A role for the fusogen eff-1 in epidermal stem cell number robustness in Caenorhabditis elegans

Abstract 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 sho...

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Autores principales:	Sneha L. Koneru, Fu Xiang Quah, Ritobrata Ghose, Mark Hintze, Nicola Gritti, Jeroen Sebastiaan van Zon, Michalis Barkoulas
Formato:	article
Lenguaje:	EN
Publicado:	Nature Portfolio 2021
Materias:	Medicine R Science Q
Acceso en línea:	https://doaj.org/article/b3d14064a7df42bfb896368139637f03
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spelling	oai:doaj.org-article:b3d14064a7df42bfb896368139637f032021-12-02T14:49:33ZA role for the fusogen eff-1 in epidermal stem cell number robustness in Caenorhabditis elegans10.1038/s41598-021-88500-42045-2322https://doaj.org/article/b3d14064a7df42bfb896368139637f032021-05-01T00:00:00Zhttps://doi.org/10.1038/s41598-021-88500-4https://doaj.org/toc/2045-2322Abstract 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.Sneha L. KoneruFu Xiang QuahRitobrata GhoseMark HintzeNicola GrittiJeroen Sebastiaan van ZonMichalis BarkoulasNature PortfolioarticleMedicineRScienceQENScientific Reports, Vol 11, Iss 1, Pp 1-13 (2021)
institution	DOAJ
collection	DOAJ
language	EN
topic	Medicine R Science Q
spellingShingle	Medicine R Science Q Sneha L. Koneru Fu Xiang Quah Ritobrata Ghose Mark Hintze Nicola Gritti Jeroen Sebastiaan van Zon Michalis Barkoulas A role for the fusogen eff-1 in epidermal stem cell number robustness in Caenorhabditis elegans
description	Abstract 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.
format	article
author	Sneha L. Koneru Fu Xiang Quah Ritobrata Ghose Mark Hintze Nicola Gritti Jeroen Sebastiaan van Zon Michalis Barkoulas
author_facet	Sneha L. Koneru Fu Xiang Quah Ritobrata Ghose Mark Hintze Nicola Gritti Jeroen Sebastiaan van Zon Michalis Barkoulas
author_sort	Sneha L. Koneru
title	A role for the fusogen eff-1 in epidermal stem cell number robustness in Caenorhabditis elegans
title_short	A role for the fusogen eff-1 in epidermal stem cell number robustness in Caenorhabditis elegans
title_full	A role for the fusogen eff-1 in epidermal stem cell number robustness in Caenorhabditis elegans
title_fullStr	A role for the fusogen eff-1 in epidermal stem cell number robustness in Caenorhabditis elegans
title_full_unstemmed	A role for the fusogen eff-1 in epidermal stem cell number robustness in Caenorhabditis elegans
title_sort	role for the fusogen eff-1 in epidermal stem cell number robustness in caenorhabditis elegans
publisher	Nature Portfolio
publishDate	2021
url	https://doaj.org/article/b3d14064a7df42bfb896368139637f03
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A role for the fusogen eff-1 in epidermal stem cell number robustness in Caenorhabditis elegans

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