Early and late paternal contribution to cell division of embryos in a time‐lapse imaging incubation system

Andrologia ◽  
2021 ◽  
Author(s):  
Amanda Souza Setti ◽  
Daniela Paes de Almeida Ferreira Braga ◽  
Livia Vingris ◽  
Assumpto Iaconelli ◽  
Edson Borges
Keyword(s):  
Cell Division ◽  
Time Lapse ◽  
Paternal Contribution ◽  
Incubation System ◽  
Time Lapse Imaging

scholarly journals Proteins P24 and P41 Function in the Regulation of Terminal-Organelle Development and Gliding Motility in Mycoplasma pneumoniae

2007 ◽  
Vol 189 (20) ◽  
pp. 7442-7449 ◽  
Author(s):  
Benjamin M. Hasselbring ◽  
Duncan C. Krause
Keyword(s):  
Cell Division ◽  
Mycoplasma Pneumoniae ◽  
Fluorescent Protein ◽  
Time Lapse ◽  
Gliding Motility ◽  
Atypical Pneumonia ◽  
Reading Frame ◽  
Spatial Positioning ◽  
Time Lapse Imaging ◽  
Gliding Mechanism

ABSTRACT Mycoplasma pneumoniae is a major cause of bronchitis and atypical pneumonia in humans. This cell wall-less bacterium has a complex terminal organelle that functions in cytadherence and gliding motility. The gliding mechanism is unknown but is coordinated with terminal-organelle development during cell division. Disruption of M. pneumoniae open reading frame MPN311 results in loss of protein P41 and downstream gene product P24. P41 localizes to the base of the terminal organelle and is required to anchor the terminal organelle to the cell body, but during cell division, MPN311 insertion mutants also fail to properly regulate nascent terminal-organelle development spatially or gliding activity temporally. We measured gliding velocity and frequency and used fluorescent protein fusions and time-lapse imaging to assess the roles of P41 and P24 individually in terminal-organelle development and gliding function. P41 was necessary for normal gliding velocity and proper spatial positioning of new terminal organelles, while P24 was required for gliding frequency and new terminal-organelle formation at wild-type rates. However, P41 was essential for P24 function, and in the absence of P41, P24 exhibited a dynamic localization pattern. Finally, protein P28 requires P41 for stability, but analysis of a P28− mutant established that the MPN311 mutant phenotype was not a function of loss of P28.

Prediction of embryo viability using validated cell division time intervals measured by time-lapse imaging

2012 ◽  
Vol 98 (3) ◽  
pp. S31
Author(s):  
A.A. Chen ◽  
K. Loewke ◽  
S.P. Willman ◽  
P.E. Chenette ◽  
R. Boostanfar ◽  
...  
Keyword(s):  
Cell Division ◽  
Time Lapse ◽  
Embryo Viability ◽  
Time Intervals ◽  
Time Lapse Imaging

scholarly journals Polarized endosome dynamics engage cytoplasmic Par-3 that recruits dynein during asymmetric cell division

2021 ◽  
Vol 7 (24) ◽  
pp. eabg1244
Author(s):  
Xiang Zhao ◽  
Jason Q. Garcia ◽  
Kai Tong ◽  
Xingye Chen ◽  
Bin Yang ◽  
...  
Keyword(s):  
Cell Division ◽  
Notch Signaling ◽  
Radial Glia ◽  
Asymmetric Cell Division ◽  
Protein Complexes ◽  
Time Lapse ◽  
Daughter Cells ◽  
Dynein Motor ◽  
Time Lapse Imaging

In the developing embryos, the cortical polarity regulator Par-3 is critical for establishing Notch signaling asymmetry between daughter cells during asymmetric cell division (ACD). How cortically localized Par-3 establishes asymmetric Notch activity in the nucleus is not understood. Here, using in vivo time-lapse imaging of mitotic radial glia progenitors in the developing zebrafish forebrain, we uncover that during horizontal ACD along the anteroposterior embryonic axis, endosomes containing the Notch ligand DeltaD (Dld) move toward the cleavage plane and preferentially segregate into the posterior (subsequently basal) Notchhi daughter. This asymmetric segregation requires the activity of Par-3 and dynein motor complex. Using label retention expansion microscopy, we further detect Par-3 in the cytosol colocalizing the dynein light intermediate chain 1 (Dlic1) onto Dld endosomes. Par-3, Dlic1, and Dld are associated in protein complexes in vivo. Our data reveal an unanticipated mechanism by which cytoplasmic Par-3 directly polarizes Notch signaling components during ACD.

scholarly journals A Modular and Affordable Time-Lapse Imaging and Incubation System Based on 3D-Printed Parts, a Smartphone, and Off-The-Shelf Electronics

PLoS ONE ◽  
2016 ◽  
Vol 11 (12) ◽  
pp. e0167583 ◽  
Author(s):  
Rodrigo Hernández Vera ◽  
Emil Schwan ◽  
Nikos Fatsis-Kavalopoulos ◽  
Johan Kreuger
Keyword(s):  
Time Lapse ◽  
Incubation System ◽  
3D Printed ◽  
Time Lapse Imaging

scholarly journals The Roles of Fission Yeast Ase1 in Mitotic Cell Division, Meiotic Nuclear Oscillation, and Cytokinesis Checkpoint Signaling

2005 ◽  
Vol 16 (3) ◽  
pp. 1378-1395 ◽  
Author(s):  
Akira Yamashita ◽  
Masamitsu Sato ◽  
Akiko Fujita ◽  
Masayuki Yamamoto ◽  
Takashi Toda
Keyword(s):  
Cell Division ◽  
Fission Yeast ◽  
Aurora Kinase ◽  
Time Lapse ◽  
Mitotic Cell ◽  
Chromosome Loss ◽  
Nuclear Movement ◽  
Checkpoint Signaling ◽  
Anaphase B ◽  
Time Lapse Imaging

The Ase1/Prc1 proteins constitute a conserved microtubule-associated protein family that is implicated in central spindle formation and cytokinesis. Here we characterize a role for fission yeast Ase1. Ase1 localizes to microtubule overlapping zones and displays dynamic alterations of localization during the cell cycle. In particular, its spindle localization during metaphase is reduced substantially, followed by robust appearance at the spindle midzone in anaphase. ase1 deletions are viable but defective in nuclear and septum positioning and completion of cytokinesis, which leads to diploidization and chromosome loss. Time-lapse imaging shows that elongating spindles collapse abruptly in the middle of anaphase B. Either absence or overproduction of Ase1 results in profound defects on microtubule bundling in an opposed manner, indicating that Ase1 is a dose-dependent microtubule-bundling factor. In contrast microtubule nucleating activities are not noticeably compromised in ase1 mutants. During meiosis astral microtubules are not bundled and oscillatory nuclear movement is impaired significantly. The Aurora kinase does not correctly localize to central spindles in the absence of Ase1. Finally Ase1 acts as a regulatory component in the cytokinesis checkpoint that operates to inhibit nuclear division when the cytokinesis apparatus is perturbed. Ase1, therefore, couples anaphase completion with cytokinesis upon cell division.

scholarly journals High proliferation and delamination during skin epidermal stratification

2021 ◽  
Vol 12 (1) ◽  
Author(s):  
Mareike Damen ◽  
Lisa Wirtz ◽  
Ekaterina Soroka ◽  
Houda Khatif ◽  
Christian Kukat ◽  
...  
Keyword(s):  
Cell Division ◽  
Asymmetric Cell Division ◽  
Growth Dynamics ◽  
Time Lapse ◽  
Tissue Growth ◽  
Epidermal Differentiation ◽  
Second Phase ◽  
Open Questions ◽  
Epithelial Barriers ◽  
Time Lapse Imaging

AbstractThe development of complex stratified epithelial barriers in mammals is initiated from single-layered epithelia. How stratification is initiated and fueled are still open questions. Previous studies on skin epidermal stratification suggested a central role for perpendicular/asymmetric cell division orientation of the basal keratinocyte progenitors. Here, we use centrosomes, that organize the mitotic spindle, to test whether cell division orientation and stratification are linked. Genetically ablating centrosomes from the developing epidermis leads to the activation of the p53-, 53BP1- and USP28-dependent mitotic surveillance pathway causing a thinner epidermis and hair follicle arrest. The centrosome/p53-double mutant keratinocyte progenitors significantly alter their division orientation in the later stages without majorly affecting epidermal differentiation. Together with time-lapse imaging and tissue growth dynamics measurements, the data suggest that the first and major phase of epidermal development is boosted by high proliferation rates in both basal and suprabasally-committed keratinocytes as well as cell delamination, whereas the second phase maybe uncoupled from the division orientation of the basal progenitors. The data provide insights for tissue homeostasis and hyperproliferative diseases that may recapitulate developmental programs.

scholarly journals Time-Lapse Imaging Reveals Symmetric Neurogenic Cell Division of GFAP-Expressing Progenitors for Expansion of Postnatal Dentate Granule Neurons

PLoS ONE ◽  
2011 ◽  
Vol 6 (9) ◽  
pp. e25303 ◽  
Author(s):  
Takashi Namba ◽  
Hideki Mochizuki ◽  
Ryusuke Suzuki ◽  
Masafumi Onodera ◽  
Masahiro Yamaguchi ◽  
...  
Keyword(s):  
Cell Division ◽  
Time Lapse ◽  
Granule Neurons ◽  
Time Lapse Imaging

scholarly journals Epidermal stratification is uncoupled from centrosome-dependent cell division orientation of the basal progenitors

2020 ◽  
Author(s):  
Mareike Damen ◽  
Ekaterina Soroka ◽  
Houda Khatif ◽  
Christian Kukat ◽  
Benjamin D. Simons ◽  
...  
Keyword(s):  
Cell Division ◽  
Asymmetric Cell Division ◽  
Time Lapse ◽  
Tissue Growth ◽  
Open Questions ◽  
Suprabasal Cell ◽  
Dependent Cell ◽  
Epithelial Barriers ◽  
Time Lapse Imaging ◽  
Basal Keratinocyte

AbstractThe development of complex stratified epithelial barriers in mammals is initiated from single-layered epithelia. How stratification is initiated and fueled are still open questions. Previous studies on skin epidermal stratification suggested a central role for perpendicular/asymmetric cell division orientations of the basal keratinocyte progenitors. Here, we use centrosomes, that organize the mitotic spindle, to test whether cell division orientations and stratification are linked. Genetically ablating centrosomes from the developing epidermis led to the activation of the p53-, 53BP1- and USP28-dependent mitotic surveillance pathway causing a thinner epidermis and hair follicle arrest. Importantly, the centrosome/p53 double mutant keratinocyte progenitors significantly altered their division orientations without affecting epidermal stratification. Time-lapse imaging and tissue growth dynamic measurements suggested that early stratification is initiated by a burst in basal and suprabasal cell proliferation as well as cell delamination. The data provide insights for tissue homeostasis and hyperproliferative diseases that may recapitulate developmental programs.

scholarly journals An extended DNA-free intranuclear compartment organizes centrosome microtubules in malaria parasites

2021 ◽  
Vol 4 (11) ◽  
pp. e202101199
Author(s):  
Caroline S Simon ◽  
Charlotta Funaya ◽  
Johanna Bauer ◽  
Yannik Voβ ◽  
Marta Machado ◽  
...  
Keyword(s):  
Cell Division ◽  
Electron Tomography ◽  
Super Resolution ◽  
Time Lapse ◽  
Amorphous Structure ◽  
Eukaryotic Cell ◽  
Model Organisms ◽  
Nuclear Pore ◽  
Microtubule Organization ◽  
Time Lapse Imaging

Proliferation of Plasmodium falciparum in red blood cells is the cause of malaria and is underpinned by an unconventional cell division mode, called schizogony. Contrary to model organisms, P. falciparum replicates by multiple rounds of nuclear divisions that are not interrupted by cytokinesis. Organization and dynamics of critical nuclear division factors remain poorly understood. Centriolar plaques, the centrosomes of P. falciparum, serve as microtubule organizing centers and have an acentriolar, amorphous structure. The small size of parasite nuclei has precluded detailed analysis of intranuclear microtubule organization by classical fluorescence microscopy. We apply recently developed super-resolution and time-lapse imaging protocols to describe microtubule reconfiguration during schizogony. Analysis of centrin, nuclear pore, and microtubule positioning reveals two distinct compartments of the centriolar plaque. Whereas centrin is extranuclear, we confirm by correlative light and electron tomography that microtubules are nucleated in a previously unknown and extended intranuclear compartment, which is devoid of chromatin but protein-dense. This study generates a working model for an unconventional centrosome and enables a better understanding about the diversity of eukaryotic cell division.

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