A cell division mutant of drosophila with a functionally abnormal spindle

Ripóll, Pedro; Pimpinelli, Sergio; Valdivia, Manuel M.; Ávila, Jesús

doi:10.1016/s0092-8674(85)80071-4

Cited by 91 publications

(86 citation statements)

References 18 publications

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“…This analysis is based on previous studies of Drosophila neuroblast cell division errors (Gatti et al, 1974;Ripoll et al, 1985;Gatti and Baker, 1989;Gatti and Goldberg, 1991). Division errors that produce chromosome aberrations can be detected by screening for chromosome fragments.…”

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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“…The precise mechanism by which Aspm maintains the orientation of the spindle axis is presently unclear, although it is likely to involve its predicted microtubule-bundling capacity (Bond et al, 2002;do Carmo Avides and Glover, 1999;Ripoll et al, 1985), which might help to buffer forces that act on the spindle poles as chromatids by electroporation of endoribonuclease-prepared siRNA (esiRNA) followed by 24-hour wholeembryo culture was performed as described previously (Fish et al, 2006), except that in some experiments a pCAGGS-Cherry plasmid instead of a pCAGGS-mRFP plasmid was used to identify the targeted APs. Aspm is not essential for correct positioning of the mitotic spindle, the axis of which in mammalian APs is typically oriented parallel to the apical surface by the end of metaphase (upper cells).…”

Section: Enhanced Cleavage Precision In Aps -A Role For Aspmmentioning

confidence: 99%

Making bigger brains–the evolution of neural-progenitor-cell division

Fish

Dehay

Kennedy

et al. 2008

Journal of Cell Science

260

232

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the basally dividing progenitors of the subventricular zone. In rodents, these basal (or intermediate) progenitors lack cell polarity, whereas in primates a subpopulation of radial, presumably polarized, progenitors has evolved (outersubventricular-zone progenitors). These cells undergo basal mitoses and are thought to retain epithelial characteristics. We propose the epithelial-progenitor hypothesis, which argues that evolutionary changes that promote the maintenance of epithelial features in neural progenitors, including outer-subventricularzone progenitors, have been instrumental in the expansion of the cerebral cortex in primates.

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“…Oregon R was the wild-type strain. , cmet Δ (a null allele of cenp-meta), and asp 1 have been previously described (Basu et al, 1999;Lei and Warrior, 2000;Lopes et al, 2005;McGrail et al, 1995;Ripoll et al, 1985;Scaerou et al, 1999;Siller et al, 2005;Williams et al, 1992;Williams et al, 2003;Yucel et al, 2000). The nudC 9jE8 allele was the kind gift of Rahul Warrior (University of California, Irvine, CA).…”

Section: Genetic Stocks and Manipulationsmentioning

confidence: 99%

Roles of theDrosophilaNudE protein in kinetochore function and centrosome migration

Wainman

Creque

Williams

et al. 2009

Journal of Cell Science

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We examined the distribution of the dynein-associated protein NudE in Drosophila larval brain neuroblasts and spermatocytes, and analyzed the phenotypic consequences of a nudE null mutation. NudE can associate with kinetochores, spindles and the nuclear envelope. In nudE mutant brain mitotic cells, centrosomes are often detached from the poles. Moreover, the centrosomes of mutant primary spermatocytes do not migrate from the cell cortex to the nuclear envelope, establishing a new role for NudE. In mutant neuroblasts, chromosomes fail to congress to a tight metaphase plate, and cell division arrests because of spindle assembly checkpoint (SAC) activation. The targeting of NudE to mitotic kinetochores requires the dyneininteracting protein Lis1, and surprisingly Cenp-meta, a Drosophila CENP-E homolog. NudE is non-essential for the targeting of all mitotic kinetochore components tested. However, in the absence of NudE, the 'shedding' of proteins off the kinetochore is abrogated and the SAC cannot be turned off, implying that NudE regulates dynein function at the kinetochore. Supplementary material available online at

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A cell division mutant of drosophila with a functionally abnormal spindle

Cited by 91 publications

References 18 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.

Making bigger brains–the evolution of neural-progenitor-cell division

Roles of theDrosophilaNudE protein in kinetochore function and centrosome migration

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