Kinase‐independent activity of Cdc2/Cyclin A prevents the S phase in the <i>Drosophila </i>cell cycle

Hayashi, Shigeo; Yamaguchi, Masamitsu

doi:10.1046/j.1365-2443.1999.00243.x

Cited by 20 publications

(11 citation statements)

References 52 publications

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“…In fact, there are several protein kinases whose biological activities do not correspond to their in vitro kinase activities (Schwartzberg et al, 1997;Hayashi and Yamaguchi, 1999;Rathjen et al, 1999;Charette et al, 2001;Hu et al, 2001;Hü ser et al, 2001;Hojjati et al, 2007;Chen et al, 2008). Hojjati et al (2007) reported that the autophosphorylation and substrate phosphorylation activities of animal aCaMKII are not required for it to function in the modulation of short-term presynaptic plasticity, suggesting that aCaMKII plays a structural role rather than an enzymatic role (Hojjati et al, 2007).…”

Section: Biological Activity Of Ccamk Is Not Solely Defined By In Vitmentioning

confidence: 99%

Rhizobial and Fungal Symbioses Show Different Requirements for Calmodulin Binding to Calcium Calmodulin–Dependent Protein Kinase in Lotus japonicus

et al. 2012

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Ca2+/calmodulin (CaM)–dependent protein kinase (CCaMK) is a key regulator of root nodule and arbuscular mycorrhizal symbioses and is believed to be a decoder for Ca2+ signals induced by microbial symbionts. However, it is unclear how CCaMK is activated by these microbes. Here, we investigated in vivo activation of CCaMK in symbiotic signaling, focusing mainly on the significance of and epistatic relationships among functional domains of CCaMK. Loss-of-function mutations in EF-hand motifs revealed the critical importance of the third EF hand for CCaMK activation to promote infection of endosymbionts. However, a gain-of-function mutation (T265D) in the kinase domain compensated for these loss-of-function mutations in the EF hands. Mutation of the CaM binding domain abolished CaM binding and suppressed CCaMKT265D activity in rhizobial infection, but not in mycorrhization, indicating that the requirement for CaM binding to CCaMK differs between root nodule and arbuscular mycorrhizal symbioses. Homology modeling and mutagenesis studies showed that the hydrogen bond network including Thr265 has an important role in the regulation of CCaMK. Based on these genetic, biochemical, and structural studies, we propose an activation mechanism of CCaMK in which root nodule and arbuscular mycorrhizal symbioses are distinguished by differential regulation of CCaMK by CaM binding.

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Section: Biological Activity Of Ccamk Is Not Solely Defined By In Vitmentioning

confidence: 99%

Rhizobial and Fungal Symbioses Show Different Requirements for Calmodulin Binding to Calcium Calmodulin–Dependent Protein Kinase in Lotus japonicus

et al. 2012

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“…Moreover, E2F transcription factors have been found to interact with A2-type cyclins (J. Boruc, L. De Veylder, 30.1 6 1.4 31.4 6 0.7 31.6 6 0.7 31.9 6 1.1 8C 22.7 6 1.6 21.4 6 1.0 29.6 6 1.7 28.1 6 2.1 16C 11.8 6 0.8 13.2 6 1.2 7.9 6 0.4 9.4 6 1.1 +10 mM b-estradiol 2C 27.2 6 2.5 35.7 6 5.1 24.5 6 1.1 40.2 6 5.0 4C 26.9 6 1.7 25.0 6 2.6 29.4 6 1.9 24.0 6 1.4 8C 27.7 6 1.6 31.9 6 1.6 36.5 6 1.4 31.9 6 3.0 16C 16.2 6 0.5 7.2 6 2.6 9.5 6 1.9 3.9 6 0.7 and E. Russinova, unpublished data), another indication that A2-type cyclins might play a role during the S phase itself. In mammals, E2F activity is regulated by CDK2-cyclin A phosphorylation (Krek et al, 1994;Xu et al, 1994;Kitagawa et al, 1995;Hayashi and Yamaguchi, 1999;Morris et al, 2000). Inactivation of E2Fs by CDK2 phosphorylation promotes the mitotic cell cycle by driving cells into the G2 phase.…”

Section: Cdkb1;1 and Cyca2;3 Colocalize In The Nucleusmentioning

confidence: 99%

CDKB1;1 Forms a Functional Complex with CYCA2;3 to Suppress Endocycle Onset

et al. 2009

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The mitosis-to-endocycle transition requires the controlled inactivation of M phase-associated cyclin-dependent kinase (CDK) activity. Previously, the B-type CDKB1;1 was identified as an important negative regulator of endocycle onset. Here, we demonstrate that CDKB1;1 copurifies and associates with the A2-type cyclin CYCA2;3. Coexpression of CYCA2;3 with CDKB1;1 triggered ectopic cell divisions and inhibited endoreduplication. Moreover, the enhanced endoreduplication phenotype observed after overexpression of a dominant-negative allele of CDKB1;1 could be partially complemented by CYCA2;3 co-overexpression, illustrating that both subunits unite in vivo to form a functional complex. CYCA2;3 protein stability was found to be controlled by CCS52A1, an activator of the anaphase-promoting complex. We conclude that CCS52A1 participates in endocycle onset by down-regulating CDKB1;1 activity through the destruction of CYCA2;3.

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“…The physical interaction between the recombinant CDT1a and CYCA2;2 proteins in an in vitro pull-down experiment (del Mar Castellano et al, 2004) supports this possibility. Animal cyclin A/CDKs also negatively regulate G1/S-related transcription factors, including E2F-DP (Dynlacht et al, 1994;Krek et al, 1994;Xu et al, 1994;Hayashi and Yamaguchi, 1999). In a transcription analysis using real-time quantitative PCR, however, significant differences in the transcript level of CDC6a, which is regulated by E2Fa-DPa , could not be detected among the wild type, the mutant, and the CYCA2;3-GFP and mDB-CYCA2;3-GFP overexpressors (see Supplemental Figure 5 online), suggesting that CYCA2;3 is not involved in transcriptional regulation.…”

Section: Molecular Mechanism For the Negative Regulation Of Endocyclesmentioning

confidence: 99%

The A-Type Cyclin CYCA2;3 Is a Key Regulator of Ploidy Levels inArabidopsisEndoreduplication

et al. 2006

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Plant cells frequently undergo endoreduplication, a process in which chromosomal DNA is successively duplicated in the absence of mitosis. It has been proposed that endoreduplication is regulated at its entry by mitotic cyclin-dependent kinase activity. However, the regulatory mechanisms for its termination remain unclear, although plants tightly control the ploidy level in each cell type. In the process of searching for regulatory factors of endoreduplication, the promoter of an Arabidopsis thaliana cyclin A gene, CYCA2;3, was revealed to be active in developing trichomes during the termination period of endoreduplication as well as in proliferating tissues. Taking advantage of the situation that plants encode highly redundant cyclin A genes, we were able to perform functional dissection of CYCA2;3 using null mutant alleles. Null mutations of CYCA2;3 semidominantly promoted endocycles and increased the ploidy levels achieved in mature organs, but they did not significantly affect the proportion of cells that underwent endoreduplication. Consistent with this result, expression of the CYCA2;3-green fluorescent protein fusion protein restrained endocycles in a dose-dependent manner. Moreover, a mutation in the destruction box of CYCA2;3 stabilized the fusion protein in the nuclei and enhanced the restraint. We conclude that CYCA2;3 negatively regulates endocycles and acts as a key regulator of ploidy levels in Arabidopsis endoreduplication.

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Kinase‐independent activity of Cdc2/Cyclin A prevents the S phase in the Drosophila cell cycle

Cited by 20 publications

References 52 publications

Rhizobial and Fungal Symbioses Show Different Requirements for Calmodulin Binding to Calcium Calmodulin–Dependent Protein Kinase in Lotus japonicus

Rhizobial and Fungal Symbioses Show Different Requirements for Calmodulin Binding to Calcium Calmodulin–Dependent Protein Kinase in Lotus japonicus

CDKB1;1 Forms a Functional Complex with CYCA2;3 to Suppress Endocycle Onset

The A-Type Cyclin CYCA2;3 Is a Key Regulator of Ploidy Levels inArabidopsisEndoreduplication

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