scholarly journals Genome-Wide Identification and Analysis of Cell Cycle Genes in Betula pendula

2021 ◽  
Author(s):  
Yijie Li ◽  
Song Chen ◽  
Yuhang Liu ◽  
Haijiao Huang
Keyword(s):  
Cell Cycle ◽  
Growth And Development ◽  
Betula Pendula ◽  
Cell Cycle Progression ◽  
Transcript Abundance ◽  
Cell Cycle Gene ◽  
Specific Expression ◽  
Cell Cycles ◽  
Cell Cycle Genes ◽  
Functional Studies

Research Highlights: This study identified the cell cycle genes in birch that likely play important roles during plant growth and development. This analysis provides a basis for understanding the regulatory mechanism of various cell cycles in Betula pendula. Background and Objectives: The cell cycle factors not only influence cell cycle progression together, but also regulate accretion, division and differentiation of cells, and then regulate growth and development of plant. In this study, we identified the putative cell cycle genes in B. pendula genome, based on the annotated cell cycle genes in A. thaliana. It could serve as a foundation for further functional studies. Materials and Methods: The transcript abundance was determined for all the cell cycle genes in xylem, root, leaf and flower tissues using RNA-seq technology. Results: We identified 59 cell cycle gene models in the genome of B. pendula, 17 highly expression genes among them. These genes were BpCDKA.1, BpCDKB1.1, BpCDKB2.1, BpCKS1.2, BpCYCB1.1, BpCYCB1.2, BpCYCB2.1, BpCYCD3.1, BpCYCD3.5, BpDEL1, BpDpa2, BpE2Fa, BpE2Fb, BpKRP1, BpKRP2, BpRb1 and BpWEE1. Conclusions: We identified 17 core cell cycle genes in the genome of birch by combining phylogenetic analysis and tissue specific expression data.

scholarly journals Genome-Wide Identification and Analysis of Cell Cycle Genes in Betula pendula

2021 ◽  
Author(s):  
Yijie Li ◽  
Song Chen ◽  
Yuhang Liu ◽  
Haijiao Huang
Keyword(s):  
Cell Cycle ◽  
Growth And Development ◽  
Betula Pendula ◽  
Cell Cycle Progression ◽  
Transcript Abundance ◽  
Specific Expression ◽  
Cell Cycles ◽  
Cell Cycle Genes ◽  
Functional Studies ◽  
Genome Wide

Research Highlights: This study identified the cell cycle genes in birch that likely play important roles during plant growth and development. This provides a basis for understanding the regulatory mechanism of various cell cycles in Betula pendula. Background and Objectives: The cell cycle factors not only influence cell cycle progression together, but also regulate accretion, division and differentiation of cells, and then regulate growth and development of plant. In this study, we identified the putative cell cycle genes in B. pendula genome, based on the annotated cell cycle genes in A. thaliana. It could serve as a foundation for further functional studies. Materials and Methods: The transcript abundance was determined for all the cell cycle genes in xylem, root, leaf and flower tissues using RNA-seq technology. Results: We identified 59cell cycle gene models in the genome of B. pendula, 17 highly expression genes among them. These genes were BpCDKA.1, BpCDKB1.1, BpCDKB2.1, BpCKS1.2, BpCYCB1.1, BpCYCB1.2, BpCYCB2.1, BpCYCD3.1, BpCYCD3.5, BpDEL1, BpDpa2, BpE2Fa, BpE2Fb, BpKRP1, BpKRP2, BpRb1 and BpWEE1. Conclusions: We identified 17 core cell cycle genes in the genome of birch by combining phylogenetic analysis and tissue specific expression data.

scholarly journals Genome-Wide Identification and Analysis of Cell Cycle Genes in Birch

Forests ◽  
2022 ◽  
Vol 13 (1) ◽  
pp. 120
Author(s):  
Yijie Li ◽  
Song Chen ◽  
Yuhang Liu ◽  
Haijiao Huang
Keyword(s):  
Cell Cycle ◽  
Growth And Development ◽  
Betula Pendula ◽  
Cell Cycle Gene ◽  
Expression Data ◽  
Rna Seq ◽  
Specific Expression ◽  
Cell Cycles ◽  
Cell Cycle Genes ◽  
Genome Wide

Research Highlights: This study identified the cell cycle genes in birch that likely play important roles during the plant’s growth and development. This analysis provides a basis for understanding the regulatory mechanism of various cell cycles in Betula pendula Roth. Background and Objectives: The cell cycle factors not only influence cell cycles progression together, but also regulate accretion, division, and differentiation of cells, and then regulate growth and development of the plant. In this study, we identified the putative cell cycle genes in the B. pendula genome, based on the annotated cell cycle genes in Arabidopsis thaliana (L.) Heynh. It can be used as a basis for further functional research. Materials and Methods: RNA-seq technology was used to determine the transcription abundance of all cell cycle genes in xylem, roots, leaves, and floral tissues. Results: We identified 59 cell cycle gene models in the genome of B. pendula, with 17 highly expression genes among them. These genes were BpCDKA.1, BpCDKB1.1, BpCDKB2.1, BpCKS1.2, BpCYCB1.1, BpCYCB1.2, BpCYCB2.1, BpCYCD3.1, BpCYCD3.5, BpDEL1, BpDpa2, BpE2Fa, BpE2Fb, BpKRP1, BpKRP2, BpRb1, and BpWEE1. Conclusions: By combining phylogenetic analysis and tissue-specific expression data, we identified 17 core cell cycle genes in the Betulapendula genome.

scholarly journals RB, p130 and p107 differentially repress G1/S and G2/M genes after p53 activation

2019 ◽  
Vol 47 (21) ◽  
pp. 11197-11208 ◽  
Author(s):  
Amy E Schade ◽  
Martin Fischer ◽  
James A DeCaprio
Keyword(s):  
Gene Expression ◽  
Cell Cycle ◽  
Dna Damage ◽  
Cell Cycle Progression ◽  
Human Fibroblasts ◽  
Cell Cycle Gene ◽  
Cycle Progression ◽  
Cell Cycle Genes ◽  
P53 Activation ◽  
S Genes

Abstract Cell cycle gene expression occurs in two waves. The G1/S genes encode factors required for DNA synthesis and the G2/M genes contribute to mitosis. The Retinoblastoma protein (RB) and DREAM complex (DP, RB-like, E2F4 and MuvB) cooperate to repress all cell cycle genes during G1 and inhibit entry into the cell cycle. DNA damage activates p53 leading to increased levels of p21 and inhibition of cell cycle progression. Whether the G1/S and G2/M genes are differentially repressed by RB and the RB-like proteins p130 and p107 in response to DNA damage is not known. We performed gene expression profiling of primary human fibroblasts upon DNA damage and assessed the effects on G1/S and G2/M genes. Upon p53 activation, p130 and RB cooperated to repress the G1/S genes. In addition, in the absence of RB and p130, p107 contributed to repression of G1/S genes. In contrast, G2/M genes were repressed by p130 and p107 after p53 activation. Furthermore, repression of G2/M genes by p107 and p130 led to reduced entry into mitosis. Our data demonstrates specific roles for RB, p130-DREAM, and p107-DREAM in p53 and p21 mediated repression of cell cycle genes.

scholarly journals A Genetic Screen for Suppressors and Enhancers of the Drosophila Cdk1-Cyclin B Identifies Maternal Factors That Regulate Microtubule and Microfilament Stability

Genetics ◽  
2002 ◽  
Vol 162 (3) ◽  
pp. 1179-1195 ◽  
Author(s):  
Jun-Yuan Ji ◽  
Marjan Haghnia ◽  
Cory Trusty ◽  
Lawrence S B Goldstein ◽  
Gerold Schubiger
Keyword(s):  
Cell Cycle ◽  
Cell Cycle Progression ◽  
Genetic Screen ◽  
Cyclin B ◽  
Gene Products ◽  
Nuclear Movement ◽  
Cell Cycles ◽  
Major Mechanism ◽  
Cytoskeletal Dynamics ◽  
Chromosome Bridges

Abstract Coordination between cell-cycle progression and cytoskeletal dynamics is important for faithful transmission of genetic information. In early Drosophila embryos, increasing maternal cyclin B leads to higher Cdk1-CycB activity, shorter microtubules, and slower nuclear movement during cycles 5-7 and delays in nuclear migration to the cortex at cycle 10. Later during cycle 14 interphase of six cycB embryos, we observed patches of mitotic nuclei, chromosome bridges, abnormal nuclear distribution, and small and large nuclei. These phenotypes indicate disrupted coordination between the cell-cycle machinery and cytoskeletal function. Using these sensitized phenotypes, we performed a dosage-sensitive genetic screen to identify maternal proteins involved in this process. We identified 10 suppressors classified into three groups: (1) gene products regulating Cdk1 activities, cdk1 and cyclin A; (2) gene products interacting with both microtubules and microfilaments, Actin-related protein 87C; and (3) gene products interacting with microfilaments, chickadee, diaphanous, Cdc42, quail, spaghetti-squash, zipper, and scrambled. Interestingly, most of the suppressors that rescue the astral microtubule phenotype also reduce Cdk1-CycB activities and are microfilament-related genes. This suggests that the major mechanism of suppression relies on the interactions among Cdk1-CycB, microtubule, and microfilament networks. Our results indicate that the balance among these different components is vital for normal early cell cycles and for embryonic development. Our observations also indicate that microtubules and cortical microfilaments antagonize each other during the preblastoderm stage.

scholarly journals Heat shock protein 27 promotes cell cycle progression by down-regulating E2F transcription factor 4 and retinoblastoma family protein p130

2018 ◽  
Vol 293 (41) ◽  
pp. 15815-15826 ◽  
Author(s):  
Ah-Mee Park ◽  
Ikuo Tsunoda ◽  
Osamu Yoshie
Keyword(s):  
Cell Cycle ◽  
Heat Shock ◽  
Heat Shock Protein ◽  
Cellular Senescence ◽  
Cell Cycle Progression ◽  
Heat Shock Protein 27 ◽  
Serum Starvation ◽  
Cell Cycle Gene ◽  
Cycle Progression ◽  
Human Lung Fibroblast

Heat shock protein 27 (HSP27) protects cells under stress. Here, we demonstrate that HSP27 also promotes cell cycle progression of MRC-5 human lung fibroblast cells. Serum starvation for 24 h induced G1 arrest in these cells, and upon serum refeeding, the cells initiated cell cycle progression accompanied by an increase in HSP27 protein levels. HSP27 levels peaked at 12 h, and transcriptional up-regulation of six G2/M-related genes (CCNA2, CCNB1, CCNB2, CDC25C, CDCA3, and CDK1) peaked at 24–48 h. siRNA-mediated HSP27 silencing in proliferating MRC-5 cells induced G2 arrest coinciding with down-regulation of these six genes. Of note, the promoters of all of these genes have the cell cycle–dependent element and/or the cell cycle gene-homology region. These promoter regions are known to be bound by the E2F family proteins (E2F-1 to E2F-8) and retinoblastoma (RB) family proteins (RB1, p107, and p130), among which E2F-4 and p130 were strongly up-regulated in HSP27-knockdown cells. E2F-4 or p130 knockdown concomitant with the HSP27 knockdown rescued MRC-5 cells from G2 arrest and up-regulated the six cell cycle genes. Moreover, we observed cellular senescence in MRC-5 cells on day 3 after the HSP27 knockdown, as evidenced by increased senescence-associated β-gal activity and up-regulated inflammatory cytokines. The cellular senescence was also suppressed by the concomitant knockdown of E2F-4/HSP27 or p130/HSP27. Our findings indicate that HSP27 promotes cell cycle progression of MRC-5 cells by suppressing expression of the transcriptional repressors E2F-4 and p130.

The NIMA-related kinase X-Nek2B is required for efficient assembly of the zygotic centrosome in Xenopus laevis

2000 ◽  
Vol 113 (11) ◽  
pp. 1973-1984 ◽  
Author(s):  
A.M. Fry ◽  
P. Descombes ◽  
C. Twomey ◽  
R. Bacchieri ◽  
E.A. Nigg
Keyword(s):  
Cell Cycle ◽  
Xenopus Laevis ◽  
Basal Body ◽  
Chromatin Condensation ◽  
Embryonic Cells ◽  
Serine Threonine Kinase ◽  
Cell Cycles ◽  
Functional Studies ◽  
Mammalian Cell Cycle ◽  
Egg Extracts

Nek2 is a mammalian cell cycle-regulated serine/threonine kinase that belongs to the family of proteins related to NIMA of Aspergillus nidulans. Functional studies in diverse species have implicated NIMA-related kinases in G(2)/M progression, chromatin condensation and centrosome regulation. To directly address the requirements for vertebrate Nek2 kinases in these cell cycle processes, we have turned to the biochemically-tractable system provided by Xenopus laevis egg extracts. Following isolation of a Xenopus homologue of Nek2, called X-Nek2B, we found that X-Nek2B abundance and activity remained constant through the first mitotic cycle implying a fundamental difference in Nek2 regulation between embryonic and somatic cell cycles. Removal of X-Nek2B from extracts did not disturb either entry into mitosis or the accompanying condensation of chromosomes providing no support for a requirement for Nek2 in these processes at least in embryonic cells. In contrast, X-Nek2B localized to centrosomes of adult Xenopus cells and was rapidly recruited to the basal body of Xenopus sperm following incubation in egg extracts. Recruitment led to phosphorylation of the X-Nek2B kinase. Most importantly, depletion of X-Nek2B from extracts significantly delayed both the assembly of microtubule asters and the recruitment of gamma-tubulin to the basal body. Hence, these studies demonstrate that X-Nek2B is required for efficient assembly of a functional zygotic centrosome and highlight the possibility of multiple roles for vertebrate Nek2 kinases in the centrosome cycle.

Stage specific expression of cell cycle genes during in vivo or in vitro development of ovarian follicles in sheep

2016 ◽  
Vol 143 ◽  
pp. 1-7 ◽  
Author(s):  
V. Praveen Chakravarthi ◽  
S.S.R. Kona ◽  
A.V.N. Siva Kumar ◽  
M. Bhaskara ◽  
V.H. Rao
Keyword(s):  
Cell Cycle ◽  
Ovarian Follicles ◽  
Specific Expression ◽  
In Vitro Development ◽  
Cell Cycle Genes ◽  
Vitro Development

Comparative genomics identifies genes mediating cardiotoxicity in the embryonic zebrafish heart

2008 ◽  
Vol 33 (2) ◽  
pp. 148-158 ◽  
Author(s):  
Jing Chen ◽  
Sara A. Carney ◽  
Richard E. Peterson ◽  
Warren Heideman
Keyword(s):  
Heart Failure ◽  
Cell Cycle ◽  
Heart Development ◽  
Cell Cycle Progression ◽  
Transcriptional Response ◽  
Cell Cycle Gene ◽  
Zebrafish Embryos ◽  
Transcriptional Responses ◽  
Cycle Progression ◽  
Necessary And Sufficient

Retinoic acid (RA) and 2,3,7,8-tetrachlorodibenzo- p-dioxin (TCDD) activate distinct ligand-dependent transcription factors, and both cause cardiac malformation and heart failure in zebrafish embryos. We hypothesized that they cause this response by hyperactivating a common set of genes critical for heart development. To test this, we used microarrays to measure transcript changes in hearts isolated from zebrafish embryos 1, 2, 4, and 12 h after exposure to 1 μM RA. We used hierarchical clustering to compare the transcriptional responses produced in the embryonic heart by RA and TCDD. We could identify no early responses in common between the two agents. However, at 12 h both treatments produced a dramatic downregulation of a common cluster of cell cycle progression genes, which we term the cell cycle gene cluster. This was associated with a halt in heart growth. These results suggest that RA and TCDD ultimately trigger a common transcriptional response associated with heart failure, but not through the direct activation of a common set of genes. Among the genes rapidly induced by RA was Nr2F5, a member of the COUP-TF family of transcriptional repressors. We found that induction of Nr2F5 was both necessary and sufficient for the cardiotoxic response to RA.

scholarly journals Progesterone Increases Rat Neural Progenitor Cell Cycle Gene Expression and Proliferation Via Extracellularly Regulated Kinase and Progesterone Receptor Membrane Components 1 and 2

Endocrinology ◽  
2009 ◽  
Vol 150 (7) ◽  
pp. 3186-3196 ◽  
Author(s):  
Lifei Liu ◽  
Junming Wang ◽  
Liqin Zhao ◽  
Jon Nilsen ◽  
Kelsey McClure ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Progesterone Receptor ◽  
Progenitor Cell ◽  
Neural Progenitor Cell ◽  
Neural Progenitor ◽  
Mammalian Brain ◽  
Cell Cycle Gene ◽  
Cell Cycle Genes ◽  
Expression Of Genes ◽  
Membrane Components

Progesterone receptor (PR) expression and regulation of neural progenitor cell (NPC) proliferation was investigated using NPC derived from adult rat brain. RT-PCR revealed that PRA mRNA was not detected in rat NPCs, whereas membrane-associated PRs, PR membrane components (PGRMCs) 1 and 2, mRNA were expressed. Progesterone-induced increase in 5-bromo-2-deoxyuridine incorporation was confirmed by fluorescent-activated cell sorting analysis, which indicated that progesterone promoted rat NPC exit of G0/G1 phase at 5 h, followed by an increase in S-phase at 6 h and M-phase at 8 h, respectively. Microarray analysis of cell-cycle genes, real-time PCR, and Western blot validation revealed that progesterone increased expression of genes that promote mitosis and decreased expression of genes that repress cell proliferation. Progesterone-induced proliferation was not dependent on conversion to metabolites and was antagonized by the ERK1/2 inhibitor UO126. Progesterone-induced proliferation was isomer and steroid specific. PGRMC1 small interfering RNA treatment, together with computational structural analysis of progesterone and its isomers, indicated that the proliferative effect of progesterone is mediated by PGRMC1/2. Progesterone mediated NPC proliferation and concomitant regulation of mitotic cell cycle genes via a PGRMC/ERK pathway mechanism is a potential novel therapeutic target for promoting neurogenesis in the mammalian brain.

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