Disease relevance of Cell Nucleus Division

• These results suggest that, in the presence of CB, cells transformed by DNA tumor viruses show uncontrolled nuclear division, whereas cells tranformed by RNA tumor viruses show controlled nuclear division [1].
• Nitric oxide, recently proposed as a hypoxia signal in Drosophila, induced a reversible arrest of the nuclear divisions comparable with that induced by hypoxia [2].
• The same dichotomy between the levels of the two decarboxylases was observed for meningiomas, in which ODC levels were higher in atypical forms (with karyokinesis) then in typical forms (without karyokinesis) [3].

High impact information on Cell Nucleus Division

• Thus, Tem1 and Lte1 are present in the same cellular compartment (the bud) only after the nucleus enters the bud during nuclear division [4].
• Ash1p is localized to the daughter nucleus in cells that have undergone nuclear division [5].
• In A. nidulans, gamma-tubulin is essential for nuclear division and microtubule assembly and is associated with the spindle pole body, the fungal microtubule organizing center [6].
• Mutation of a gene that encodes a kinesin-like protein blocks nuclear division in A. nidulans [7].
• We show that the engrailed gene is needed for the processes that organize the embryo during the nuclear divisions that precede cellularization [8].

Biological context of Cell Nucleus Division

• These results constitute genetic proof that the intact myosin molecule is required for cytokinesis and not for karyokinesis [9].
• Tousled-like kinase functions with the chromatin assembly pathway regulating nuclear divisions [10].
• Although FAR1 mRNA levels rise again during late S or G2 phase, reaccumulation of Far1 protein to functional levels is restricted until after nuclear division [11].
• In cells whose actin cytoskeleton has been perturbed, bud formation is frequently delayed and the morphogenesis checkpoint introduces a compensatory delay of nuclear division until a bud has been formed [12].
• Thermosensitive mutations in the DBF2 gene arrest the cell cycle during nuclear division [13].

Anatomical context of Cell Nucleus Division

• Microinjection of anti-PRC1 antibodies into HeLa cells blocked cellular cleavage, but not nuclear division, indicating a functional role for PRC1 in the process of cytokinesis [14].
• Although actin caps and metaphase furrows have been implicated in maintaining the fidelity of nuclear division and the positions of nuclei within the cortex, our observations indicate that these structures are dispensible during the early syncytial blastoderm cell cycles [15].
• Selective destruction of cultured tumor cells with uncontrolled nuclear division by cytochalasin B and cytosine arabinoside [16].
• Cell lines were assayed for: (a) multinucleation or uncontrolled nuclear division (UND+) and uncontrolled DNA synthesis in cytochalasin B (CB) medium; and (b) the continuation of DNA synthesis in media containing reduced (0.5%) amounts of serum [17].
• This suggests that centrin could be involved in the centrosome reproduction cycle, in the coordination of cytoplasmic and nuclear division or in cytokinesis [18].

Associations of Cell Nucleus Division with chemical compounds

• Phenylalanine residues implicated in calmodulin localization and nuclear division are located in the amino-terminal half of the protein, whereas those implicated in actin organization and bud emergence are located in the carboxyl-terminal half [19].
• The multiple septa typically divide two nuclei, but the nuclei frequently do not stain equally with 4',6-diamidino-2-phenylindole (DAPI), suggesting that byr4 is required for proper karyokinesis [20].
• The timing of nuclear division in cells that cannot make a bud is exquisitely sensitive to the dosage of SWE1 and MIH1 genes, which control phosphorylation of Cdc28 at tyrosine 19 [21].
• The timing of the nuclear division cycle in Neurospora crassa was studied by inhibiting DNA synthesis with hydroxyurea added to exponentially growing cultures at concentrations that do not inhibit cytoplasmic growth [22].
• Addition of inhibitors of DNA synthesis or nuclear division did not affect the pattern of CO2 evolution in synchronous cultures [23].

Gene context of Cell Nucleus Division

• SMC1: an essential yeast gene encoding a putative head-rod-tail protein is required for nuclear division and defines a new ubiquitous protein family [24].
• Dual functions of CDC6: a yeast protein required for DNA replication also inhibits nuclear division [25].
• We propose a model in which the Elm1 kinase functions in a mitotic signaling network that controls events required for normal bud growth and cytokinesis, while the Swe1 kinase functions in a checkpoint pathway that delays nuclear division in response to defects in these events [26].
• We have isolated a gene, NDD1, which at a high dosage suppresses the nuclear-division defect of cdc28-1N [27].
• We have isolated three mutant alleles of CDC4 (cdc4-10, cdc4-11, and cdc4-16) which suppress the nuclear division defect of cdc20-1 cells [28].

Analytical, diagnostic and therapeutic context of Cell Nucleus Division

• In addition, these cells contained one, two, or multiple nuclei indicative of a G2/M delay in nuclear division and also a defect in cytokinesis and/or cell separation [29].
• By carrying out time-lapse and optical sectioning video microscopy analysis of cells that express green fluorescent protein (GFP)-tagged nuclear envelope and actomyosin ring components, we found that nuclear division is temporally coupled to cytokinesis [30].
• Light and electron microscopy analysis also showed that nuclear envelope fission and the division of the nucleoplasm are severely delayed in cytokinesis mutants, resulting in discoupling between the nuclear division cycle and the budding cycle [30].

References