B-type nuclear lamin and the nuclear pore complex Nup107-160 influences maintenance of the spindle envelope required for cytokinesis in<i>Drosophila</i>male meiosis

Hayashi, Daisuke; Tanabe, Karin; Katsube, Hiroka; Inoué, Yoshihiro

doi:10.1242/bio.017566

Cited by 21 publications

(26 citation statements)

References 68 publications

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“…Some or all of these defects could be indirectly due to disruptions in the nuclear import of factors required for a fully functional spindle to assemble, and we did detect variable and sometimes lower levels of some kinetochore proteins after LMN-1 knockdown (data not shown). Nevertheless, our results indicate that the nuclear lamina plays an important role in C. elegans oocyte meiotic spindle assembly, and roles for lamins in spindle assembly have also been reported in Xenopus extracts and during Drosophila male meiosis(Goodman et al, 2010; Hayashi et al, 2016; Tsai et al, 2006).…”

Section: Discussionsupporting

confidence: 58%

Microtubule Assembly and Pole Coalescence: Early Steps in C. elegans Oocyte Meiosis I Spindle Assembly

Chuang

Schlientz

Yang

et al. 2020

Preprint

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How oocytes assemble bipolar meiotic spindles in the absence of centrosomes as microtubule organizing centers remains poorly understood. We have used live cell imaging in C. elegans to investigate requirements for the nuclear lamina and for conserved regulators of microtubule dynamics during oocyte meiosis I spindle assembly, assessing these requirements with respect to recently identified spindle assembly steps. We show that the nuclear lamina is required for microtubule bundles to form a cage-like structure that appears shortly after oocyte nuclear envelope breakdown and surrounds the oocyte chromosomes, although bipolar spindles still assembled in its absence. Although two conserved regulators of microtubule nucleation, RAN-1 and γ-tubulin, are not required for bipolar spindle assembly, both contribute to normal levels of spindle-associated microtubules and spindle assembly dynamics. Finally, the XMAP215 ortholog ZYG-9 and the nearly identical minus-end directed kinesins KLP-15/16 are required for proper assembly of the early cage-like structure of microtubule bundles, and for early spindle pole foci to coalesce into a bipolar structure. Our results provide a framework for assigning molecular mechanisms to recently described steps in C. elegans oocyte meiosis I spindle assembly.

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Section: Discussionsupporting

confidence: 58%

Microtubule Assembly and Pole Coalescence: Early Steps in C. elegans Oocyte Meiosis I Spindle Assembly

Chuang

Schlientz

Yang

et al. 2020

Preprint

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“…To further validate the contribution of compromised NE integrity to the mitotic phenotypes induced by TGFβ, we selected LaminB1, a major determinant of nuclear shape and size with a dual role in regulating cytokinesis, spindle matrix and chromatin condensation (Gruenbaum and Foisner, 2015; Guttinger et al, 2009; Hayashi et al, 2016; Martin et al, 2010; Tsai et al, 2006; Verstraeten et al, 2011), for more detailed analysis. TGFβ suppressed Lamins A and B1 proteins in MCF10A, SKBR3 as well as CDβgeo cells, whereas its removal restored the levels of Lamins (Fig.…”

Section: Resultsmentioning

confidence: 99%

“…Specifically, LaminB1, suppressed by TGFβ and SNAIL, plays an important role in cytokinesis, spindle assembly and chromatin condensation (Funkhouser et al, 2013; Hayashi et al, 2016; Martin et al, 2010; Tsai et al, 2006; Verstraeten et al, 2011). Disruption of LaminB1 causes cause nuclear blebbing (Funkhouser et al, 2013), and cytokinesis failure leading to BN and MN cells (Funkhouser et al, 2013; Hayashi et al, 2016; Martin et al, 2010; Tsai et al, 2006; Verstraeten et al, 2011), thus, phenocopying the effects of TGFβ. Accordingly, restoring LaminB1 partially rescues the mitotic abnormalities induced by TGFβ suggesting that additional NE components suppressed by TGFβ are also likely to contribute to the cytokinesis and mitotic defects observed in cells undergoing EMT.…”

Section: Discussionmentioning

confidence: 99%

Genomic Instability Is Induced by Persistent Proliferation of Cells Undergoing Epithelial-to-Mesenchymal Transition

et al. 2016

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Summary TGFβ secreted by tumor stroma induces Epithelial-to-Mesenchymal Transition (EMT) in cancer cells, a reversible phenotype linked to cancer progression and drug resistance. However, exposure to stromal signals may also lead to heritable changes in cancer cells, which are poorly understood. We show that epithelial cells failing to undergo proliferation arrest during TGFβ-induced EMT sustain mitotic abnormalities due to failed cytokinesis, resulting in aneuploidy. This genomic instability is associated with suppression of multiple nuclear envelope proteins implicated in mitotic regulation, and is phenocopied by modulating the expression of LaminB1. While TGFβ-induced mitotic defects in proliferating cells are reversible upon its withdrawal, the acquired genomic abnormalities persist, leading to increased tumorigenic phenotypes. In metastatic breast cancer patients, increased mesenchymal marker expression within single circulating tumor cells is correlated with genomic instability. These observations identify a mechanism whereby microenvironment-derived signals trigger heritable genetic changes within cancer cells contributing to tumor evolution.

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“…FG-Nups bind to proteins that shuttle between the nucleus and cytoplasm [10,11]. The FG-barrier constructed by the FG-Nups allows the selective transport of these proteins [12][13][14].As most of the Nups are well-conserved in Drosophila, we decided to investigate the role of the NPC in spermatogenesis using this model animal that allows well-advanced genetic analyses [15][16][17]. A previous study using spermatocyte-specific RNAi experiments investigated whether the depletion of the 30 Nups affected the progression of premeiotic cells through meiosis [17].…”

mentioning

confidence: 99%

Nuclear Export of Cyclin B Mediated by the Nup62 Complex Is Required for Meiotic Initiation in Drosophila Males

Okazaki

Yamazoe

Inoué

2020

Cells

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Background: The central channel of the nuclear pore complex plays an important role in the selective transport of proteins between the nucleus and cytoplasm. Previous studies have demonstrated that the depletion of the Nup62 complex, constructing the nuclear pore channel in premeiotic Drosophila cells, resulted in the absence of meiotic cells. We attempted to understand the mechanism underlying the cell cycle arrest before meiosis. Methods: We induced dsRNAs against the nucleoporin mRNAs using the Gal4/UAS system in Drosophila. Results: The cell cycle of the Nup62-depleted cells was arrested before meiosis without CDK1 activation. The ectopic over-expression of CycB, but not constitutively active CDK1, resulted in partial rescue from the arrest. CycB continued to exist in the nuclei of Nup62-depleted cells and cells depleted of exportin encoded by emb. Protein complexes containing CycB, Emb, and Nup62 were observed in premeiotic spermatocytes. CycB, which had temporally entered the nucleus, was associated with Emb, and the complex was transported back to the cytoplasm through the central channel, interacting with the Nup62 complex. Conclusion: We proposed that CycB is exported with Emb through the channel interacting with the Nup62 complex before the onset of meiosis. The nuclear export ensures the modification and formation of sufficient CycB-CDK1 in the cytoplasm.

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B-type nuclear lamin and the nuclear pore complex Nup107-160 influences maintenance of the spindle envelope required for cytokinesis inDrosophilamale meiosis

Cited by 21 publications

References 68 publications

Microtubule Assembly and Pole Coalescence: Early Steps in C. elegans Oocyte Meiosis I Spindle Assembly

Microtubule Assembly and Pole Coalescence: Early Steps in C. elegans Oocyte Meiosis I Spindle Assembly

Genomic Instability Is Induced by Persistent Proliferation of Cells Undergoing Epithelial-to-Mesenchymal Transition

Nuclear Export of Cyclin B Mediated by the Nup62 Complex Is Required for Meiotic Initiation in Drosophila Males

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