scholarly journals SCL28 promotes cell expansion and endoreplication in Arabidopsis by activating SIAMESE-RELATED cyclin-dependent kinase inhibitors.

2021 ◽  
Author(s):  
Camila Goldy ◽  
Virginia L Barrera ◽  
Isaiah Taylor ◽  
Celeste Buchensky ◽  
Rodrigo Vena ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Cell Wall ◽  
Cell Expansion ◽  
Kinase Inhibitors ◽  
Mitotic Cell ◽  
Specific Cell ◽  
Mitotic Cell Cycle ◽  
Cyclin Dependent Kinase ◽  
Division Plane ◽  
Division Plane Orientation

The processes that contribute to plant organ morphogenesis are spatial-temporally organized. Within the meristem the mitotic cell cycle produces new cells that subsequently engage in specific cell expansion and differentiation programs once they exit the division competent zone. The latter is frequently accompanied by endoreplication, being an alternative cell cycle that replicates the DNA without nuclear division, causing a stepwise increase in somatic ploidy. We have previously shown that the Arabidopsis SCL28 transcription factor promotes progression through G2/M and modulates division plane orientation. Here, we demonstrate that SCL28 co-express and regulates genes specific to cell elongation and differentiation, including genes related to cell wall and cytoskeleton assembly. Consistently, this correlates with defects in post-mitotic cell expansion in a scl28 mutant. Strikingly, SCL28 controls expression of 6 members of the SIAMESE/SIAMESE-RELATED (SIM/SMR) family, encoding cyclin-dependent kinase inhibitors with a role in promoting mitotic cell cycle exit and endoreplication onset, both in response to developmental and environmental cues. Consistent with this role, scl28 mutants displayed reduced endoreplication, both in roots and leaves. Altogether, these results suggest that SCL28 controls cell expansion and differentiation by promoting endoreplication onset and by modulating aspects of the biogenesis, assembly and remodeling of the cytoskeleton and cell wall.

scholarly journals Prevention of DNA Rereplication Through a Meiotic Recombination Checkpoint Response

2016 ◽  
Vol 6 (12) ◽  
pp. 3869-3881
Author(s):  
Nicole A Najor ◽  
Layne Weatherford ◽  
George S Brush
Keyword(s):  
Cell Cycle ◽  
Dna Replication ◽  
Protein Kinase ◽  
Meiotic Recombination ◽  
Mitotic Cell ◽  
Mitotic Cell Cycle ◽  
Cyclin Dependent Kinase ◽  
Checkpoint Response ◽  
Recombination Checkpoint ◽  
Dna Rereplication

Abstract In the budding yeast Saccharomyces cerevisiae, unnatural stabilization of the cyclin-dependent kinase inhibitor Sic1 during meiosis can trigger extra rounds of DNA replication. When programmed DNA double-strand breaks (DSBs) are generated but not repaired due to absence of DMC1, a pathway involving the checkpoint gene RAD17 prevents this DNA rereplication. Further genetic analysis has now revealed that prevention of DNA rereplication also requires MEC1, which encodes a protein kinase that serves as a central checkpoint regulator in several pathways including the meiotic recombination checkpoint response. Downstream of MEC1, MEK1 is required through its function to inhibit repair between sister chromatids. By contrast, meiotic recombination checkpoint effectors that regulate gene expression and cyclin-dependent kinase activity are not necessary. Phosphorylation of histone H2A, which is catalyzed by Mec1 and the related Tel1 protein kinase in response to DSBs, and can help coordinate activation of the Rad53 checkpoint protein kinase in the mitotic cell cycle, is required for the full checkpoint response. Phosphorylation sites that are targeted by Rad53 in a mitotic S phase checkpoint response are also involved, based on the behavior of cells containing mutations in the DBF4 and SLD3 DNA replication genes. However, RAD53 does not appear to be required, nor does RAD9, which encodes a mediator of Rad53, consistent with their lack of function in the recombination checkpoint pathway that prevents meiotic progression. While this response is similar to a checkpoint mechanism that inhibits initiation of DNA replication in the mitotic cell cycle, the evidence points to a new variation on DNA replication control.

scholarly journals Time-Series Single-Cell RNA-Seq Data Reveal Auxin Fluctuation during Endocycle

2019 ◽  
Vol 61 (2) ◽  
pp. 243-254 ◽  
Author(s):  
Kotaro Torii ◽  
Akane Kubota ◽  
Takashi Araki ◽  
Motomu Endo
Keyword(s):  
Cell Cycle ◽  
Cell Division ◽  
Single Cell ◽  
Molecular Mechanisms ◽  
Mitotic Cell ◽  
Specific Cell ◽  
Mitotic Cell Cycle ◽  
Transcriptome Data ◽  
Cell Transcriptome ◽  
Single Cell Transcriptome

Abstract Appropriate cell cycle regulation is crucial for achieving coordinated development and cell differentiation in multicellular organisms. In Arabidopsis, endoreduplication is often observed in terminally differentiated cells and several reports have shown its molecular mechanisms. Auxin is a key factor for the mode transition from mitotic cell cycle to endocycle; however, it remains unclear if and how auxin maintains the endocycle mode. In this study, we reanalyzed root single-cell transcriptome data and reconstructed cell cycle trajectories of the mitotic cell cycle and endocycle. With progression of the endocycle, genes involved in auxin synthesis, influx and efflux were induced at the specific cell phase, suggesting that auxin concentration fluctuated dynamically. Such induction of auxin-related genes was not observed in the mitotic cell cycle, suggesting that the auxin fluctuation plays some roles in maintaining the endocycle stage. In addition, the expression level of CYCB1;1, which is required for cell division in the M phase, coincided with the expected amount of auxin and cell division. Our analysis also provided a set of genes expressed in specific phases of the cell cycle. Taking these findings together, reconstruction of single-cell transcriptome data enables us to identify properties of the cell cycle more accurately.

Paclitaxel inhibits osteoclast formation and bone resorption via influencing mitotic cell cycle arrest and RANKL-induced activation of NF-κB and ERK

2012 ◽  
Vol 113 (3) ◽  
pp. 946-955 ◽  
Author(s):  
Estabelle S. M. Ang ◽  
Nathan J. Pavlos ◽  
Shek Man Chim ◽  
Hao Tian Feng ◽  
Robin M. Scaife ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Bone Resorption ◽  
Cell Cycle Arrest ◽  
Mitotic Cell ◽  
Osteoclast Formation ◽  
Mitotic Cell Cycle ◽  
Cycle Arrest

scholarly journals Functions of Cyclin A1 in the Cell Cycle and Its Interactions with Transcription Factor E2F-1 and the Rb Family of Proteins

1999 ◽  
Vol 19 (3) ◽  
pp. 2400-2407 ◽  
Author(s):  
Rong Yang ◽  
Carsten Müller ◽  
Vong Huynh ◽  
Yuen K. Fung ◽  
Amy S. Yee ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Transcription Factor ◽  
Mitotic Cell ◽  
Histone H1 ◽  
Mitotic Cell Cycle ◽  
Osteosarcoma Cell ◽  
Cell Cycle Regulators ◽  
Cyclin A1 ◽  
Transcription Factor E2f

ABSTRACT Human cyclin A1, a newly discovered cyclin, is expressed in testis and is thought to function in the meiotic cell cycle. Here, we show that the expression of human cyclin A1 and cyclin A1-associated kinase activities was regulated during the mitotic cell cycle. In the osteosarcoma cell line MG63, cyclin A1 mRNA and protein were present at very low levels in cells at the G0 phase. They increased during the progression of the cell cycle and reached the highest levels in the S and G2/M phases. Furthermore, the cyclin A1-associated histone H1 kinase activity peaked at the G2/M phase. We report that cyclin A1 could bind to important cell cycle regulators: the Rb family of proteins, the transcription factor E2F-1, and the p21 family of proteins. The in vitro interaction of cyclin A1 with E2F-1 was greatly enhanced when cyclin A1 was complexed with CDK2. Associations of cyclin A1 with Rb and E2F-1 were observed in vivo in several cell lines. When cyclin A1 was coexpressed with CDK2 in sf9 insect cells, the CDK2-cyclin A1 complex had kinase activities for histone H1, E2F-1, and the Rb family of proteins. Our results suggest that the Rb family of proteins and E2F-1 may be important targets for phosphorylation by the cyclin A1-associated kinase. Cyclin A1 may function in the mitotic cell cycle in certain cells.

scholarly journals Protein kinase C acts downstream of calcium at entry into the first mitotic interphase of Xenopus laevis.

1990 ◽  
Vol 1 (3) ◽  
pp. 315-326 ◽  
Author(s):  
W M Bement ◽  
D G Capco
Keyword(s):  
Cell Cycle ◽  
Protein Kinase C ◽  
Protein Kinase ◽  
Xenopus Laevis ◽  
Mitotic Cell ◽  
Cortical Granule ◽  
Mitotic Cell Cycle ◽  
Cleavage Furrow ◽  
Kinase C ◽  
Cortical Granule Exocytosis

Transit into interphase of the first mitotic cell cycle in amphibian eggs is a process referred to as activation and is accompanied by an increase in intracellular free calcium [( Ca2+]i), which may be transduced into cytoplasmic events characteristic of interphase by protein kinase C (PKC). To investigate the respective roles of [Ca2+]i and PKC in Xenopus laevis egg activation, the calcium signal was blocked by microinjection of the calcium chelator BAPTA, or the activity of PKC was blocked by PKC inhibitors sphingosine or H7. Eggs were then challenged for activation by treatment with either calcium ionophore A23187 or the PKC activator PMA. BAPTA prevented cortical contraction, cortical granule exocytosis, and cleavage furrow formation in eggs challenged with A23187 but not with PMA. In contrast, sphingosine and H7 inhibited cortical granule exocytosis, cortical contraction, and cleavage furrow formation in eggs challenged with either A23187 or PMA. Measurement of egg [Ca2+]i with calcium-sensitive electrodes demonstrated that PMA treatment does not increase egg [Ca2+]i in BAPTA-injected eggs. Further, PMA does not increase [Ca2+]i in eggs that have not been injected with BAPTA. These results show that PKC acts downstream of the [Ca2+]i increase to induce cytoplasmic events of the first Xenopus mitotic cell cycle.

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