Using positional information to provide context for biological image analysis with MorphoGraphX 2.0
- Max Planck Institute for Plant Breeding Research, Germany
- John Innes Centre, United Kingdom
- RWTH Aachen University, Germany
- Université de Montréal, Canada
- University of Montreal, Canada
- Technical University of Munich, Germany
- University of Warwick, United Kingdom
Abstract
Positional information is a central concept in developmental biology. In developing organs, positional information can be idealized as a local coordinate system that arises from morphogen gradients controlled by organizers at key locations. This offers a plausible mechanism for the integration of the molecular networks operating in individual cells into the spatially-coordinated multicellular responses necessary for the organization of emergent forms. Understanding how positional cues guide morphogenesis requires the quantification of gene expression and growth dynamics in the context of their underlying coordinate systems. Here we present recent advances in the MorphoGraphX software (Barbier de Reuille et al., 2015) that implement a generalized framework to annotate developing organs with local coordinate systems. These coordinate systems introduce an organ-centric spatial context to microscopy data, allowing gene expression and growth to be quantified and compared in the context of the positional information thought to control them.
Data availability
Datasets and software are available at www.MorphoGraphX.org and Dryad
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MorphoGraphX2: Datasets that demostrate how to create positional information with local coordinate systemsDryad Digital Repository, doi:10.5061/dryad.m905qfv1r.
Article and author information
Author details
Anne-Lise Routier-Kierzkowska
Constance Le Gloanec
Daniel Kierzkowski
Johannes Stegmaier
Funding
Deutsche Forschungsgemeinschaft (Forschunggruppe 2581)
- Kay Schneitz
- Miltos Tsiantis
- Richard S Smith
Human Frontiers Science Program (RGP0002/2020)
- George Bassel
Max Planck Society (Core grant)
- Miltos Tsiantis
Fonds Nature et Technologies (282285)
- Anne-Lise Routier-Kierzkowska
- Daniel Kierzkowski
Deutsche Forschungsgemeinschaft (ERA-CAPS V-Morph)
- Richard S Smith
Biotechnology and Biological Sciences Research Council (ISP to John Innes Centre)
- Richard S Smith
Bundesministerium für Bildung und Forschung (031A494 & 031A492)
- Richard S Smith
Deutsche Forschungsgemeinschaft (STE2802/2-1)
- Dennis Eschweiler
New Frontiers in Research Fund (2018-00953)
- Anne-Lise Routier-Kierzkowska
- Daniel Kierzkowski
Natural Sciences and Engineering Research Council of Canada (RGPIN-2018-04897)
- Daniel Kierzkowski
Natural Sciences and Engineering Research Council of Canada (RGPIN-2018-05762)
- Anne-Lise Routier-Kierzkowska
Leverhulme Trust (RPG-2019-267)
- George Bassel
Biotechnology and Biological Sciences Research Council (BB/S002804/1)
- George Bassel
The funders had no role in study design, data collection and interpretation, or the decision to submit the work for publication.
Copyright
© 2022, Strauss et al.
This article is distributed under the terms of the Creative Commons Attribution License permitting unrestricted use and redistribution provided that the original author and source are credited.
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Using positional information to provide context for biological image analysis with MorphoGraphX 2.0
eLife 11:e72601.
https://doi.org/10.7554/eLife.72601
Further reading
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Congenital malformations can originate from numerous genetic or non-genetic factors but in most cases the causes are unknown. Genetic disruption of nicotinamide adenine dinucleotide (NAD) de novo synthesis causes multiple malformations, collectively termed Congenital NAD Deficiency Disorder (CNDD), highlighting the necessity of this pathway during embryogenesis. Previous work in mice shows that NAD deficiency perturbs embryonic development specifically when organs are forming. While the pathway is predominantly active in the liver postnatally, the site of activity prior to and during organogenesis is unknown. Here, we used a mouse model of human CNDD and assessed pathway functionality in embryonic livers and extraembryonic tissues via gene expression, enzyme activity and metabolic analyses. We found that the extra-embryonic visceral yolk sac endoderm exclusively synthesises NAD de novo during early organogenesis before the embryonic liver takes over this function. Under CNDD-inducing conditions, visceral yolk sacs had reduced NAD levels and altered NAD-related metabolic profiles, affecting embryo metabolism. Expression of requisite pathway genes is conserved in the equivalent yolk sac cell type in humans. Our findings show that visceral yolk sac-mediated NAD de novo synthesis activity is essential for mouse embryogenesis and its perturbation causes CNDD. As mouse and human yolk sacs are functionally homologous, our data improve the understanding of human congenital malformation causation.
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- Developmental Biology
- Stem Cells and Regenerative Medicine
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