scholarly journals Microdomains bounded by endoplasmic reticulum segregate cell cycle calcium transients in syncytial Drosophila embryos

2005 ◽  
Vol 171 (1) ◽  
pp. 47-59 ◽  
Author(s):  
Huw Parry ◽  
Alex McDougall ◽  
Michael Whitaker
Keyword(s):  
Cell Cycle ◽  
Endoplasmic Reticulum ◽  
Mitotic Spindle ◽  
Spatial Organization ◽  
Cell Types ◽  
Calcium Transients ◽  
Calcium Signals ◽  
Calcium Store ◽  
Internal Calcium ◽  
Drosophila Embryos

Cell cycle calcium signals are generated by the inositol trisphosphate (InsP3)–mediated release of calcium from internal stores (Ciapa, B., D. Pesando, M. Wilding, and M. Whitaker. 1994. Nature. 368:875–878; Groigno, L., and M. Whitaker. 1998. Cell. 92:193–204). The major internal calcium store is the endoplasmic reticulum (ER); thus, the spatial organization of the ER during mitosis may be important in shaping and defining calcium signals. In early Drosophila melanogaster embryos, ER surrounds the nucleus and mitotic spindle during mitosis, offering an opportunity to determine whether perinuclear localization of ER conditions calcium signaling during mitosis. We establish that the nuclear divisions in syncytial Drosophila embryos are accompanied by both cortical and nuclear localized calcium transients. Constructs that chelate InsP3 also prevent nuclear division. An analysis of nuclear calcium concentrations demonstrates that they are differentially regulated. These observations demonstrate that mitotic calcium signals in Drosophila embryos are confined to mitotic microdomains and offer an explanation for the apparent absence of detectable global calcium signals during mitosis in some cell types.

scholarly journals Endoplasmic reticulum generates calcium signalling microdomains around the nucleus and spindle in syncytial Drosophila embryos

2006 ◽  
Vol 34 (3) ◽  
pp. 385-388 ◽  
Author(s):  
H. Parry ◽  
A. McDougall ◽  
M. Whitaker
Keyword(s):  
Endoplasmic Reticulum ◽  
Mitotic Spindle ◽  
Spatial Organization ◽  
Calcium Influx ◽  
Calcium Signalling ◽  
Calcium Transients ◽  
Calcium Store ◽  
Internal Calcium ◽  
Er Calcium ◽  
Drosophila Embryos

Cell cycle calcium signals are generated by inositol trisphosphate-mediated release of calcium from internal stores [Ciapa, Pesando, Wilding and Whitaker (1994) Nature (London) 368, 875–878; Groigno and Whitaker (1998) Cell 92, 193–204]. The major internal calcium store is the ER (endoplasmic reticulum): the spatial organization of the ER during mitosis is important in defining a microdomain around the nucleus and mitotic spindle in early Drosophila embryos [Parry, McDougall and Whitaker (2005) J. Cell Biol. 171, 47–59]. Nuclear divisions in syncytial Drosophila embryos are accompanied by both cortical and nuclear localized calcium transients. Mitosis is prevented by the InsP3 antagonists Xestospongin C and heparin. Nuclear-localized transients and cortical transients rely on extraembryonic calcium, suggesting that ER calcium levels are maintained by calcium influx.

scholarly journals RHBDL4 protects against endoplasmic reticulum stress by regulating the morphology and distribution of ER sheets

2021 ◽  
Author(s):  
Viorica Liebe Lastun ◽  
Matthew Freeman
Keyword(s):  
Cell Cycle ◽  
Endoplasmic Reticulum ◽  
Endoplasmic Reticulum Stress ◽  
Er Stress ◽  
Liver Steatosis ◽  
Physiological Role ◽  
Cell Types ◽  
Rhomboid Protease ◽  
Rapid Changes

In metazoans, the architecture of the endoplasmic reticulum (ER) differs between cell types, and undergoes major changes through the cell cycle and according to physiological needs. Although much is known about how the different ER morphologies are generated and maintained, especially the ER tubules, how context dependent changes in ER shape and distribution are regulated and the factors involved are less characterized. Here, we show that RHBDL4, an ER-resident rhomboid protease, modulates the shape and distribution of the ER, especially under conditions that require rapid changes in the ER sheet distribution, including ER stress. RHBDL4 interacts with CLIMP-63, a protein involved in ER sheet stabilisation, and with the cytoskeleton. Mice lacking RHBDL4 are sensitive to ER stress and develop liver steatosis, a phenotype associated with unresolved ER stress. Our data introduce a new physiological role of RHBDL4 and also imply that this function does not require its enzymatic activity.

scholarly journals Cell Cycle-dependent Regulation of Structure of Endoplasmic Reticulum and Inositol 1,4,5-Trisphosphate-induced Ca2+ Release in Mouse Oocytes and Embryos

2003 ◽  
Vol 14 (1) ◽  
pp. 288-301 ◽  
Author(s):  
Greg FitzHarris ◽  
Petros Marangos ◽  
John Carroll
Keyword(s):  
Cell Cycle ◽  
Endoplasmic Reticulum ◽  
Mitotic Spindle ◽  
Mitotic Division ◽  
Cyclin B ◽  
Dependent Manner ◽  
Inositol 1,4,5 Trisphosphate ◽  
A Cell ◽  
Cycle Dependent ◽  
Mouse Eggs

The organization of endoplasmic reticulum (ER) was examined in mouse eggs undergoing fertilization and in embryos during the first cell cycle. The ER in meiosis II (MII)-arrested mouse eggs is characterized by accumulations (clusters) that are restricted to the cortex of the vegetal hemisphere of the egg. Monitoring ER structure with DiI18 after egg activation has demonstrated that ER clusters disappear at the completion of meiosis II. The ER clusters can be maintained by inhibiting the decrease in cdk1-cyclin B activity by using the proteasome inhibitor MG132, or by microinjecting excess cyclin B. A role for cdk1-cyclin B in ER organization is further suggested by the finding that the cdk inhibitor roscovitine causes the loss of ER clusters in MII eggs. Cortical clusters are specific to meiosis as they do not return in the first mitotic division; rather, the ER aggregates around the mitotic spindle. Inositol 1,4,5-trisphosphate-induced Ca2+ release is also regulated in a cell cycle-dependent manner where it is increased in MII and in the first mitosis. The cell cycle dependent effects on ER structure and inositol 1,4,5-trisphosphate-induced Ca2+ release have implications for understanding meiotic and mitotic control of ER structure and inheritance, and of the mechanisms regulating mitotic Ca2+signaling.

scholarly journals Local perinuclear calcium signals associated with mitosis-entry in early sea urchin embryos.

1996 ◽  
Vol 135 (1) ◽  
pp. 191-199 ◽  
Author(s):  
M Wilding ◽  
E M Wright ◽  
R Patel ◽  
G Ellis-Davies ◽  
M Whitaker
Keyword(s):  
Cell Cycle ◽  
Confocal Microscopy ◽  
Sea Urchin ◽  
Calcium Release ◽  
Flash Photolysis ◽  
Mitotic Cell ◽  
Calcium Transients ◽  
Perinuclear Region ◽  
Calcium Signals ◽  
Sea Urchin Embryos

Using calcium-sensitive dyes together with their dextran conjugates and confocal microscopy, we have looked for evidence of localized calcium signaling in the region of the nucleus before entry into mitosis, using the sea urchin egg first mitotic cell cycle as a model. Global calcium transients that appear to originate from the nuclear area are often observed just before nuclear envelope breakdown (NEB). In the absence of global increases in calcium, confocal microscopy using Calcium Green-1 dextran indicator dye revealed localized calcium transients in the perinuclear region. We have also used a photoinactivatable calcium chelator, nitrophenyl EGTA (NP-EGTA), to test whether the chelator-induced block of mitosis entry can be reversed after inactivation of the chelator. Cells arrested before NEB by injection of NP-EGTA resume the cell cycle after flash photolysis of the chelator. Photolysis of chelator triggers calcium release. TreatmenT with caFfeine to enhance calcium-induced calcium release increases the amplitude of NEB-associated calcium transients. These results indicate that calcium increases local to the nucleus are required to trigger entry into mitosis. Local calcium transients arise in the perinuclear region and can spread from this region into the cytoplasm. Thus, cell cycle calcium signals are generated by the perinuclear mitotic machinery in early sea urchin embryos.

scholarly journals Polo kinase mediates the phosphorylation and cellular localization of Nuf/FIP3, a Rab11 effector

2017 ◽  
Vol 28 (11) ◽  
pp. 1435-1443
Author(s):  
Lotti Brose ◽  
Justin Crest ◽  
Li Tao ◽  
William Sullivan
Keyword(s):  
Cell Cycle ◽  
Cellular Localization ◽  
Cell Types ◽  
Recycling Endosome ◽  
Polo Kinase ◽  
A Cell ◽  
Cycle Dependent ◽  
Drosophila Embryos

Animal cytokinesis involves both actin-myosin–based contraction and vesicle-mediated membrane addition. In many cell types, including early Drosophila embryos, Nuf/FIP3, a Rab11 effector, mediates recycling endosome (RE)–based vesicle delivery to the cytokinesis furrow. Nuf exhibits a cell cycle–regulated concentration at the centrosome that is accompanied by dramatic changes in its phosphorylation state. Here we demonstrate that maximal phosphorylation of Nuf occurs at prophase, when centrosome-associated Nuf disperses throughout the cytoplasm. Accordingly, ectopic Cdk1 activation results in immediate Nuf dispersal from the centrosome. Screening of candidate kinases reveals a specific, dosage-sensitive interaction between Nuf and Polo with respect to Nuf-mediated furrow formation. Inhibiting Polo activity results in Nuf underphosphorylation and prolonged centrosome association. In vitro, Polo directly binds and is required for Nuf phosphorylation at Ser-225 and Thr-227, matching previous in vivo–mapped phosphorylation sites. These results demonstrate a role for Polo kinase in directly mediating Nuf cell cycle–dependent localization.

scholarly journals Calcium signalling in early embryos

2008 ◽  
Vol 363 (1495) ◽  
pp. 1401-1418 ◽  
Author(s):  
Michael Whitaker
Keyword(s):  
Cell Cycle ◽  
Second Messengers ◽  
Calcium Signalling ◽  
Embryonic Cell ◽  
Calcium Transients ◽  
Calcium Signal ◽  
Calcium Signals ◽  
Cell Cycles ◽  
Early Embryos ◽  
And Control

The onset of development in most species studied is triggered by one of the largest and longest calcium transients known to us. It is the most studied and best understood aspect of the calcium signals that accompany and control development. Its properties and mechanisms demonstrate what embryos are capable of and thus how the less-understood calcium signals later in development may be generated. The downstream targets of the fertilization calcium signal have also been identified, providing some pointers to the probable targets of calcium signals further on in the process of development. In one species or another, the fertilization calcium signal involves all the known calcium-releasing second messengers and many of the known calcium-signalling mechanisms. These calcium signals also usually take the form of a propagating calcium wave or waves. Fertilization causes the cell cycle to resume, and therefore fertilization signals are cell-cycle signals. In some early embryonic cell cycles, calcium signals also control the progress through each cell cycle, controlling mitosis. Studies of these early embryonic calcium-signalling mechanisms provide a background to the calcium-signalling events discussed in the articles in this issue.

Prevalence of the pit and antipit in the genus Glycine

1987 ◽  
Vol 45 ◽  
pp. 986-987
Author(s):  
R. W. Yaklich ◽  
E. L. Vigil ◽  
W. P. Wergin
Keyword(s):  
Amino Acids ◽  
Endoplasmic Reticulum ◽  
Glycine Max ◽  
Seed Coat ◽  
Cell Types ◽  
Abaxial Surface ◽  
Legume Seed ◽  
Initial Report ◽  
Cone Cells ◽  
Glycine Max L

The legume seed coat is the site of sucrose unloading and the metabolism of imported ureides and synthesis of amino acids for the developing embryo. The cell types directly responsible for these functions in the seed coat are not known. We recently described a convex layer of tissue on the inside surface of the soybean (Glycine max L. Merr.) seed coat that was termed “antipit” because it was in direct opposition to the concave pit on the abaxial surface of the cotyledon. Cone cells of the antipit contained numerous hypertrophied Golgi apparatus and laminated rough endoplasmic reticulum common to actively secreting cells. The initial report by Dzikowski (1936) described the morphology of the pit and antipit in G. max and found these structures in only 68 of the 169 seed accessions examined.

scholarly journals OASIS/CREB3L1 is a factor that responds to nuclear envelope stress

2021 ◽  
Vol 7 (1) ◽  
Author(s):  
Yasunao Kamikawa ◽  
Atsushi Saito ◽  
Koji Matsuhisa ◽  
Masayuki Kaneko ◽  
Rie Asada ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Endoplasmic Reticulum ◽  
Nuclear Envelope ◽  
Genome Instability ◽  
Nuclear Lamina ◽  
Nuclear Deformation ◽  
Membrane Domain ◽  
Stress Response Pathway ◽  
Envelope Stress ◽  
Genome Activity

AbstractThe nuclear envelope (NE) safeguards the genome and is pivotal for regulating genome activity as the structural scaffold of higher-order chromatin organization. NE had been thought as the stable during the interphase of cell cycle. However, recent studies have revealed that the NE can be damaged by various stresses such as mechanical stress and cellular senescence. These types of stresses are called NE stress. It has been proposed that NE stress is closely related to cellular dysfunctions such as genome instability and cell death. Here, we found that an endoplasmic reticulum (ER)-resident transmembrane transcription factor, OASIS, accumulates at damaged NE. Notably, the major components of nuclear lamina, Lamin proteins were depleted at the NE where OASIS accumulates. We previously demonstrated that OASIS is cleaved at the membrane domain in response to ER stress. In contrast, OASIS accumulates as the full-length form to damaged NE in response to NE stress. The accumulation to damaged NE is specific for OASIS among OASIS family members. Intriguingly, OASIS colocalizes with the components of linker of nucleoskeleton and cytoskeleton complexes, SUN2 and Nesprin-2 at the damaged NE. OASIS partially colocalizes with BAF, LEM domain proteins, and a component of ESCRT III, which are involved in the repair of ruptured NE. Furthermore, OASIS suppresses DNA damage induced by NE stress and restores nuclear deformation under NE stress conditions. Our findings reveal a novel NE stress response pathway mediated by OASIS.

scholarly journals Histone modifications form a cell-type-specific chromosomal bar code that persists through the cell cycle

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
John A. Halsall ◽  
Simon Andrews ◽  
Felix Krueger ◽  
Charlotte E. Rutledge ◽  
Gabriella Ficz ◽  
...  
Keyword(s):  
Gene Expression ◽  
Cell Cycle ◽  
Histone Modifications ◽  
Expression Patterns ◽  
Cell Types ◽  
Cell Type ◽  
Bar Code ◽  
Genes Encoding ◽  
Cell Type Specific ◽  
Rolling Windows

AbstractChromatin configuration influences gene expression in eukaryotes at multiple levels, from individual nucleosomes to chromatin domains several Mb long. Post-translational modifications (PTM) of core histones seem to be involved in chromatin structural transitions, but how remains unclear. To explore this, we used ChIP-seq and two cell types, HeLa and lymphoblastoid (LCL), to define how changes in chromatin packaging through the cell cycle influence the distributions of three transcription-associated histone modifications, H3K9ac, H3K4me3 and H3K27me3. We show that chromosome regions (bands) of 10–50 Mb, detectable by immunofluorescence microscopy of metaphase (M) chromosomes, are also present in G1 and G2. They comprise 1–5 Mb sub-bands that differ between HeLa and LCL but remain consistent through the cell cycle. The same sub-bands are defined by H3K9ac and H3K4me3, while H3K27me3 spreads more widely. We found little change between cell cycle phases, whether compared by 5 Kb rolling windows or when analysis was restricted to functional elements such as transcription start sites and topologically associating domains. Only a small number of genes showed cell-cycle related changes: at genes encoding proteins involved in mitosis, H3K9 became highly acetylated in G2M, possibly because of ongoing transcription. In conclusion, modified histone isoforms H3K9ac, H3K4me3 and H3K27me3 exhibit a characteristic genomic distribution at resolutions of 1 Mb and below that differs between HeLa and lymphoblastoid cells but remains remarkably consistent through the cell cycle. We suggest that this cell-type-specific chromosomal bar-code is part of a homeostatic mechanism by which cells retain their characteristic gene expression patterns, and hence their identity, through multiple mitoses.

scholarly journals Self-Organized Nuclear Positioning Synchronizes the Cell Cycle in Drosophila Embryos

Cell ◽  
2019 ◽  
Vol 177 (4) ◽  
pp. 925-941.e17 ◽  
Author(s):  
Victoria E. Deneke ◽  
Alberto Puliafito ◽  
Daniel Krueger ◽  
Avaneesh V. Narla ◽  
Alessandro De Simone ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Nuclear Positioning ◽  
Self Organized ◽  
Drosophila Embryos
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