Cyk-4

Jantsch, Verena; Gönczy, Pierre; Romano, Alper; Schnabel, Heinke; Hamill, Danielle R.; Schnabel, Ralf; Hyman, Anthony A.; Glotzer, Michael

doi:10.1083/jcb.149.7.1391

Cited by 352 publications

(169 citation statements)

References 56 publications

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“…One mediator of H-Ras-induced cytoskeletal rearrangements is RhoA, which is activated upon overexpression of activated H-Ras (27,28). RhoA is also the only member of the Rhoprotein family of small GTPases that is required for cytokinesis in mammalian cells (29,30). Properly localized activity of both RhoA and its downstream mediator ROCK is necessary for ingression of the cleavage furrow (22, 23).…”

Section: Discussionmentioning

confidence: 99%

Oncogenic H-Ras V12 promotes anchorage-independent cytokinesis in human fibroblasts

Thullberg

Gad

Guyader

et al. 2007

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

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Cell anchorage is required for cell proliferation of untransformed cells, whereas anchorage-independent growth can be induced by oncogenes and is a hallmark of transformation. Whereas anchorage-dependent control of the progression of the G1 phase of the cell cycle has been extensively studied, it is less clear whether and how anchorage may control other cell cycle phases and whether oncogenes may affect such controls. Here, we found that lack of cell anchorage did not influence progression through the cell cycle S phase, G2 phase, or most of mitosis of primary human fibroblasts. However, unanchored fibroblasts could not complete cytokinesis. The cleavage furrow and central spindle were still formed in the absence of anchorage, but cells were unable to complete ingression, causing binucleation. Importantly, V12 H-Ras-transformed fibroblasts and two cancer cell lines progressed through the entire cell cycle without anchorage, including through cytokinesis. This indicates that oncogenic signaling may contribute to anchorageindependent growth and tumorigenesis by promoting the final cleavage furrow ingression during cytokinesis.cell adhesion ͉ integrin ͉ extracellular matrix ͉ signaling ͉ cell cycle

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Section: Discussionmentioning

confidence: 99%

Oncogenic H-Ras V12 promotes anchorage-independent cytokinesis in human fibroblasts

Thullberg

Gad

Guyader

et al. 2007

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

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“…Staining of rho-1(dn) animals with the DNA dye 4Ј,6-diamidino-2-phenylindole (DAPI) revealed many, but not all, of these cells to be multinucleate (Fig. 2 C and D), suggesting rho-1(dn) can cause a cytokinesis defect in these cells (23).…”

Section: Methodsmentioning

confidence: 99%

A RHO GTPase-mediated pathway is required during P cell migration in Caenorhabditis elegans

Spencer

Orita

Malone

et al. 2001

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

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The Rho family of guanine triphosphate hydrolases controls various cellular processes, including cell migration. We describe here the demonstration of a role for a RhoA GTPase homologue during cell migration in Caenorhabditis elegans. We show that eliminating or reducing rho-1 gene function by using a dominant-negative transgene or dsRNA interference results in a severe defect in migration of hypodermal P cells to a ventral position. Biochemical and genetic data also suggest that unc-73, which encodes a Trio-like guanine nucleotide exchange factor, may act as an activator of rho-1 in the migration process. Mutations in let-502 ROCK, a homologue of a RhoA effector in mammals, also cause defects in P cell migration, suggesting that it may be one of several effectors acting downstream of rho-1 during P cell migration. Finally, we provide evidence to support the idea that other small Rac subfamily small GTPases act redundantly and in parallel to RHO-1 in this specific cell migration event.rho-1 ͉ rac ͉ unc-73

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“…Cytokinesis in C. elegans requires complex formation between Zen-4 (homolog of the human MKlp1) and ZYG-4, a Rho GTPase activator (Jantsch-Plunger et al, 2000;Mishima et al, 2002). Regulation of Rho, in turn, was shown to be required for successful cytokinesis (reviewed in .…”

Section: Plk1 and Cytokinesismentioning

confidence: 99%