Coordinating cell cycle progression via cyclin specificity

Pagliuca, Felicia W.; Collins, Mark O.; Choudhary, Jyoti S.

doi:10.4161/cc.10.24.18395

Cited by 7 publications

(7 citation statements)

References 10 publications

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“…Furthermore, this connection seemed to be specific, because other cyclins and cyclin-dependent kinases involved in cell cycle regulation, i.e., cyclin A, cyclin E, cdk4 and cdk6, 41,[44][45][46][47] were not affected by the upregulation of PLCβ1. Therefore, we decided to study the connection between PLCβ1 and cyclin D3 in terms of cell proliferation in K562 cells.…”

Section: Human Erythroleukemia Cells K562 Overexpressing Plcβ1mentioning

confidence: 99%

K562 cell proliferation is modulated by PLCβ1 through a PKCα-mediated pathway

et al. 2013

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Section: Human Erythroleukemia Cells K562 Overexpressing Plcβ1mentioning

confidence: 99%

K562 cell proliferation is modulated by PLCβ1 through a PKCα-mediated pathway

et al. 2013

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“…Moreover, interaction between the two proteins was detected also in G1/S cycling cells, which confirmed the capacity of PKC⍺ and Cyclin B1 to complex during cell cycle progression ( Supplementary Figure 6 ). Next, in order to further investigate the existence of this complex, we again immunoprecipitated PKC⍺ and we found it was able to interact with cdk1/cdc2, the kinase that forms the MPF associating with Cyclin B1 [ 20 – 25 ], [ 26 ], [ 27 , 28 ]. As positive control of the experiment, we immunoprecipitated Cyclin B1 finding it perfectly complexed with cdk1/cdc2 (Figure 3E ).…”

Section: Resultsmentioning

confidence: 99%

A novel DAG-dependent mechanism links PKCa and Cyclin B1 regulating cell cycle progression

et al. 2014

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Through the years, different studies showed the involvement of Protein Kinase C (PKC) in cell cycle control, in particular during G1/S transition. Little is known about their role at G2/M checkpoint. In this study, using K562 human erythroleukemia cell line, we found a novel and specific mechanism through which the conventional isoform PKC⍺ positively affects Cyclin B1 modulating G2/M progression of cell cycle. Since the kinase activity of this PKC isoform was not necessary in this process, we demonstrated that PKC⍺, physically interacting with Cyclin B1, avoided its degradation and stimulated its nuclear import at mitosis. Moreover, the process resulted to be strictly connected with the increase in nuclear diacylglycerol levels (DAG) at G2/M checkpoint, due to the activity of nuclear Phospholipase C β1 (PLCβ1), the only PLC isoform mainly localized in the nucleus of K562 cells. Taken together, our findings indicated a novel DAG dependent mechanism able to regulate the G2/M progression of the cell cycle.

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“…Perturbing the expression of core cell cycle regulators, such as cyclin‐dependent kinase A‐1 (CDKA;1) or cyclin‐dependent kinase B2 (CDKB2), causes a significant decrease of cell number in the meristem, leading to a severe root growth defect (Andersen et al 2008; Nowack et al 2012). Cyclins are primary regulators of cyclin‐dependent kinases (CDKs) via activating CDKs or determining their substrate specificity (Loog and Morgan 2005; Pagliuca et al 2011). In Arabidopsis , there are more genes encoding cyclins than encoding CDKs, which may benefit plants to specifically adapt to a variety of developmental processes (Wang et al 2004; Pagliuca et al 2011).…”

Section: Introductionmentioning

confidence: 99%

“…Cyclins are primary regulators of cyclin‐dependent kinases (CDKs) via activating CDKs or determining their substrate specificity (Loog and Morgan 2005; Pagliuca et al 2011). In Arabidopsis , there are more genes encoding cyclins than encoding CDKs, which may benefit plants to specifically adapt to a variety of developmental processes (Wang et al 2004; Pagliuca et al 2011). Many cyclins are specific to tissues or developmental stages (Wang et al 2004).…”

Section: Introductionmentioning

confidence: 99%

The epidermis‐specific cyclin CYCP3;1 is involved in the excess brassinosteroid signaling‐inhibited root meristem cell division

Chen

Sun

Wang

2020

JIPB

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Cell division is precisely regulated and highly tissue-specific; studies have suggested that diverse signals in the epidermis, especially the epidermal brassinosteroids (BRs), can regulate root growth. However, the underlying molecular mechanisms that integrate hormonal cues such as BR signaling with other endogenous, tissue-specific developmental programs to regulate epidermal cell proliferation remain unclear. In this study, we used molecular and biochemical approaches, microscopic imaging and genetic analysis to investigate the function and mechanisms of a P-type cyclin in root growth regulation. We found that CYCP3;1, specifically expressed in the root meristem epidermis and lateral root cap, can regulate meristem cell division. Mitotic analyses and biochemical studies demonstrated that CYCP3;1 promotes cell division at the G2-M duration by associating and activating cyclin-dependent kinase B2-1 (CDKB2;1). Furthermore, we found that CYCP3;1 expression was inhibited by BR signaling through BRI1-EMS-SUPPRESSOR1 (BES1), a positive downstream transcription factor in the BR signaling pathway. These findings not only provide a mechanism of how root epidermal-specific regulators modulate root growth, but also reveal why the excess of BRs or enhanced BR signaling inhibits cell division in the meristem to negatively regulate root growth.

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Coordinating cell cycle progression via cyclin specificity

Cited by 7 publications

References 10 publications

K562 cell proliferation is modulated by PLCβ1 through a PKCα-mediated pathway

K562 cell proliferation is modulated by PLCβ1 through a PKCα-mediated pathway

A novel DAG-dependent mechanism links PKCa and Cyclin B1 regulating cell cycle progression

The epidermis‐specific cyclin CYCP3;1 is involved in the excess brassinosteroid signaling‐inhibited root meristem cell division

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