Identification of a novel cyclin required for the intrinsic apoptosis pathway in lymphoid cells

Roig, Maurici B.; Roset, Ramon; Ortet, Laura; Balsiger, Norman A.; Anfosso, A.; Cabellos, Laia; Garrido, Marta; Alameda, Francesc; Brady, Hugh J.M.; Gil‐Gómez, Gabriel

doi:10.1038/cdd.2008.145

Cited by 19 publications

(19 citation statements)

References 30 publications

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“…Ccno in mouse lymphoid cells can bind and activate CDK2 to respond to DNA damage-induced intrinsic apoptosis stimuli. When Ccno was knocked down, DNA damageinduced apoptosis could be abrogated [21].…”

Section: Introductionmentioning

confidence: 99%

Cyclin O Regulates Germinal Vesicle Breakdown in Mouse Oocytes1

Ma¹,

Ouyang²,

Yibo³

et al. 2013

Biology of Reproduction

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It is well accepted that oocyte meiotic resumption is mainly regulated by the maturation-promoting factor (MPF), which is composed of cyclin B1 (CCNB1) and cyclin-dependent kinase 1 (CDC2). Maturation-promoting factor activity is regulated by the expression level of CCNB1, phosphorylation of CDC2, and their germinal vesicle (GV) localization. In addition to CCNB1, cyclin O (CCNO) is highly expressed in oocytes, but its biological functions are still not clear. By employing short interfering RNA microinjection of GV-stage oocytes, we found that Ccno knockdown inhibited CDC2 (Tyr15) dephosphorylation and arrested oocytes at the GV stage. To rescue meiotic resumption, cell division cycle 25 B kinase (Cdc25b) and Ccnb1 were overexpressed in the Ccno knockdown oocytes. Unexpectedly, we found that Ccno knockdown did not affect CDC25B entry into the GV, and overexpression of CDC25B was not able to rescue resumption of oocyte meiosis. However, GV breakdown (GVBD) was significantly increased after overexpression of Ccnb1 in Ccno knockdown oocytes, indicating that GVBD block caused by cyclin O knockdown can be rescued by cyclin B1 overexpression. We thus conclude that cyclin O, as an upstream regulator of MPF, plays an important role in oocyte meiotic resumption in mouse oocytes.

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Section: Introductionmentioning

confidence: 99%

Cyclin O Regulates Germinal Vesicle Breakdown in Mouse Oocytes1

Ma¹,

Ouyang²,

Yibo³

et al. 2013

Biology of Reproduction

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“…Downstream from the MCIDAS/E2F complex also lies CCNO ( Fig. 1) (Stubbs et al 2012;Ma et al 2014;Wallmeier et al 2014), a cyclin-like protein first shown to be involved in oocyte meiosis resumption and apoptosis (Roig et al 2009;Ma et al 2013), and then shown to be expressed in MCC progenitors in the Xenopus skin and in the mouse brain, airways, and oviducts (Stubbs et al 2012;Funk et al 2015;Amirav et al 2016). Although its partners and molecular function remain to be determined, CCNO mutations or depletion lead to defects comparable to the C-MYB phenotype: defects in BB amplification, docking, and ciliogenesis Funk et al 2015).…”

Section: Downstream Effectors Of the MCC Differentiation Programmentioning

confidence: 99%

Multiciliated Cells in Animals

Meunier¹,

Azimzadeh²

2016

Cold Spring Harb Perspect Biol

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Many animal cells assemble single cilia involved in motile and/or sensory functions. In contrast, multiciliated cells (MCCs) assemble up to 300 motile cilia that beat in a coordinate fashion to generate a directional fluid flow. In the human airways, the brain, and the oviduct, MCCs allow mucus clearance, cerebrospinal fluid circulation, and egg transportation, respectively. Impairment of MCC function leads to chronic respiratory infections and increased risks of hydrocephalus and female infertility. MCC differentiation during development or repair involves the activation of a regulatory cascade triggered by the inhibition of Notch activity in MCC progenitors. The downstream events include the simultaneous assembly of a large number of basal bodies (BBs)-from which cilia are nucleated-in the cytoplasm of the differentiating MCCs, their migration and docking at the plasma membrane associated to an important remodeling of the actin cytoskeleton, and the assembly and polarization of motile cilia. The direction of ciliary beating is coordinated both within cells and at the tissue level by a combination of planar polarity cues affecting BB position and hydrodynamic forces that are both generated and sensed by the cilia. Herein, we review the mechanisms controlling the specification and differentiation of MCCs and BB assembly and organization at the apical surface, as well as ciliary assembly and coordination in MCCs.

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“…Therefore, it is not surprising that several studies have assigned CCNO a role in multiciliogenesis and mucociliary disorders [73][74][75][76][77][78] and infertility [79]. CCNO has also been shown to promote apoptosis in lymphoid cells [80].…”

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confidence: 99%

Atypical cyclins: the extended family portrait

Quandt

Ribeiro

Clotet

2019

Cell. Mol. Life Sci.

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Regulation of cell division is orchestrated by cyclins, which bind and activate their catalytic workmates, the cyclin-dependent kinases (CDKs). Cyclins have been traditionally defined by an oscillating (cyclic) pattern of expression and by the presence of a characteristic "cyclin box" that determines binding to the CDKs. Noteworthy, the Human Genome Sequence Project unveiled the existence of several other proteins containing the "cyclin box" domain. These potential "cyclins" have been named new, orphan or atypical, creating a conundrum in cyclins nomenclature. Moreover, although many years have passed after their discovery, the scarcity of information regarding these possible members of the family has hampered the establishment of criteria for systematization. Here, we discuss the criteria that define cyclins and we propose a classification and nomenclature update based on structural features, interactors, and phylogenetic information. The application of these criteria allows to systematically define, for the first time, the subfamily of atypical cyclins and enables the use of a common nomenclature for this extended family.

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Identification of a novel cyclin required for the intrinsic apoptosis pathway in lymphoid cells

Cited by 19 publications

References 30 publications

Cyclin O Regulates Germinal Vesicle Breakdown in Mouse Oocytes1

Cyclin O Regulates Germinal Vesicle Breakdown in Mouse Oocytes1

Multiciliated Cells in Animals

Atypical cyclins: the extended family portrait

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