Genetics of the cell cycle: Adaptive modification of the CycB 2g mutation expression in dividing cells of Drosophila melanogaster

2005 ◽  
Vol 41 (3) ◽  
pp. 237-243 ◽  
Author(s):  
L. I. Lebedeva ◽  
S. A. Trunova ◽  
L. V. Omelyanchuk
Keyword(s):  
Cell Cycle ◽  
Drosophila Melanogaster ◽  
Adaptive Modification ◽  
Dividing Cells

Mutations of the fizzy locus cause metaphase arrest in Drosophila melanogaster embryos

Development ◽  
1993 ◽  
Vol 117 (1) ◽  
pp. 359-376 ◽  
Author(s):  
I.A. Dawson ◽  
S. Roth ◽  
M. Akam ◽  
S. Artavanis-Tsakonas
Keyword(s):  
Cell Cycle ◽  
Cell Death ◽  
Drosophila Melanogaster ◽  
Double Mutant ◽  
Nuclear Division ◽  
Normal Function ◽  
Metaphase Arrest ◽  
Nervous Systems ◽  
Dividing Cells ◽  
A Cell

We describe the effects of mutations in the fizzy gene of Drosophila melanogaster and show that fizzy mutations cause cells in mitosis to arrest at metaphase. We show that maternally supplied fizzy activity is required for normal nuclear division in the preblastoderm embryo and, during later embryogenesis, that zygotic fizzy activity is required for the development of the ventrally derived epidermis and the central and peripheral nervous systems. In fizzy embryos, dividing cells in these tissues arrest at metaphase, fail to differentiate and ultimately die. In the ventral epidermis, if cells are prevented from entering mitosis by using a string mutation, cell death is prevented and the ability to differentiate ventral epidermis is restored in fizzy; string double mutant embryos. These results demonstrate that fizzy is a cell cycle mutation and that the normal function of the fizzy gene is required for dividing cells to exit metaphase and complete mitosis.

scholarly journals Dual roles for the Drosophila PI 4-kinase Four wheel drive in localizing Rab11 during cytokinesis

2009 ◽  
Vol 187 (6) ◽  
pp. 847-858 ◽  
Author(s):  
Gordon Polevoy ◽  
Ho-Chun Wei ◽  
Raymond Wong ◽  
Zsofia Szentpetery ◽  
Yeun Ju Kim ◽  
...  
Keyword(s):  
Drosophila Melanogaster ◽  
Critical Role ◽  
Successful Completion ◽  
Dual Roles ◽  
Recycling Endosome ◽  
Golgi Membranes ◽  
Wheel Drive ◽  
Dividing Cells ◽  
Four Wheel Drive

Successful completion of cytokinesis relies on addition of new membrane, and requires the recycling endosome regulator Rab11, which localizes to the midzone. Despite the critical role of Rab11 in this process, little is known about the formation and composition of Rab11-containing organelles. Here, we identify the phosphatidylinositol (PI) 4-kinase III β Four wheel drive (Fwd) as a key regulator of Rab11 during cytokinesis in Drosophila melanogaster spermatocytes. We show Fwd is required for synthesis of PI 4-phosphate (PI4P) on Golgi membranes and for formation of PI4P-containing secretory organelles that localize to the midzone. Fwd binds and colocalizes with Rab11 on Golgi membranes, and is required for localization of Rab11 in dividing cells. A kinase-dead version of Fwd also binds Rab11 and partially restores cytokinesis to fwd mutant flies. Moreover, activated Rab11 partially suppresses loss of fwd. Our data suggest Fwd plays catalytic and noncatalytic roles in regulating Rab11 during cytokinesis.

Clonal heterogeneity in the germinal zone of the developing rat telencephalon

Development ◽  
1993 ◽  
Vol 118 (1) ◽  
pp. 175-192 ◽  
Author(s):  
S.E. Acklin ◽  
D. van der Kooy
Keyword(s):  
Cell Cycle ◽  
Cell Lines ◽  
Spatial Organization ◽  
Precursor Cell ◽  
Clonal Heterogeneity ◽  
Double Labeling ◽  
Germinal Zone ◽  
Dividing Cells ◽  
Cellular Phenotypes ◽  
Developing Rat

A double-labeling technique, combining retroviral tagging of individual cell lines (one clone per brain hemisphere) with the simultaneous [3H]thymidine-labeling of dividing cells in S phase, was used to study proliferation characteristics of individual precursor cell lines in the germinal zone of the developing rat forebrain. The cortical germinal zone was found to be segregated into three spatially distinct horizontal populations of precursor cell lineages, which differed in cell cycle kinetics, amount of cell death, and synchronous versus asynchronous mode of proliferation. The striatal germinal zone demonstrated a similar heterogeneity in the cell cycle characteristics of proliferating clones, but did not show nearly as distinct a spatial segregation of these different populations. The results demonstrate the clonal heterogeneity among precursor populations in the telencephalon and the differential spatial organization of the cortical and the striatal germinal zones. This germinal zone heterogeneity may predict some of the differences found among cellular phenotypes in the adult forebrain.

Transcription of the histone H5 gene is not S-phase regulated

1986 ◽  
Vol 6 (2) ◽  
pp. 601-606
Author(s):  
S Dalton ◽  
J R Coleman ◽  
J R Wells
Keyword(s):  
Cell Cycle ◽  
Steady State ◽  
Northern Blotting ◽  
S Phase ◽  
Erythroid Cells ◽  
Dividing Cells ◽  
Steady State Levels ◽  
Avian Erythroblastosis Virus ◽  
Histone H5

Levels of the tissue-specific linker histone H5 are elevated in mature erythroid cells as compared with levels in dividing cells of the same lineage. We examined levels of H5 mRNA in relation to the cell cycle in early erythroid cells transformed by avian erythroblastosis virus to determine whether the gene for this unusual histone is S-phase regulated. Northern blotting analyses revealed that during the cell cycle steady-state levels of H5 mRNA remained relatively constant in contrast to levels of the major core and H1 mRNAs which increased approximately 15-fold during S phase. In vitro pulse-labeling experiments involving nuclei isolated from synchronized cells at various stages of the cell cycle revealed that transcription of the H5 gene was not initiated at any particular stage of the cell cycle but was constitutive. In contrast, transcription of the H2A gene(s) initiated in early S phase, was present throughout the DNA replicative phase, and was essentially absent in G1 and G2 phases.

Excision and replication of extrachromosomal DNA of pea (Pisum sativum)

1983 ◽  
Vol 3 (2) ◽  
pp. 172-181
Author(s):  
J Van't Hof ◽  
C A Bjerknes ◽  
N C Delihas
Keyword(s):  
Cell Cycle ◽  
Pisum Sativum ◽  
S Phase ◽  
Velocity Sedimentation ◽  
Extrachromosomal Dna ◽  
Chromosomal Dna ◽  
Root Tips ◽  
Dividing Cells ◽  
G2 Phase ◽  
Pea Roots

Experiments with cultured pea roots were conducted to determine (i) whether extrachromosomal DNA was produced by cells in the late S phase or in the G2 phase of the cell cycle, (ii) whether the maturation of nascent DNA replicated by these cells achieved chromosomal size, (iii) when extrachromosomal DNA was removed from the chromosomal duplex, and (iv) the replication of nascent chains by the extrachromosomal DNA after its release from the chromosomal duplex. Autoradiography and cytophotometry of cells of carbohydrate-starved root tips revealed that extrachromosomal DNA was produced by a small fraction of cells accumulated in the late S phase after they had replicated about 80% of their DNA. Velocity sedimentation of nascent chromosomal DNA in alkaline sucrose gradients indicated that the DNA of cells in the late S phase failed to achieve chromosomal size. After reaching sizes of 70 X 10(6) to 140 X 10(6) daltons, some of the nascent chromosomal molecules were broken, presumably releasing extrachromosomal DNA several hours later. Sedimentation of selectively extracted extrachromosomal DNA either from dividing cells or from those in the late S phase showed that it replicated two nascent chains, one of 3 X 10(6) daltons and another of 7 X 10(6) daltons. Larger molecules of extrachromosomal DNA were detectable after cells were labeled for 24 h. These two observations were compatible with the idea that the extrachromosomal DNA was first replicated as an integral part of the chromosomal duplex, was cut from the duplex, and then, once free of the chromosome, replicated two smaller chains of 3 X 10(6) and 7 X 10(6) daltons.

scholarly journals Fate of the M-phase-assembled centrioles during the cell cycle in the TP53;PCNT;CEP215-deleted cells

2020 ◽  
Author(s):  
Gee In Jung ◽  
Kunsoo Rhee
Keyword(s):  
Cell Cycle ◽  
Cancer Cells ◽  
Cell Lines ◽  
S Phase ◽  
M Phase ◽  
Dividing Cells ◽  
Centriole Assembly

ABSTRACTCancer cells frequently include supernumerary centrioles. Here, we generated TP53;PCNT;CEP215 triple knockout cell lines and observed precocious separation and amplification of the centrioles at M phase. Many of the triple KO cells maintained supernumerary centrioles throughout the cell cycle. The M-phase-assembled centrioles lack an ability to function as templates for centriole assembly during S phase. They also lack an ability to organize microtubules in interphase. However, we found that a fraction of them acquired an ability to organize microtubules during M phase. Our works provide an example how supernumerary centrioles behave in dividing cells.

scholarly journals Ras controls growth, survival and differentiation in the Drosophila eye by different thresholds of MAP kinase activity

Development ◽  
2001 ◽  
Vol 128 (9) ◽  
pp. 1687-1696 ◽  
Author(s):  
K. Halfar ◽  
C. Rommel ◽  
H. Stocker ◽  
E. Hafen
Keyword(s):  
Cell Cycle ◽  
Cell Cycle Progression ◽  
Kinase Activity ◽  
Photoreceptor Cells ◽  
Loss Of Function ◽  
Cellular Functions ◽  
Partial Loss ◽  
Cycle Progression ◽  
Mapk Activity ◽  
Dividing Cells

Ras mediates a plethora of cellular functions during development. In the developing eye of Drosophila, Ras performs three temporally separate functions. In dividing cells, it is required for growth but is not essential for cell cycle progression. In postmitotic cells, it promotes survival and subsequent differentiation of ommatidial cells. In the present paper, we have analyzed the different roles of Ras during eye development by using molecularly defined complete and partial loss-of-function mutations of Ras. We show that the three different functions of Ras are mediated by distinct thresholds of MAPK activity. Low MAPK activity prolongs cell survival and permits differentiation of R8 photoreceptor cells while high or persistent MAPK activity is sufficient to precociously induce R1-R7 photoreceptor differentiation in dividing cells.

Stage specificity in the mesenchyme requirement of rodent lung epithelium in vitro: a matter of growth control?

Development ◽  
1983 ◽  
Vol 74 (1) ◽  
pp. 183-206
Author(s):  
Kirstie A. Lawson
Keyword(s):  
Cell Cycle ◽  
Bronchial Epithelium ◽  
Branching Morphogenesis ◽  
S Phase ◽  
Growth Fraction ◽  
Early Event ◽  
Rat Lung ◽  
Lung Epithelium ◽  
Dividing Cells

Epithelia from lung rudiments in which secondary bronchial buds are already established (14th and 13th gestational day for rat and mouse respectively) are able to undergo branching morphogenesis and cytodifferentiation in submandibular mesenchyme in vitro, whereas lung epithelium from one day younger foetuses rarely gives a morphogenetic response to submandibular mesenchyme and usually differentiates into primary (non-budding) bronchial epithelium. The failure of 13-day rat lung epithelium to respond to submandibular mesenchyme can be prevented by peeling off the submandibular mesenchyme from the lung epithelium after 2½ days culture and replacing the same mesenchyme, or renewing it with fresh salivary mesenchyme ex vivo. Changes in the epithelial contour are visible by 10 h and buds form within 24 h; this is followed by branching morphogenesis in more than 66% of the samples. The number of cells in S-phase in the epithelium is doubled within 3 to 5 h after the operation and the number of mitotic cells (colchicine block) is increased during an 11 to 19 h period after the operation. Substituting stomach mesenchyme for submandibular mesenchyme after the operation failed to elicit morphogenesis or an increase in the number of S-phase cells in the epithelium. The proportion of epithelial cells in S-phase in unoperated recombinates does not differ from the proportion in the primary bronchial epithelium (non-budding) of homotypic lung recombinates, whereas the proportion of S-phase cells in operated recombinates approaches that found in the buds of homotypic lung recombinates. The distribution of S-phase cells in visibly responding recombinates 15 to 17 h after operation shows the same heterogeneity as in homotypic lung recombinates, newly formed buds having twice as many cells labelled with [3H]thymidine as the non-budding area. Cell cycle parameters of intact rat lung growing in vitro were estimated using the labelled mitoses method. Primary bronchial epithelium and bronchial buds both had a total cell cycle time of about 13 h and an S-phase of about 10 h. The growth fraction was 0·54 in the primary bronchus and 0·95 in the buds. It is suggested that, also in the recombinates, differences in the proportion of S-phase cells at any one time in morphogenetically active and inactive areas of the epithelium are due to differences in the growth fraction. It is concluded that an early event in the morphogenetic response of lung epithelium to submandibular mesenchyme after removing and restoring the mesenchyme is an increase in the size of the population of dividing cells and it is suggested that a high proportion of dividing cells in an epithelial population is a prerequisite for further interaction of epithelium and mesenchyme leading to branching morphogenesis.

Search, capture and signal: games microtubules and centrosomes play

2001 ◽  
Vol 114 (2) ◽  
pp. 247-255 ◽  
Author(s):  
S.C. Schuyler ◽  
D. Pellman
Keyword(s):  
Cell Cycle ◽  
Cell Cycle Progression ◽  
Cytoplasmic Dynein ◽  
Cell Cycle Checkpoint ◽  
Cellular Polarity ◽  
Cycle Progression ◽  
Cycle Checkpoint ◽  
Dividing Cells ◽  
Actin Cables ◽  
Type V

Accurate distribution of the chromosomes in dividing cells requires coupling of cellular polarity cues with both the orientation of the mitotic spindle and cell cycle progression. Work in budding yeast has demonstrated that cytoplasmic dynein and the kinesin Kip3p define redundant pathways that ensure proper spindle orientation. Furthermore, it has been shown that the Kip3p pathway components Kar9p and Bim1p (Yeb1p) form a complex that provides a molecular link between cortical polarity cues and spindle microtubules. Recently, other studies indicated that the cortical localization of Kar9p depends upon actin cables and Myo2p, a type V myosin. In addition, a BUB2-dependent cell cycle checkpoint has been described that inhibits the mitotic exit network and cytokinesis until proper centrosome position is achieved. Combined, these studies provide molecular insight into how cells link cellular polarity, spindle position and cell cycle progression.

Telomerase and immortalization

2019 ◽  
pp. 209-220
Author(s):  
Laura Collopy ◽  
Kazunori Tomita
Keyword(s):  
Cell Cycle ◽  
Growth And Development ◽  
Normal Cell ◽  
Chromosome Instability ◽  
Growth Arrest ◽  
Proliferative Capacity ◽  
Differentiated Cells ◽  
Dividing Cells ◽  
History Of ◽  
A Cell

The lifetime of a cell is set by the terminal ends of our chromosomes, ageing timers called telomeres. Most dividing cells, not exceptional for cancers, require telomeres to protect chromosomes. However, telomere erosion occurs at every cell cycle, thus imposing a proliferative capacity, eventually triggering a growth arrest. Cancer cells must overcome this proliferative limit in order to continue dividing. In the vast majority of cases, the growth and progression of cancers correlates with the upregulation of telomerase, an enzyme that replenishes telomeres. Telomerase is not active in normal, differentiated cells and its reactivation in cancer renders cells immortal and promotes their continued growth and development. Curiously, in cancer telomerase maintains short telomeres, retaining chromosome instability. Here, we briefly take you through history of cellular mortality with the connection to telomeres and telomerase and review their function in the normal cell to address their role during the transformation to malignancy.

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