The FA2 gene of Chlamydomonas encodes a NIMA family kinase with roles in cell cycle progression and microtubule severing during deflagellation

2002 ◽  
Vol 115 (8) ◽  
pp. 1759-1768 ◽  
Author(s):  
Moe R. Mahjoub ◽  
Ben Montpetit ◽  
Lifan Zhao ◽  
Rip J. Finst ◽  
Benjamin Goh ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Chlamydomonas Reinhardtii ◽  
Basal Body ◽  
Cell Cycle Progression ◽  
Chromatin Condensation ◽  
Eukaryotic Cell ◽  
Genetic Screen ◽  
Cycle Progression ◽  
Microtubule Severing

The NIMA kinases are one of several families of kinases that participate in driving the eukaryotic cell cycle. NIMA-related kinases have been implicated in G2/M progression, chromatin condensation and regulation of the centrosome cycle. Here we report the identification of a new member of this family, FA2, from Chlamydomonas reinhardtii. FA2 was originally discovered in a genetic screen for deflagellation-defective mutants. We have previously shown that FA2 is essential for basal-body/centriole-associated microtubule severing. We now report that the FA2 NIMA-related kinase also plays a role in cell cycle progression in Chlamydomonas. This is the first indication that members of the NIMA family might exert their effects through the regulation of microtubule severing.

scholarly journals Katanin Knockdown Supports a Role for Microtubule Severing in Release of Basal Bodies before Mitosis in Chlamydomonas

2009 ◽  
Vol 20 (1) ◽  
pp. 379-388 ◽  
Author(s):  
M. Qasim Rasi ◽  
Jeremy D.K. Parker ◽  
Jessica L. Feldman ◽  
Wallace F. Marshall ◽  
Lynne M. Quarmby
Keyword(s):  
Cell Cycle ◽  
Rna Interference ◽  
Transition Zone ◽  
Basal Body ◽  
Cell Cycle Progression ◽  
Basal Bodies ◽  
Cycle Progression ◽  
Microtubule Severing ◽  
Regulation Of Cell Cycle ◽  
Precise Role

Katanin is a microtubule-severing protein that participates in the regulation of cell cycle progression and in ciliary disassembly, but its precise role is not known for either activity. Our data suggest that in Chlamydomonas, katanin severs doublet microtubules at the proximal end of the flagellar transition zone, allowing disengagement of the basal body from the flagellum before mitosis. Using an RNA interference approach we have discovered that severe knockdown of the p60 subunit of katanin, KAT1, is achieved only in cells that also carry secondary mutations that disrupt ciliogenesis. Importantly, we observed that cells in the process of cell cycle-induced flagellar resorption sever the flagella from the basal bodies before resorption is complete, and we find that this process is defective in KAT1 knockdown cells.

scholarly journals To Divide or Not to Divide? How Deuterium Affects Growth and Division of Chlamydomonas reinhardtii

Biomolecules ◽  
2021 ◽  
Vol 11 (6) ◽  
pp. 861
Author(s):  
Veronika Kselíková ◽  
Vilém Zachleder ◽  
Kateřina Bišová
Keyword(s):  
Cell Cycle ◽  
Chlamydomonas Reinhardtii ◽  
Cell Cycle Progression ◽  
Model Organism ◽  
Cycle Progression ◽  
Synchronous Cultures ◽  
Multiple Fission ◽  
First Choice ◽  
High Doses

Extensive in vivo replacement of hydrogen by deuterium, a stable isotope of hydrogen, induces a distinct stress response, reduces cell growth and impairs cell division in various organisms. Microalgae, including Chlamydomonas reinhardtii, a well-established model organism in cell cycle studies, are no exception. Chlamydomonas reinhardtii, a green unicellular alga of the Chlorophyceae class, divides by multiple fission, grows autotrophically and can be synchronized by alternating light/dark regimes; this makes it a model of first choice to discriminate the effect of deuterium on growth and/or division. Here, we investigate the effects of high doses of deuterium on cell cycle progression in C. reinhardtii. Synchronous cultures of C. reinhardtii were cultivated in growth medium containing 70 or 90% D2O. We characterize specific deuterium-induced shifts in attainment of commitment points during growth and/or division of C. reinhardtii, contradicting the role of the “sizer” in regulating the cell cycle. Consequently, impaired cell cycle progression in deuterated cultures causes (over)accumulation of starch and lipids, suggesting a promising potential for microalgae to produce deuterated organic compounds.

scholarly journals Centrin Gene Disruption Impairs Stage-specific Basal Body Duplication and Cell Cycle Progression inLeishmania

2004 ◽  
Vol 279 (24) ◽  
pp. 25703-25710 ◽  
Author(s):  
Angamuthu Selvapandiyan ◽  
Alain Debrabant ◽  
Robert Duncan ◽  
Jacqueline Muller ◽  
Poonam Salotra ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Basal Body ◽  
Gene Disruption ◽  
Cell Cycle Progression ◽  
Cycle Progression

Cyclin specificity: how many wheels do you need on a unicycle?

2001 ◽  
Vol 114 (10) ◽  
pp. 1811-1820 ◽  
Author(s):  
M.E. Miller ◽  
F.R. Cross
Keyword(s):  
Cell Cycle ◽  
Subcellular Localization ◽  
Cell Cycle Progression ◽  
Eukaryotic Cell ◽  
Cyclin Dependent Kinase ◽  
Temporal Expression ◽  
Cycle Progression

Cyclin-dependent kinase (CDK) activity is essential for eukaryotic cell cycle events. Multiple cyclins activate CDKs in all eukaryotes, but it is unclear whether multiple cyclins are really required for cell cycle progression. It has been argued that cyclins may predominantly act as simple enzymatic activators of CDKs; in opposition to this idea, it has been argued that cyclins might target the activated CDK to particular substrates or inhibitors. Such targeting might occur through a combination of factors, including temporal expression, protein associations, and subcellular localization.

Characterization of HDACI OSU42 as a Novel Histone Deacetylase Inhibitor in AML Cell Lines.

Blood ◽  
2006 ◽  
Vol 108 (11) ◽  
pp. 1988-1988
Author(s):  
Jin Sun ◽  
Shujun Liu ◽  
Jianhua Yu ◽  
Min Wei ◽  
Charlene Mao ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Gene Silencing ◽  
Cell Cycle Progression ◽  
Chromatin Condensation ◽  
Regulation Of Gene Expression ◽  
Histone H3 ◽  
Malignant Cells ◽  
Cycle Progression ◽  
Nb4 Cells ◽  
Histone Hypoacetylation

Abstract Histone acetylation plays a key role in the regulation of gene expression. Histone hyperacetylation is associated with chromatin opening and gene transcription, while histone hypoacetylation is associated with chromatin condensation and gene silencing. Abnormal histone hypoacetylation mediated by aberrant activity of histone deacetylases (HDACs) has been found to be associated with silencing of tumor suppressor and growth inhibitory genes in malignant cells. HDAC inhibitors (HDACIs) can relieve HDAC-mediated gene silencing and thereby induce normal patterns of cell cycle, differentiation and apoptosis in malignant cells. HDACI OSU 42 is a novel hydroxamate tethered phenylbutyrate derivative that was designed and synthesized at our institution, and exhibited IC50s at submicromolar level, compared with millimolar level for other members of this classes of HDACIs such as valproic acid (VPA). We characterized the activity of this compound in acute myeloid leukemia (AML) cells. It is known that the fusion proteins AML1/ETO and PML / RAR alpha that characterized t(8;21) and t(15;17) AML silence target genes through recruitment of HDACs to their promoter regions. Therefore we utilized AML1/ETO-positive Kasumi-1 and PML/RARA-positive NB4 cells to test the activity of HDACI OSU 42 and used THP-1 cells, characterized by AF9/MLL fusion gene, as a control. We hypothesized that by virtue of the fusion genes, Kasumi-1 and NB4 are more susceptible to HDACI treatment. IC50s for proliferation inhibition in Kasumi-1 cells treated with HDACI OSU42 were 71.8±14.3nM for 24hr and 31.3± 0.4nM for 48hr, significantly lower than VPA (2.0mM for 24hr, 0.9mM for 48hr). The IC50s for NB4 were 237.7±6.5nM for 24hr and 119±6.4nM for 48hr. As a contrast, IC50 for THP-1 was 507.3±68.3nM for 48hr. HDACI OSU42 inhibited 80% of total HDAC activity at 125nM in both Kasumi-1 and NB4; 30nM HDACI OSU42 induced hyperacetylation of histone H3 and H4. Apoptosis analysis showed that nearly 60% more of Kasumi-1 and NB4 underwent apoptosis after treated with 1μM of HDACI OSU42 for 24hr, compared with their untreated control. On the other hand, the same treatment only induced 15% more of THP-1 undergoing apoptosis. Apoptotic effect of HDACI OSU42 was mediated by activation of caspase 9 and caspase 3. Cell cycle analysis demonstrated that treatment of Kasumi-1 and NB4 with 150nM of HDACI OSU 42 inhibited cell cycle progression and arrested 20% to 30% more cells at S phase or G2/M phase, whereas this treatment had not effect on cell cycle progression of THP-1. This was consistent with the up-regulated expression of p21 at both transcription level and protein level. Q-PCR data suggested that Kasumi-1 and NB4 treated with HDACI OSU42 expressed ~10 folds of p21 higher than untreated cells. Chromatin immunoprecipitation assay revealed 10 to 50 folds increase in acetylation level of histone H3 and H4 associated with p21 promoter. Kasumi-1 and NB4 cells also show differentiation ability (increase in CD14 and CD 13 expression by flow cytometry) when treated with 30nM of HDACI OSU42, whereas THP-1 remained undifferentiated. These results support the activity of HDACI OSU42 as a new potent HDACI in AML.

Epigenetic dynamics across the cell cycle

2010 ◽  
Vol 48 ◽  
pp. 107-120 ◽  
Author(s):  
Tony Bou Kheir ◽  
Anders H. Lund
Keyword(s):  
Cell Cycle ◽  
Chromosome Segregation ◽  
Cell Cycle Progression ◽  
Current Knowledge ◽  
Chromatin Condensation ◽  
Chromatin Modifications ◽  
Cycle Progression ◽  
Daughter Cells ◽  
Mammalian Cell Cycle ◽  
Regulate Cell Cycle Progression

Progression of the mammalian cell cycle depends on correct timing and co-ordination of a series of events, which are managed by the cellular transcriptional machinery and epigenetic mechanisms governing genome accessibility. Epigenetic chromatin modifications are dynamic across the cell cycle, and are shown to influence and be influenced by cell-cycle progression. Chromatin modifiers regulate cell-cycle progression locally by controlling the expression of individual genes and globally by controlling chromatin condensation and chromosome segregation. The cell cycle, on the other hand, ensures a correct inheritance of epigenetic chromatin modifications to daughter cells. In this chapter, we summarize the current knowledge on the dynamics of epigenetic chromatin modifications during progression of the cell cycle.

Changes in nitric oxide/hydrogen peroxide content and cell cycle progression: Study with synchronized cultures of green alga Chlamydomonas reinhardtii

2017 ◽  
Vol 208 ◽  
pp. 84-93 ◽  
Author(s):  
Wojciech Pokora ◽  
Anna Aksmann ◽  
Agnieszka Baścik-Remisiewicz ◽  
Agnieszka Dettlaff-Pokora ◽  
Max Rykaczewski ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Cell Cycle ◽  
Hydrogen Peroxide ◽  
Chlamydomonas Reinhardtii ◽  
Green Alga ◽  
Cell Cycle Progression ◽  
Cycle Progression ◽  
Peroxide Content ◽  
Synchronized Cultures

scholarly journals A fission yeast homolog of CDC20/p55CDC/Fizzy is required for recovery from DNA damage and genetically interacts with p34cdc2.

1997 ◽  
Vol 17 (2) ◽  
pp. 742-750 ◽  
Author(s):  
T Matsumoto
Keyword(s):  
Cell Cycle ◽  
Dna Damage ◽  
Dna Repair ◽  
Fission Yeast ◽  
Cell Cycle Progression ◽  
Eukaryotic Cell ◽  
Cycle Progression ◽  
Cell Cycle Delay ◽  
Successful Recovery ◽  
Synthetically Lethal

Successful recovery from DNA damage requires coordination of several biological processes. Eukaryotic cell cycle progression is delayed when the cells encounter DNA-damaging agents. This cell cycle delay allows the cells to cope with DNA damage by utilizing DNA repair enzymes. Thus, at least two processes, induction of the cell cycle delay and repair of damaged DNA, are coordinately required for recovery. In this study, a fission yeast rad mutant (slp1-362) was genetically investigated. In response to radiation, slp1 stops cell division; however, it does not restart it. This defect is suppressed when slp1-362 is combined with wee1-50 or cdc2-3w; in these mutants, the onset of mitosis is advanced due to the premature activation of p34cdc2. In contrast, slp1 is synthetically lethal with cdc25, nim1/cdr1, or cdr2, all of which are unable to activate the p34cdc2 kinase correctly. These genetic interactions of slp1 with cdc2 and its modulators imply that slp1 is not defective in either "induction of cell cycle delay" or "DNA repair." slp1+ may be involved in a critical process which restarts cell cycle progression after the completion of DNA repair. Molecular cloning of slp1+ revealed that slp1+ encodes a putative 488-amino-acid polypeptide exhibiting significant homology to WD-domain proteins, namely, CDC20 (budding yeast), p55CDC (human), and Fizzy (fly). A possible role of slp1+ is proposed.

scholarly journals Alpha-Tubulin Acetylation in Trypanosoma cruzi: A Dynamic Instability of Microtubules Is Required for Replication and Cell Cycle Progression

2021 ◽  
Vol 11 ◽  
Author(s):  
Victoria Lucia Alonso ◽  
Mara Emilia Carloni ◽  
Camila Silva Gonçalves ◽  
Gonzalo Martinez Peralta ◽  
Maria Eugenia Chesta ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Trypanosoma Cruzi ◽  
Basal Body ◽  
Mitotic Spindle ◽  
Cell Cycle Progression ◽  
Dynamic Instability ◽  
Cycle Progression ◽  
Alpha Tubulin ◽  
Over Expression ◽  
Tubulin Acetylation

Trypanosomatids have a cytoskeleton arrangement that is simpler than what is found in most eukaryotic cells. However, it is precisely organized and constituted by stable microtubules. Such microtubules compose the mitotic spindle during mitosis, the basal body, the flagellar axoneme and the subpellicular microtubules, which are connected to each other and also to the plasma membrane forming a helical arrangement along the central axis of the parasite cell body. Subpellicular, mitotic and axonemal microtubules are extensively acetylated inTrypanosoma cruzi. Acetylation on lysine (K) 40 of α-tubulin is conserved from lower eukaryotes to mammals and is associated with microtubule stability. It is also known that K40 acetylation occurs significantly on flagella, centrioles, cilia, basal body and the mitotic spindle in eukaryotes. Several tubulin posttranslational modifications, including acetylation of K40, have been cataloged in trypanosomatids, but the functional importance of these modifications for microtubule dynamics and parasite biology remains largely undefined. The primary tubulin acetyltransferase was recently identified in several eukaryotes as Mec-17/ATAT, a Gcn5-related N-acetyltransferase. Here, we report thatT. cruziATAT acetylates α-tubulinin vivoand is capable of auto-acetylation.TcATAT is located in the cytoskeleton and flagella of epimastigotes and colocalizes with acetylated α-tubulin in these structures. We have expressedTcATAT with an HA tag using the inducible vector pTcINDEX-GW inT. cruzi. Over-expression ofTcATAT causes increased levels of the alpha tubulin acetylated species, induces morphological and ultrastructural defects, especially in the mitochondrion, and causes a halt in the cell cycle progression of epimastigotes, which is related to an impairment of the kinetoplast division. Finally, as a result ofTcATAT over-expression we observed that parasites became more resistant to microtubule depolymerizing drugs. These results support the idea that α-tubulin acetylation levels are finely regulated for the normal progression ofT. cruzicell cycle.

scholarly journals Control of cell cycle progression by phosphorylation of cyclin-dependent kinase (CDK) substrates

2010 ◽  
Vol 30 (4) ◽  
pp. 243-255 ◽  
Author(s):  
Randy Suryadinata ◽  
Martin Sadowski ◽  
Boris Sarcevic
Keyword(s):  
Cell Cycle ◽  
Cell Division ◽  
Cell Cycle Progression ◽  
Genetic Material ◽  
Eukaryotic Cell ◽  
S Phase ◽  
Cycle Progression ◽  
M Phase ◽  
Unicellular Organisms ◽  
Multicellular Organisms

The eukaryotic cell cycle is a fundamental evolutionarily conserved process that regulates cell division from simple unicellular organisms, such as yeast, through to higher multicellular organisms, such as humans. The cell cycle comprises several phases, including the S-phase (DNA synthesis phase) and M-phase (mitotic phase). During S-phase, the genetic material is replicated, and is then segregated into two identical daughter cells following mitotic M-phase and cytokinesis. The S- and M-phases are separated by two gap phases (G1 and G2) that govern the readiness of cells to enter S- or M-phase. Genetic and biochemical studies demonstrate that cell division in eukaryotes is mediated by CDKs (cyclin-dependent kinases). Active CDKs comprise a protein kinase subunit whose catalytic activity is dependent on association with a regulatory cyclin subunit. Cell-cycle-stage-dependent accumulation and proteolytic degradation of different cyclin subunits regulates their association with CDKs to control different stages of cell division. CDKs promote cell cycle progression by phosphorylating critical downstream substrates to alter their activity. Here, we will review some of the well-characterized CDK substrates to provide mechanistic insights into how these kinases control different stages of cell division.

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