Publications by authors named "Chikage Umeda-Hara"

Somatic polyploidization often increases cell and organ size, thereby contributing to plant biomass production. However, as most woody plants do not undergo polyploidization, explaining the polyploidization effect on organ growth in trees remains difficult. Here we developed a new method to generate tetraploid lines in poplars through colchicine treatment of lateral buds.

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For the full activation of cyclin-dependent kinases (CDKs), not only cyclin binding but also CDK phosphorylation is required. This activating phosphorylation is mediated by CDK-activating kinases (CAKs). Arabidopsis has four genes showing similarity to vertebrate-type CAKs, three CDKDs (CDKD;1-CDKD;3) and one CDKF (CDKF;1).

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Visualization of the spatiotemporal pattern of cell division is crucial to understand how multicellular organisms develop and how they modify their growth in response to varying environmental conditions. The mitotic cell cycle consists of four phases: S (DNA replication), M (mitosis and cytokinesis), and the intervening G1 and G2 phases; however, only G2/M-specific markers are currently available in plants, making it difficult to measure cell cycle duration and to analyze changes in cell cycle progression in living tissues. Here, we developed another cell cycle marker that labels S-phase cells by manipulating Arabidopsis CDT1a, which functions in DNA replication origin licensing.

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DNA damage checkpoints delay mitotic cell-cycle progression in response to DNA stress, stalling the cell cycle to allow time for repair. CDKB is a plant-specific cyclin-dependent kinase (CDK) that is required for the G₂/M transition of the cell cycle. In Arabidopsis, DNA damage leads the degradation of CDKB2, and the subsequent G₂ arrest gives cells time to repair damaged DNA.

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A-type cyclins (CYCAs) are a type of mitotic cyclin and are closely related to cyclin B. Plant CYCAs are classified into three subtypes (CYCA1-CYCA3), among which CYCA3 has been suggested to show a biased expression during the G1-to-S phase. We characterised Arabidopsis CYCA3s (CYCA3;1-CYCA3;4) in terms of expression pattern and protein function.

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Cyclin D (CYCD) plays an important role in cell cycle progression and reentry in response to external signals. Here, we demonstrate that Arabidopsis thaliana CYCD4 is associated with specific cell divisions in the hypocotyl. We observed that cycd4 T-DNA insertion mutants had a reduced number of nonprotruding cells and stomata in the hypocotyl epidermis.

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The Arabidopsis genome encodes 10 D-type cyclins (CYCD); however, their differential role in cell cycle control is not well known. Among them, CYCD4;2 is unique in the amino acid sequence; namely, it lacks the Rb-binding motif and the PEST sequence that are conserved in CYCDs. Here, we have shown that CYCD4;2 suppressed G1 cyclin mutations in yeast and formed a kinase complex with CDKA;1, an ortholog of yeast Cdc28, in insect cells.

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Cyclin-dependent kinases (CDKs) play essential roles in coordinate control of cell cycle progression. Activation of CDKs requires interaction with specific cyclin partners and phosphorylation of their T-loops by CDK-activating kinases (CAKs). The Arabidopsis thaliana genome encodes four potential CAKs.

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We generated transgenic tobacco and rice plants harboring a chimeric gene consisting of the 5'-upstream sequence of the rice metallothionein gene (ricMT) fused to the beta-glucuronidase (GUS) gene. The activity and tissue-specific expression of the ricMT promoter were demonstrated in these transgenic plants. In the transgenic rice plants, despite substantial levels of GUS activity in the shoot and root, almost no GUS signal was detected in the endosperm.

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B-type cyclin-dependent kinases (CDKs) are unique to plants and are assumed to be involved in the control of the G2-to-M phase progression and mitotic events. However, little is known about their cyclin partners. In Arabidopsis, we isolated cDNA encoding the D-type cyclin CYCD4;1 by a yeast (Saccharomyces cerevisiae) two-hybrid screening using CDKB2;1 as bait.

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