scholarly journals Redistribution of FLAgellar Member 8 during the trypanosome life cycle: consequences for cell fate prediction

2021 ◽  
Author(s):  
Estefanía Calvo Alvarez ◽  
Serge Bonnefoy ◽  
Audrey Salles ◽  
Fiona E. Benson ◽  
Paul G. McKean ◽  
...  
Keyword(s):  
Life Cycle ◽  
Cell Fate ◽  
Cell Fate Prediction

scholarly journals A polynomial based model for cell fate prediction in human diseases

2017 ◽  
Vol 11 (S7) ◽  
Author(s):  
Lichun Ma ◽  
Jie Zheng
Keyword(s):  
Cell Fate ◽  
Human Diseases ◽  
Cell Fate Prediction

scholarly journals Reprogramming DNA methylation in the mammalian life cycle: building and breaking epigenetic barriers

2013 ◽  
Vol 368 (1609) ◽  
pp. 20110330 ◽  
Author(s):  
Stefanie Seisenberger ◽  
Julian R. Peat ◽  
Timothy A. Hore ◽  
Fátima Santos ◽  
Wendy Dean ◽  
...  
Keyword(s):  
Dna Methylation ◽  
Life Cycle ◽  
Cell Fate ◽  
Excision Repair ◽  
Primordial Germ Cells ◽  
Biological Significance ◽  
Epigenetic Reprogramming ◽  
Developmental Potential ◽  
Methylation Patterns

In mammalian development, epigenetic modifications, including DNA methylation patterns, play a crucial role in defining cell fate but also represent epigenetic barriers that restrict developmental potential. At two points in the life cycle, DNA methylation marks are reprogrammed on a global scale, concomitant with restoration of developmental potency. DNA methylation patterns are subsequently re-established with the commitment towards a distinct cell fate. This reprogramming of DNA methylation takes place firstly on fertilization in the zygote, and secondly in primordial germ cells (PGCs), which are the direct progenitors of sperm or oocyte. In each reprogramming window, a unique set of mechanisms regulates DNA methylation erasure and re-establishment. Recent advances have uncovered roles for the TET3 hydroxylase and passive demethylation, together with base excision repair (BER) and the elongator complex, in methylation erasure from the zygote. Deamination by AID, BER and passive demethylation have been implicated in reprogramming in PGCs, but the process in its entirety is still poorly understood. In this review, we discuss the dynamics of DNA methylation reprogramming in PGCs and the zygote, the mechanisms involved and the biological significance of these events. Advances in our understanding of such natural epigenetic reprogramming are beginning to aid enhancement of experimental reprogramming in which the role of potential mechanisms can be investigated in vitro . Conversely, insights into in vitro reprogramming techniques may aid our understanding of epigenetic reprogramming in the germline and supply important clues in reprogramming for therapies in regenerative medicine.

scholarly journals Monitoring single-cell dynamics of entry into quiescence during an unperturbed lifecycle

eLife ◽  
2021 ◽  
Vol 10 ◽  
Author(s):  
Basile Jacquel ◽  
Théo Aspert ◽  
Damien Laporte ◽  
Isabelle Sagot ◽  
Gilles Charvin
Keyword(s):  
Life Cycle ◽  
Single Cell ◽  
Cell Fate ◽  
Cell Tracking ◽  
Cellular Responses ◽  
Quiescent State ◽  
Cell Dynamics ◽  
Quiescent Cells ◽  
Internal Ph ◽  
Bona Fide

The life cycle of microorganisms is associated with dynamic metabolic transitions and complex cellular responses. In yeast, how metabolic signals control the progressive choreography of structural reorganizations observed in quiescent cells during a natural life cycle remains unclear. We have developed an integrated microfluidic device to address this question, enabling continuous single-cell tracking in a batch culture experiencing unperturbed nutrient exhaustion to unravel the coordination between metabolic and structural transitions within cells. Our technique reveals an abrupt fate divergence in the population, whereby a fraction of cells is unable to transition to respiratory metabolism and undergoes a reversible entry into a quiescence-like state leading to premature cell death. Further observations reveal that non-monotonous internal pH fluctuations in respiration-competent cells orchestrate the successive waves of protein super-assemblies formation that accompany the entry into a bona fide quiescent state. This ultimately leads to an abrupt cytosolic glass transition that occurs stochastically long after proliferation cessation. This new experimental framework provides a unique way to track single-cell fate dynamics over a long timescale in a population of cells that continuously modify their ecological niche.

scholarly journals Redistribution of FLAgellar Member 8 during the trypanosome life cycle: consequences for cell fate prediction

2020 ◽  
Author(s):  
Estefanía Calvo Alvarez ◽  
Serge Bonnefoy ◽  
Audrey Salles ◽  
Fiona E. Benson ◽  
Paul G. McKean ◽  
...  
Keyword(s):  
Cell Fate ◽  
Daughter Cell ◽  
Parasite Development ◽  
African Trypanosomes ◽  
Specific Distribution ◽  
Summary Statement ◽  
Maturation State ◽  
Cell Fate Prediction ◽  
First Time ◽  
Single Flagellum

AbstractThe single flagellum of African trypanosomes is essential in multiple aspects of the parasite development. The FLAgellar Member 8 protein (FLAM8), localised to the tip of the flagellum in cultured insect forms, was identified as a marker of the locking event that controls flagellum length. Here, we investigated whether FLAM8 could also reflect the flagellum maturation state in other stages. We observed that FLAM8 distribution extended along the entire flagellar cytoskeleton in mammalian infective forms. Then, a rapid FLAM8 concentration to the distal tip occurs during differentiation into early insect forms, illustrating for the first time the remodeling of an existing flagellum in trypanosomes. In the tsetse cardia, FLAM8 further localizes to the entire length of the new flagellum during an asymmetric division. Strikingly, in parasites dividing in the tsetse midgut and in the salivary glands, the amount and distribution of FLAM8 in the new flagellum was seen to predict the daughter cell fate. We propose and discuss how FLAM8 could be considered as a meta-marker of the flagellum stage and maturation state in trypanosomes.Summary statementThe trypanosome protein FLAM8 displays a dynamic and stage-specific distribution during the entire parasite cycle, representing a novel marker of the flagellum stage and maturation state.

Basic study on establishment of the morphological database of the nucleus for cell fate prediction

2018 ◽  
Vol 2018.26 (0) ◽  
pp. 511
Author(s):  
Tatsuya SASAKI ◽  
Kazuaki NAGAYAMA
Keyword(s):  
Cell Fate ◽  
Basic Study ◽  
Cell Fate Prediction

scholarly journals Generative modeling of single-cell time series with PRESCIENT enables prediction of cell trajectories with interventions

2021 ◽  
Vol 12 (1) ◽  
Author(s):  
Grace Hui Ting Yeo ◽  
Sachit D. Saksena ◽  
David K. Gifford
Keyword(s):  
Time Series ◽  
Single Cell ◽  
Cell Fate ◽  
Lineage Tracing ◽  
Pancreatic Β Cell ◽  
Β Cell ◽  
Modeling Framework ◽  
Generative Modeling ◽  
Cell Fate Prediction ◽  
Cell Trajectories

AbstractExisting computational methods that use single-cell RNA-sequencing (scRNA-seq) for cell fate prediction do not model how cells evolve stochastically and in physical time, nor can they predict how differentiation trajectories are altered by proposed interventions. We introduce PRESCIENT (Potential eneRgy undErlying Single Cell gradIENTs), a generative modeling framework that learns an underlying differentiation landscape from time-series scRNA-seq data. We validate PRESCIENT on an experimental lineage tracing dataset, where we show that PRESCIENT is able to predict the fate biases of progenitor cells in hematopoiesis when accounting for cell proliferation, improving upon the best-performing existing method. We demonstrate how PRESCIENT can simulate trajectories for perturbed cells, recovering the expected effects of known modulators of cell fate in hematopoiesis and pancreatic β cell differentiation. PRESCIENT is able to accommodate complex perturbations of multiple genes, at different time points and from different starting cell populations, and is available at https://github.com/gifford-lab/prescient.

Ultrastructural analysis of “Sensory” surface nerve endings and “putative” neurotransmitter sites in Schistosoma mansoni Miracidia

1989 ◽  
Vol 47 ◽  
pp. 962-963
Author(s):  
Betty Ruth Jones ◽  
Steve Chi-Tang Pan
Keyword(s):  
Nervous System ◽  
Life Cycle ◽  
Schistosoma Mansoni ◽  
Snail Host ◽  
Complex Life Cycle ◽  
Rational Approach ◽  
Effective Control ◽  
The Social ◽  
Social And Economic Development ◽  
Basic Biology

INTRODUCTION: Schistosomiasis has been described as “one of the most devastating diseases of mankind, second only to malaria in its deleterious effects on the social and economic development of populations in many warm areas of the world.” The disease is worldwide and is probably spreading faster and becoming more intense than the overall research efforts designed to provide the basis for countering it. Moreover, there are indications that the development of water resources and the demands for increasing cultivation and food in developing countries may prevent adequate control of the disease and thus the number of infections are increasing.Our knowledge of the basic biology of the parasites causing the disease is far from adequate. Such knowledge is essential if we are to develop a rational approach to the effective control of human schistosomiasis. The miracidium is the first infective stage in the complex life cycle of schistosomes. The future of the entire life cycle depends on the capacity and ability of this organism to locate and enter a suitable snail host for further development, Little is known about the nervous system of the miracidium of Schistosoma mansoni and of other trematodes. Studies indicate that miracidia contain a well developed and complex nervous system that may aid the larvae in locating and entering a susceptible snail host (Wilson, 1970; Brooker, 1972; Chernin, 1974; Pan, 1980; Mehlhorn, 1988; and Jones, 1987-1988).

A freeze-fracture-etched study of the physarum polycephalum plasma membrane during early formation of the macroplasmodial stage

1993 ◽  
Vol 51 ◽  
pp. 346-347
Author(s):  
Randolph W. Taylor ◽  
Henrie Treadwell
Keyword(s):  
Plasma Membrane ◽  
Life Cycle ◽  
Growth Phase ◽  
Filter Paper ◽  
Physarum Polycephalum ◽  
Freeze Fracture ◽  
Petri Dish ◽  
Wire Screen ◽  
Wide Mouth ◽  
Sterile Filter

The plasma membrane of the Slime Mold, Physarum polycephalum, process unique morphological distinctions at different stages of the life cycle. Investigations of the plasma membrane of P. polycephalum, particularly, the arrangements of the intramembranous particles has provided useful information concerning possible changes occurring in higher organisms. In this report Freeze-fracture-etched techniques were used to investigate 3 hours post-fusion of the macroplasmodia stage of the P. polycephalum plasma membrane.Microplasmodia of Physarum polycephalum (M3C), axenically maintained, were collected in mid-expotential growth phase by centrifugation. Aliquots of microplasmodia were spread in 3 cm circles with a wide mouth pipette onto sterile filter paper which was supported on a wire screen contained in a petri dish. The cells were starved for 2 hrs at 24°C. After starvation, the cells were feed semidefined medium supplemented with hemin and incubated at 24°C. Three hours after incubation, samples were collected randomly from the petri plates, placed in plancettes and frozen with a propane-nitrogen jet freezer.

Centrosome Aurora A gradient ensures single polarity axis in C. elegans embryos

2020 ◽  
Vol 48 (3) ◽  
pp. 1243-1253 ◽  
Author(s):  
Sukriti Kapoor ◽  
Sachin Kotak
Keyword(s):  
Symmetry Breaking ◽  
Cell Fate ◽  
Cell Cortex ◽  
Axis Formation ◽  
Aurora A Kinase ◽  
Aurora A ◽  
C Elegans ◽  
Cell Embryo ◽  
Polarity Establishment

Cellular asymmetries are vital for generating cell fate diversity during development and in stem cells. In the newly fertilized Caenorhabditis elegans embryo, centrosomes are responsible for polarity establishment, i.e. anterior–posterior body axis formation. The signal for polarity originates from the centrosomes and is transmitted to the cell cortex, where it disassembles the actomyosin network. This event leads to symmetry breaking and the establishment of distinct domains of evolutionarily conserved PAR proteins. However, the identity of an essential component that localizes to the centrosomes and promotes symmetry breaking was unknown. Recent work has uncovered that the loss of Aurora A kinase (AIR-1 in C. elegans and hereafter referred to as Aurora A) in the one-cell embryo disrupts stereotypical actomyosin-based cortical flows that occur at the time of polarity establishment. This misregulation of actomyosin flow dynamics results in the occurrence of two polarity axes. Notably, the role of Aurora A in ensuring a single polarity axis is independent of its well-established function in centrosome maturation. The mechanism by which Aurora A directs symmetry breaking is likely through direct regulation of Rho-dependent contractility. In this mini-review, we will discuss the unconventional role of Aurora A kinase in polarity establishment in C. elegans embryos and propose a refined model of centrosome-dependent symmetry breaking.

Centromere assembly and non-random sister chromatid segregation in stem cells

2020 ◽  
Vol 64 (2) ◽  
pp. 223-232 ◽  
Author(s):  
Ben L. Carty ◽  
Elaine M. Dunleavy
Keyword(s):  
Stem Cells ◽  
Cell Division ◽  
Cell Fate ◽  
Sister Chromatid ◽  
Asymmetric Cell Division ◽  
Protein A ◽  
Germline Stem Cells ◽  
Sister Chromatids ◽  
Centromere Protein A ◽  
Oocyte Meiosis

Abstract Asymmetric cell division (ACD) produces daughter cells with separate distinct cell fates and is critical for the development and regulation of multicellular organisms. Epigenetic mechanisms are key players in cell fate determination. Centromeres, epigenetically specified loci defined by the presence of the histone H3-variant, centromere protein A (CENP-A), are essential for chromosome segregation at cell division. ACDs in stem cells and in oocyte meiosis have been proposed to be reliant on centromere integrity for the regulation of the non-random segregation of chromosomes. It has recently been shown that CENP-A is asymmetrically distributed between the centromeres of sister chromatids in male and female Drosophila germline stem cells (GSCs), with more CENP-A on sister chromatids to be segregated to the GSC. This imbalance in centromere strength correlates with the temporal and asymmetric assembly of the mitotic spindle and potentially orientates the cell to allow for biased sister chromatid retention in stem cells. In this essay, we discuss the recent evidence for asymmetric sister centromeres in stem cells. Thereafter, we discuss mechanistic avenues to establish this sister centromere asymmetry and how it ultimately might influence cell fate.

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