Maintenance of sister-chromatid cohesion at the centromere by the <i>Drosophila</i> MEI-S332 protein

Tang, Tracy Tzu-Ling; Bickel, Sharon E.; Young, Lynn; Orr‐Weaver, Terry L.

doi:10.1101/gad.12.24.3843

Cited by 108 publications

(110 citation statements)

References 31 publications

(45 reference statements)

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“…Cohesin binds densely to pericentric heterochromatin, and cohesin at centromeres is protected in both mitotic and meiotic cells by a member of the Shugoshin/Mei-S332 protein family (Kitajima et al 2004;McGuinness et al 2005;Salic et al 2004;Tang et al 1998Tang et al , 2004. Although Nipped-B completely colocalizes with Smc1 and Smc3 along meiotic chromosome cores, we did not see Nipped-B staining around the centromeres, where cohesin staining is the strongest.…”

Section: Does Nipped-b Regulate Cohesin Function At Centromeres?contrasting

confidence: 58%

Functional links between Drosophila Nipped-B and cohesin in somatic and meiotic cells

et al. 2007

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Drosophila Nipped-B is an essential protein that has multiple functions. It facilitates expression of homeobox genes and is also required for sister chromatid cohesion. Nipped-B is conserved from yeast to man, and its orthologs also play roles in deoxyribonucleic acid repair and meiosis. Mutation of the human ortholog, Nipped-B-Like (NIPBL), causes Cornelia de Lange syndrome (CdLS), associated with multiple developmental defects. The Nipped-B protein family is required for the cohesin complex that mediates sister chromatid cohesion to bind to chromosomes. A key question, therefore, is whether the Nipped-B family regulates gene expression, meiosis, and development by controlling cohesin. To gain insights into Nipped-B's functions, we compared the effects of several Nipped-B mutations on gene expression, sister chromatid cohesion, and meiosis. We also examined association of Nipped-B and cohesin with somatic and meiotic chromosomes by immunostaining. Missense Nipped-B alleles affecting the same HEAT repeat motifs as CdLS-causing NIPBL mutations have intermediate effects on both gene expression and mitotic chromatid cohesion, linking these two functions and the role of NIPBL in human development. Nipped-B colocalizes extensively with cohesin on chromosomes in both somatic and meiotic cells and is present in soluble complexes

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Section: Does Nipped-b Regulate Cohesin Function At Centromeres?contrasting

confidence: 58%

Functional links between Drosophila Nipped-B and cohesin in somatic and meiotic cells

et al. 2007

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“…Protein extracts were made by homogenizing embryos (1-2 hours) or dissected tissues in urea sample buffer (Tang et al, 1998). Proteins were transferred to nitrocellulose for immunoblotting using standard techniques.…”

Section: Protein Extracts and Immunoblotsmentioning

confidence: 99%

no polesencodes a predicted E3 ubiquitin ligase required for early embryonic development ofDrosophila

et al. 2009

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In a screen for cell-cycle regulators, we identified a Drosophilamaternal effect-lethal mutant that we named `no poles'(nopo). Embryos from nopo females undergo mitotic arrest with barrel-shaped, acentrosomal spindles during the rapid S-M cycles of syncytial embryogenesis. We identified CG5140, which encodes a candidate RING domain-containing E3 ubiquitin ligase, as the nopogene. A conserved residue in the RING domain is altered in our EMS-mutagenized allele of nopo, suggesting that E3 ligase activity is crucial for NOPO function. We show that mutation of a DNA checkpoint kinase, CHK2,suppresses the spindle and developmental defects of nopo-derived embryos, revealing that activation of a DNA checkpoint operational in early embryos contributes significantly to the nopo phenotype. CHK2-mediated mitotic arrest has been previously shown to occur in response to mitotic entry with DNA damage or incompletely replicated DNA. Syncytial embryos lacking NOPO exhibit a shorter interphase during cycle 11, suggesting that they may enter mitosis prior to the completion of DNA replication. We show that Bendless (BEN), an E2 ubiquitin-conjugating enzyme, interacts with NOPO in a yeast two-hybrid assay; furthermore, ben-derived embryos arrest with a nopo-like phenotype during syncytial divisions. These data support our model that an E2-E3 ubiquitination complex consisting of BEN-UEV1A (E2 heterodimer) and NOPO (E3 ligase) is required for the preservation of genomic integrity during early embryogenesis.

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“…The chromosome morphology of nurse cells was examined after 4Ј,6-diamidino-2-phenylindole (DAPI) or propidium iodide staining as described (16). Mitotic spindles were examined in embryos after staining with rat anti-␣-tubulin antibodies from Accurate Chemical and Accurate Scientific (Westbury, NY) as described by Tang et al (22), except that the embryos were fixed in methanol. Anti-cyclin B staining of egg chambers was done as previously described (16).…”

Section: Immunostaining Of Ovaries and Embryosmentioning

confidence: 99%

The anaphase promoting complex/cyclosome is required during development for modified cell cycles

Kashevsky

Wallace

Reed

et al. 2002

Proc. Natl. Acad. Sci. U.S.A.

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Animals and plants use modified cell cycles to achieve particular developmental strategies. In one common example, most animals and plants have tissues in which the cells become polyploid or polytene by means of an S-G cycle, but the mechanism by which mitosis is inhibited in the endo cycle is not understood. The Drosophila morula (mr) gene regulates variant cell cycles, because in addition to disrupting the archetypal cycle (G 1-S-G2-M), mr mutations affect the rapid embryonic (S-M) divisions as well as the endo cycle (S-G) that produces polyploid cells. In dividing cells mr mutations cause a metaphase arrest, and endo cycling nurse cells inappropriately reenter mitosis in mr mutants. We show mr encodes the APC2 subunit of the anaphase promoting complex͞ cyclosome. This finding demonstrates that anaphase promoting complex͞cyclosome is required not only in proliferating cells but also to block mitosis in some endo cycles. The mr mutants further indicate that transient mitotic functions in endo cycles change chromosome morphology from polytene to polyploid.

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Maintenance of sister-chromatid cohesion at the centromere by the Drosophila MEI-S332 protein

Cited by 108 publications

References 31 publications

Functional links between Drosophila Nipped-B and cohesin in somatic and meiotic cells

Functional links between Drosophila Nipped-B and cohesin in somatic and meiotic cells

no polesencodes a predicted E3 ubiquitin ligase required for early embryonic development ofDrosophila

The anaphase promoting complex/cyclosome is required during development for modified cell cycles

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