific and are accompanied by increased levels of sporadic aneuploidy. The study aimed at following the epigenetic markers and aneuploidy levels in cells of patients with haematological malignancies from diagnosis to full remission, as achieved by allogeneic stem cell transplantation (alloSCT).
Asynchronous Replication of alleles in genomes carrying an extra autosomeEuropean Journal of Human Genetics, 1999Co-Authors: Aliza Amiel, Elena Gabe, Avital Korenstei, Lydia AviviAbstract:
Transcriptional activity of genes appears to be highly related to their Replication timing; alleles showing the common biallelic mode of expression replicate highly synchronously, whereas those with a monoallelic mode of expression replicate Asynchronously. Here we used FISH to determine the level of synchronisation in Replication timing of alleles in amniotic fluid cells derived from normal foetuses and from those with either of the trisomies for autosomes 21, 18 or 13, or for sex chromosomes (47,XXX and 47,XXY). Two pairs of alleles, not associated with the extra chromosome, were studied in subjects with each trisomy and three in normal subjects. In cells derived from normal foetuses and from foetuses with sex chromosome trisomies, each pair of alleles replicated synchronously; yet these very same alleles replicated Asynchronously in cells derived from foetuses with trisomy for any of the three autosomes studied. The results suggest that the gross phenotypic abnormalities associated with an extra autosome are brought about not only by over-expression of genes present in three doses, but also by modifications in the expression of genes present in the normal two doses.
Asynchronous Replication of allelic loci in down syndromeEuropean Journal of Human Genetics, 1998Co-Authors: Aliza Amiel, Elena Gabe, Lydia Avivi, Moshe D FejgiAbstract:
We have used FISH to determine the level of synchronisation in Replication timing of four pairs of alleles, unrelated to chromosome 21 (p53, HER2, RB1, and c-myc), in foetal (amniotic fluid) cell samples of Down syndrome and in normal foetuses. All samples derived from the Down syndrome subjects showed large temporal differences in Replication timing, in contrast to the high level of synchrony shown in all samples of normal individuals. Thus, as judged by four independent loci which are not associated with chromosome 21, the additional chromosome in the Down syndrome genome induces changes in the Replication pattern of an allelic pair: from a synchronous pattern characteristic to concomitantly expressed alleles to an unsynchronised one shown by alleles displaying an allele-specific mode of expression.