Person: Joyce, Eric F.
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Joyce
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Eric F.
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Joyce, Eric F.
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Publication Identification of Genes That Promote or Antagonize Somatic Homolog Pairing Using a High-Throughput FISH–Based Screen(Public Library of Science, 2012) Joyce, Eric F.; Williams, Benjamin R.; Xie, Tiao; Wu, C.-tingThe pairing of homologous chromosomes is a fundamental feature of the meiotic cell. In addition, a number of species exhibit homolog pairing in nonmeiotic, somatic cells as well, with evidence for its impact on both gene regulation and double-strand break (DSB) repair. An extreme example of somatic pairing can be observed in Drosophila melanogaster, where homologous chromosomes remain aligned throughout most of development. However, our understanding of the mechanism of somatic homolog pairing remains unclear, as only a few genes have been implicated in this process. In this study, we introduce a novel high-throughput fluorescent in situ hybridization (FISH) technology that enabled us to conduct a genome-wide RNAi screen for factors involved in the robust somatic pairing observed in Drosophila. We identified both candidate “pairing promoting genes” and candidate “anti-pairing genes,” providing evidence that pairing is a dynamic process that can be both enhanced and antagonized. Many of the genes found to be important for promoting pairing are highly enriched for functions associated with mitotic cell division, suggesting a genetic framework for a long-standing link between chromosome dynamics during mitosis and nuclear organization during interphase. In contrast, several of the candidate anti-pairing genes have known interphase functions associated with S-phase progression, DNA replication, and chromatin compaction, including several components of the condensin II complex. In combination with a variety of secondary assays, these results provide insights into the mechanism and dynamics of somatic pairing.Publication Germline Progenitors Escape the Widespread Phenomenon of Homolog Pairing during Drosophila Development(Public Library of Science, 2013) Joyce, Eric F.; Apostolopoulos, N; Beliveau, Brian; Wu, C. -tingHomolog pairing, which plays a critical role in meiosis, poses a potential risk if it occurs in inappropriate tissues or between nonallelic sites, as it can lead to changes in gene expression, chromosome entanglements, and loss-of-heterozygosity due to mitotic recombination. This is particularly true in Drosophila, which supports organismal-wide pairing throughout development. Discovered over a century ago, such extensive pairing has led to the perception that germline pairing in the adult gonad is an extension of the pairing established during embryogenesis and, therefore, differs from the mechanism utilized in most species to initiate pairing specifically in the germline. Here, we show that, contrary to long-standing assumptions, Drosophila meiotic pairing in the gonad is not an extension of pairing established during embryogenesis. Instead, we find that homologous chromosomes are unpaired in primordial germ cells from the moment the germline can be distinguished from the soma in the embryo and remain unpaired even in the germline stem cells of the adult gonad. We further establish that pairing originates immediately after the stem cell stage. This pairing occurs well before the initiation of meiosis and, strikingly, continues through the several mitotic divisions preceding meiosis. These discoveries indicate that the spatial organization of the Drosophila genome differs between the germline and the soma from the earliest moments of development and thus argue that homolog pairing in the germline is an active process as versus a passive continuation of pairing established during embryogenesis.Publication Single-molecule super-resolution imaging of chromosomes and in situ haplotype visualization using Oligopaint FISH probes(Nature Pub. Group, 2015) Beliveau, Brian; Boettiger, Alistair; Avendaño, Maier S.; Jungmann, Ralf; McCole, Ruth; Joyce, Eric F.; Kim-Kiselak, Caroline; Bantignies, Frédéric; Fonseka, Chamith; Erceg, Jelena; Hannan, Mohammed; Hoang, Hien G.; Colognori, David; Lee, Jeannie; Shih, William; Yin, Peng; Zhuang, Xiaowei; Wu, Chao-tingFluorescence in situ hybridization (FISH) is a powerful single-cell technique for studying nuclear structure and organization. Here we report two advances in FISH-based imaging. We first describe the in situ visualization of single-copy regions of the genome using two single-molecule super-resolution methodologies. We then introduce a robust and reliable system that harnesses single-nucleotide polymorphisms (SNPs) to visually distinguish the maternal and paternal homologous chromosomes in mammalian and insect systems. Both of these new technologies are enabled by renewable, bioinformatically designed, oligonucleotide-based Oligopaint probes, which we augment with a strategy that uses secondary oligonucleotides (oligos) to produce and enhance fluorescent signals. These advances should substantially expand the capability to query parent-of-origin-specific chromosome positioning and gene expression on a cell-by-cell basis.Publication The Histone H4 Lysine 20 Monomethyl Mark, Set by PR-Set7 and Stabilized by L(3)mbt, Is Necessary for Proper Interphase Chromatin Organization(Public Library of Science, 2012) Sakaguchi, Ayako; Joyce, Eric F.; Aoki, Tsutomu; Schedl, Paul; Steward, RuthDrosophila PR-Set7 or SET8 is a histone methyltransferase that specifically monomethylates histone H4 lysine 20 (H4K20). L(3)MBT has been identified as a reader of methylated H4K20. It contains several conserved domains including three MBT repeats binding mono- and dimethylated H4K20 peptides. We find that the depletion of PR-Set7 blocks de novo H4K20me1 resulting in the immediate activation of the DNA damage checkpoint, an increase in the size of interphase nuclei, and drastic reduction of cell viability. L(3)mbt on the other hand stabilizes the monomethyl mark, as L(3)mbt-depleted S2 cells show a reduction of more than 60% of bulk monomethylated H4K20 (H4K20me1) while viability is barely affected. Ploidy and basic chromatin structure show only small changes in PR-Set7-depleted cells, but higher order interphase chromatin organization is significantly affected presumably resulting in the activation of the DNA damage checkpoint. In the absence of any other known functions of PR-Set7, the setting of the de novo monomethyl mark appears essential for cell viability in the presence or absence of the DNA damage checkpoint, but once newly assembled chromatin is established the monomethyl mark, protected by L(3)mbt, is dispensable.Publication Oligopaints: highly efficient, bioinformatically designed probes for fluorescence in situ hybridization(BioMed Central, 2013) Beliveau, Brian; Joyce, Eric F.; Apostolopoulosa, Nicholas; Yilmaza, Feyza; Fonseka, Chamith Y; McCole, Ruth; Chang, Yiming; Li, Jin Billy; Senaratne, Niroshi Niroshini; Williams, Benjamin R; Rouillard, Jean-Marie; Wu, Chao-ting