Autoradiographic study of protein and RNA formation during early development of Drosophila eggs

Zalokar, Marko

doi:10.1016/0012-1606(76)90185-8

Cited by 282 publications

(105 citation statements)

References 28 publications

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“…This cross is sterile, producing two classes of aneuploid progeny with respect to chromosome two: C(2)EN/2 individuals and 2/0 individuals. Because there is little gene expression during the initial embryonic divisions (McKnight and Miller, 1976;Zalokar, 1976;Anderson and Lengyel, 1981;Edgar and Schubiger, 1986;Merrill et al, 1988;Wieschaus and Sweeton, 1988), these aneuploid individuals can develop relatively normally through the syncytial divisions. We could distinguish between these two classes during the syncytial divisions because 2/0 embryos and C(2)EN/2 embryos possess one and three copies of the Kruppel gene, respectively.…”

Section: Resultsmentioning

confidence: 99%

Delays in anaphase initiation occur in individual nuclei of the syncytial Drosophila embryo.

Sullivan

Daily

Fogarty

et al. 1993

MBoC

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The syncytial divisions of the Drosophila melanogaster embryo lack some of the well established cell-cycle checkpoints. It has been suggested that without these checkpoints the divisions would display a reduced fidelity. To test this idea, we examined division error frequencies in individuals bearing an abnormally long and rearranged second chromosome, designated C(2)EN. Relative to a normal chromosome, this chromosome imposes additional structural demands on the mitotic apparatus in both the early syncytial embryonic divisions and the later somatic divisions. We demonstrate that the C(2)EN chromosome does not increase the error frequency of the late larva neuroblast divisions. However, in the syncytial embryonic nuclear divisions, the C(2)EN chromosome produces a 10-fold increase in division errors relative to embryos with a normal karyotype. During late anaphase of the neuroblast divisions, the sister C(2)EN chromosomes cleanly separate from one another. In contrast, during late anaphase of the syncytial divisions in C(2)EN-bearing nuclei, large amounts of chromatin often lag on the metaphase plate. Live analysis of C(2)EN-bearing embryos demonstrates that individual nuclei in the syncytial population of dividing nuclei often delay in their initiation of anaphase. These delays frequently lead to division errors. Eventually the products of the nuclei delayed in anaphase sink inward and are removed from the dividing population of syncytial nuclei. These results suggest that the Drosophila embryo may be equipped with mechanisms that monitor the fidelity of the syncytial nuclear divisions. Unlike checkpoints that rely on cell cycle delays to identify and correct division errors, these embryonic mechanisms rely on cell cycle delays to identify and discard the products of division errors.

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Section: Resultsmentioning

confidence: 99%

Delays in anaphase initiation occur in individual nuclei of the syncytial Drosophila embryo.

Sullivan

Daily

Fogarty

et al. 1993

MBoC

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“…Furthermore, reducing the function of mdf-2 and a Mad3-like gene called san-1 decreased the observed frequency of metaphase stage cells after microtubule destabilization, suggesting that a spindle checkpoint functions in the early embryo (Nystul et al, 2003). Studies in Drosophila have shown that microtubule inhibitors arrest early embryos with metaphase-like chromatin (Zalokar 1976;Foe and Alberts, 1983), and abnormally compacted chromosomes delay anaphase and result in nuclear "fallout" (Sullivan et al, 1993). However, the failure of microtubule depolymerizing drugs such as nocodazole to arrest mitosis in early embryonic cells has led to suggestions that the rapid mitotic divisions that occur in some early embryos do not use a spindle checkpoint (Murray and Hunt, 1997).…”

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confidence: 99%

A Spindle Checkpoint Functions during Mitosis in the EarlyCaenorhabditis elegansEmbryo

Encalada

Willis

Lyczak

et al. 2005

MBoC

118

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During mitosis, chromosome segregation is regulated by a spindle checkpoint mechanism. This checkpoint delays anaphase until all kinetochores are captured by microtubules from both spindle poles, chromosomes congress to the metaphase plate, and the tension between kinetochores and their attached microtubules is properly sensed. Although the spindle checkpoint can be activated in many different cell types, the role of this regulatory mechanism in rapidly dividing embryonic animal cells has remained controversial. Here, using time-lapse imaging of live embryonic cells, we show that chemical or mutational disruption of the mitotic spindle in early Caenorhabditis elegans embryos delays progression through mitosis. By reducing the function of conserved checkpoint genes in mutant embryos with defective mitotic spindles, we show that these delays require the spindle checkpoint. In the absence of a functional checkpoint, more severe defects in chromosome segregation are observed in mutants with abnormal mitotic spindles. We also show that the conserved kinesin CeMCAK, the CENP-F-related proteins HCP-1 and HCP-2, and the core kinetochore protein CeCENP-C all are required for this checkpoint. Our analysis indicates that spindle checkpoint mechanisms are functional in the rapidly dividing cells of an early animal embryo and that this checkpoint can prevent chromosome segregation defects during mitosis. INTRODUCTIONDuring mitosis, some microtubules emanating from bipolar microtubule organizing centers grow toward chromosomes and attach to specialized chromosomal regions called kinetochores (Skibbens and Hieter, 1998;Cleveland et al., 2003). Once captured, sister chromatids are segregated, one to each of two daughter cells. Eukaryotic cells have evolved a mechanism called the spindle checkpoint, to monitor chromosomal segregation and increase the fidelity of mitosis (reviewed in Gardner and Burke, 2000;McIntosh et al., 2002). Until spindle microtubules from both poles capture and align all sister chromatid pairs at a metaphase plate, the spindle checkpoint produces a delay in the onset of anaphase. If this delay is bypassed by reducing checkpoint function, anaphase starts prematurely, and daughter cells may receive unequal complements of chromosomes. Such genomic instability can result in lethality and in tumorigenesis (Hartwell and Kastan, 1994;Basu et al., 1999).Originally identified and characterized in Saccharomyces cerevisiae, seven spindle assembly checkpoint genes (MAD1, MAD2, MAD3, BUB1, BUB2, BUB3, and MPS1) are known to function at kinetochores to inhibit anaphase onset, or to mediate mitotic exit in the presence of spindle abnormalities (Hoyt et al., 1991;Li and Murray, 1991). Mutations in these genes reduce or eliminate the cell cycle delays that normally occur after treatment with microtubule depolymerizing drugs (Wang and Burke, 1995;Pangilinan and Spencer, 1996). Bub1 and Bub3 form a protein kinase complex that, in concert with Mps1, functions at kinetochores upstream of Mad1 and Mad2 (Roberts et al., 1994;H...

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“…The labeling of somatic nuclei and not the germline nuclei with the mRNA precursor [H3]-uridine in Drosophila early embryos provided the first clue that germline specification might require transcriptional repression. 25 Later, studies in C. elegans also concluded the same by using in situ hybridization to detect zygotic mRNAs in somatic, but not germline, blastomeres. 26,27 Transcriptional quiescence in PGCs is achieved by direct inhibition of RNA polymerase II transcriptional initiation and elongation functions in early embryos by PIE-1 and Pgc in C. elegans and Drosophila, respectively.…”

Section: Transcriptional Repression In Germ Cell Precursorsmentioning

confidence: 97%

A twist of fate: How a meiotic protein is providing new perspectives on germ cell development

Rana

Yanowitz

2016

Worm

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The molecular pathways that govern how germ line fate is acquired is an area of intense investigation that has major implications for the development of assisted reproductive technologies, infertility interventions, and treatment of germ cell cancers. Transcriptional repression has emerged as a primary mechanism to ensure suppression of somatic growth programs in primordial germ cells. In this commentary, we address how xnd-1 illuminates our understanding of transcriptional repression and how it is coordinated with the germ cell differentiation program. We recently identified xnd-1 as a novel, early determinant of germ cell fates in Caenorhabditis elegans. Our study revealed that XND-1 is maternally deposited into early embryos where it is selectively enriched in the germ lineage and then exclusively found on chromatin in the germ lineage throughout development and into adulthood when it dissociates from chromosomes in late pachytene. This localization is consistent with a range of interesting germ cell defects that suggest xnd-1 is a pivotal determinant of germ cell characteristics. Loss of xnd-1 results in a unique "one PGC (primordial germ cell)" phenotype due to G2 cell cycle arrest of the germline precursor blastomere, P 4 , which predisposes the animal and its progeny for reduced fecundity. The sterility in xnd-1 mutants is correlated with an increase in the transcriptional activationassociated histone modification, dimethylation of histone H3 lysine 4 (H3K4me2), and aberrant expression of somatic transgenes but overlapping roles with nos-2 and nos-1 suggest that transcriptional repression is achieved by multiple redundant mechanisms.

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Autoradiographic study of protein and RNA formation during early development of Drosophila eggs

Cited by 282 publications

References 28 publications

Delays in anaphase initiation occur in individual nuclei of the syncytial Drosophila embryo.

Delays in anaphase initiation occur in individual nuclei of the syncytial Drosophila embryo.

A Spindle Checkpoint Functions during Mitosis in the EarlyCaenorhabditis elegansEmbryo

A twist of fate: How a meiotic protein is providing new perspectives on germ cell development

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