A role for the fusogen eff-1 in epidermal stem cell number robustness in Caenorhabditis elegans
| Autor: | Fu Xiang Quah, Mark Hintze, Ritobrata Ghose, Nicola Gritti, Jeroen S. van Zon, Sneha L. Koneru, Michalis Barkoulas |
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| Rok vydání: | 2020 |
| Předmět: |
0301 basic medicine
animal structures Cell division Cèl·lules Science Cellular differentiation Cell Population Cell fate determination Development Article Cell Fusion 03 medical and health sciences 0302 clinical medicine medicine Animals education Caenorhabditis elegans Caenorhabditis elegans Proteins Cell Shape Tissue homeostasis education.field_of_study Multidisciplinary Cell fusion Membrane Glycoproteins biology Stem Cells biology.organism_classification Cell biology 030104 developmental biology medicine.anatomical_structure Epidermal Cells Differentiation embryonic structures Medicine Epidermis Genètica 030217 neurology & neurosurgery |
| Zdroj: | Scientific Reports Scientific Reports, Vol 11, Iss 1, Pp 1-13 (2021) |
| ISSN: | 2045-2322 |
| Popis: | Developmental patterning in Caenorhabditis elegans is known to proceed in a highly stereotypical manner, which raises the question of how developmental robustness is achieved despite the inevitable stochastic noise. We focus here on a population of epidermal cells, the seam cells, which show stem cell-like behaviour and divide symmetrically and asymmetrically over post-embryonic development to generate epidermal and neuronal tissues. We have conducted a mutagenesis screen to identify mutants that introduce phenotypic variability in the normally invariant seam cell population. We report here that a null mutation in the fusogen eff-1 increases seam cell number variability. Using time-lapse microscopy and single molecule fluorescence hybridisation, we find that seam cell division and differentiation patterns are mostly unperturbed in eff-1 mutants, indicating that cell fusion is uncoupled from the cell differentiation programme. Nevertheless, seam cell losses due to the inappropriate differentiation of both daughter cells following division, as well as seam cell gains through symmetric divisions towards the seam cell fate were observed at low frequency. We show that these stochastic errors likely arise through accumulation of defects interrupting the continuity of the seam and changing seam cell shape, highlighting the role of tissue homeostasis in suppressing phenotypic variability during development. Funding: Some C. elegans strains were provided by the CGC, which is funded by NIH Office of Research Infrastructure Programs (P40 OD010440). This work was funded by the European Research Council (ROBUSTNET-639485) |
| Databáze: | OpenAIRE |
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