scholarly journals Organ geometry channels reproductive cell fate in the Arabidopsis ovule primordium

eLife ◽  
2021 ◽  
Vol 10 ◽  
Author(s):  
Elvira Hernandez-Lagana ◽  
Gabriella Mosca ◽  
Ethel Mendocilla-Sato ◽  
Nuno Pires ◽  
Anja Frey ◽  
...  

In multicellular organisms, sexual reproduction requires the separation of the germline from the soma. In flowering plants, the female germline precursor differentiates as a single spore mother cell (SMC) as the ovule primordium forms. Here, we explored how organ growth contributes to SMC differentiation. We generated 92 annotated 3D images at cellular resolution in Arabidopsis. We identified the spatio-temporal pattern of cell division that acts in a domain-specific manner as the primordium forms. Tissue growth models uncovered plausible morphogenetic principles involving a spatially confined growth signal, differential mechanical properties, and cell growth anisotropy. Our analysis revealed that SMC characteristics first arise in more than one cell but SMC fate becomes progressively restricted to a single cell during organ growth. Altered primordium geometry coincided with a delay in the fate restriction process in katanin mutants. Altogether, our study suggests that tissue geometry channels reproductive cell fate in the Arabidopsis ovule primordium.

Author(s):  
Elvira Hernandez-Lagana ◽  
Gabriella Mosca ◽  
Ethel Mendocilla Sato ◽  
Nuno Pires ◽  
Anja Frey ◽  
...  

SummaryIn multicellular organisms, sexual reproduction requires the separation of the germline from the soma. In flowering plants, the first cells of the germline, so-called spore mother cells (SMCs), differentiate as the reproductive organs form. Here, we explored how organ growth influences and contributes to SMC differentiation. We generated a collection of 92 annotated 3D images capturing ovule primordium ontogeny at cellular resolution in Arabidopsis. We identified a spatio-temporal pattern of cell divisions that acts in a domain-specific manner as the primordium forms, which is coupled with the emergence of a single SMC. Using tissue growth models, we uncovered plausible morphogenetic principles involving a spatially confined growth signal, differential mechanical properties, and cell growth anisotropy. Our analysis also reveals that SMC characteristics first arise in more than one cell but SMC fate becomes progressively restricted to a single cell during organ growth. Altered primordium geometry coincided with a delay in this fate restriction process in katanin mutants. Altogether, our study suggests that tissue geometry canalizes and modulates reproductive cell fate in the Arabidopsis ovule primordium.


2015 ◽  
Author(s):  
Patrick Smadbeck ◽  
Michael P.H. Stumpf

Development is a process that needs to tightly coordinated in both space and time. Cell tracking and lineage tracing have become important experimental techniques in developmental biology and allow us to map the fate of cells and their progeny in both space and time. A generic feature of developing (as well as homeostatic) tissues that these analyses have revealed is that relatively few cells give rise to the bulk of the cells in a tissue; the lineages of most cells come to an end fairly quickly. This has spurned the interest also of computational and theoretical biologists/physicists who have developed a range of modelling -- perhaps most notably are the agent-based modelling (ABM) --- approaches. These can become computationally prohibitively expensive but seem to capture some of the features observed in experiments. Here we develop a complementary perspective that allows us to understand the dynamics leading to the formation of a tissue (or colony of cells). Borrowing from the rich population genetics literature we develop genealogical models of tissue development that trace the ancestry of cells in a tissue back to their most recent common ancestors. We apply this approach to tissues that grow under confined conditions --- as would, for example, be appropriate for the neural crest --- and unbounded growth --- illustrative of the behaviour of 2D tumours or bacterial colonies. The classical coalescent model from population genetics is readily adapted to capture tissue genealogies for different models of tissue growth and development. We show that simple but universal scaling relationships allow us to establish relationships between the coalescent and different fractal growth models that have been extensively studied in many different contexts, including developmental biology. Using our genealogical perspective we are able to study the statistical properties of the processes that give rise to tissues of cells, without the need for large-scale simulations.


Author(s):  
Nkosingiphile Mnguni ◽  
Sameerah Jamal

Abstract This paper considers two categories of fractional-order population growth models, where a time component is defined by Riemann–Liouville derivatives. These models are studied under the Lie symmetry approach, and we reduce the fractional partial differential equations to nonlinear ordinary differential equations. Subsequently, solutions of the latter are determined numerically or with the aid of Laplace transforms. Graphical representations for integral and trigonometric solutions are presented. A key feature of these models is the connection between spatial patterning of organisms versus competitive coexistence.


2020 ◽  
Author(s):  
Elizabeth W. Kahney ◽  
Lydia Sohn ◽  
Kayla Viets-Layng ◽  
Robert Johnston ◽  
Xin Chen

ABSTRACTStem cells have the unique ability to undergo asymmetric division which produces two daughter cells that are genetically identical, but commit to different cell fates. The loss of this balanced asymmetric outcome can lead to many diseases, including cancer and tissue dystrophy. Understanding this tightly regulated process is crucial in developing methods to treat these abnormalities. Here, we report that produced from a Drosophila female germline stem cell asymmetric division, the two daughter cells differentially inherit histones at key genes related to either maintaining the stem cell state or promoting differentiation, but not at constitutively active or silenced genes. We combined histone labeling with DNA Oligopaints to distinguish old versus new histone distribution and visualize their inheritance patterns at single-gene resolution in asymmetrically dividing cells in vivo. This strategy can be widely applied to other biological contexts involving cell fate establishment during development or tissue homeostasis in multicellular organisms.


2020 ◽  
Vol 21 (21) ◽  
pp. 8126
Author(s):  
Michał Kuczak ◽  
Ewa Kurczyńska

Changes in the composition of the cell walls are postulated to accompany changes in the cell’s fate. We check whether there is a relationship between the presence of selected pectic, arabinogalactan proteins (AGPs), and extensins epitopes and changes in cell reprogramming in order to answer the question of whether they can be markers accompanying changes of cell fate. Selected antibodies were used for spatio-temporal immunolocalization of wall components during the induction of somatic embryogenesis. Based on the obtained results, it can be concluded that (1) the LM6 (pectic), LM2 (AGPs) epitopes are positive markers, but the LM5, LM19 (pectic), JIM8, JIM13 (AGPs) epitopes are negative markers of cells reprogramming to the meristematic/pluripotent state; (2) the LM8 (pectic), JIM8, JIM13, LM2 (AGPs) and JIM11 (extensin) epitopes are positive markers, but LM6 (pectic) epitope is negative marker of cells undergoing detachment; (3) JIM4 (AGPs) is a positive marker, but LM5 (pectic), JIM8, JIM13, LM2 (AGPs) are negative markers for pericycle cells on the xylem pole; (4) LM19, LM20 (pectic), JIM13, LM2 (AGPs) are constitutive wall components, but LM6, LM8 (pectic), JIM4, JIM8, JIM16 (AGPs), JIM11, JIM12 and JIM20 (extensins) are not constitutive wall components; (5) the extensins do not contribute to the cell reprogramming.


Mathematics ◽  
2020 ◽  
Vol 8 (11) ◽  
pp. 2000
Author(s):  
Domingo Benítez ◽  
Gustavo Montero ◽  
Eduardo Rodríguez ◽  
David Greiner ◽  
Albert Oliver ◽  
...  

A novel phenomenological epidemic model is proposed to characterize the state of infectious diseases and predict their behaviors. This model is given by a new stochastic partial differential equation that is derived from foundations of statistical physics. The analytical solution of this equation describes the spatio-temporal evolution of a Gaussian probability density function. Our proposal can be applied to several epidemic variables such as infected, deaths, or admitted-to-the-Intensive Care Unit (ICU). To measure model performance, we quantify the error of the model fit to real time-series datasets and generate forecasts for all the phases of the COVID-19, Ebola, and Zika epidemics. All parameters and model uncertainties are numerically quantified. The new model is compared with other phenomenological models such as Logistic Grow, Original, and Generalized Richards Growth models. When the models are used to describe epidemic trajectories that register infected individuals, this comparison shows that the median RMSE error and standard deviation of the residuals of the new model fit to the data are lower than the best of these growing models by, on average, 19.6% and 35.7%, respectively. Using three forecasting experiments for the COVID-19 outbreak, the median RMSE error and standard deviation of residuals are improved by the performance of our model, on average by 31.0% and 27.9%, respectively, concerning the best performance of the growth models.


Open Biology ◽  
2017 ◽  
Vol 7 (5) ◽  
pp. 170030 ◽  
Author(s):  
Peng Dong ◽  
Zhe Liu

Animal development is orchestrated by spatio-temporal gene expression programmes that drive precise lineage commitment, proliferation and migration events at the single-cell level, collectively leading to large-scale morphological change and functional specification in the whole organism. Efforts over decades have uncovered two ‘seemingly contradictory’ mechanisms in gene regulation governing these intricate processes: (i) stochasticity at individual gene regulatory steps in single cells and (ii) highly coordinated gene expression dynamics in the embryo. Here we discuss how these two layers of regulation arise from the molecular and the systems level, and how they might interplay to determine cell fate and to control the complex body plan. We also review recent technological advancements that enable quantitative analysis of gene regulation dynamics at single-cell, single-molecule resolution. These approaches outline next-generation experiments to decipher general principles bridging gaps between molecular dynamics in single cells and robust gene regulations in the embryo.


2011 ◽  
Vol 21 (12) ◽  
pp. 1009-1017 ◽  
Author(s):  
Diana Lieber ◽  
Jorge Lora ◽  
Sandra Schrempp ◽  
Michael Lenhard ◽  
Thomas Laux
Keyword(s):  

2019 ◽  
Author(s):  
Guak-Kim Tan ◽  
Brian A. Pryce ◽  
Anna Stabio ◽  
John V. Brigande ◽  
ChaoJie Wang ◽  
...  

AbstractStudies of cell fate focus on specification, but little is known about maintenance of the differentiated state. We find that TGFβ signaling plays an essential role in maintenance of the tendon cell fate. To examine the role TGFβ signaling in tenocytes TGFβ type II receptor was targeted in the Scleraxis cell lineage. Tendon development was not disrupted in mutant embryos, but shortly after birth tenocytes lost differentiation markers and reverted to a more stem/progenitor state. Targeting of Tgfbr2 using other Cre drivers did not cause tenocyte dedifferentiation suggesting a critical significance for the spatio-temporal activity of ScxCre. Viral reintroduction of Tgfbr2 to mutants was sufficient to prevent and even rescue mutant tenocytes suggesting a continuous and cell-autonomous role for TGFβ signaling in cell fate maintenance. These results uncover the critical importance of molecular pathways that maintain the differentiated cell fate and a key role for TGFβ signaling in these processes.


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