scholarly journals LIN-28 balances longevity and germline stem cell number inCaenorhabditis elegansthrough let-7/AKT/DAF-16 axis

Aging Cell ◽  
2016 ◽  
Vol 16 (1) ◽  
pp. 113-124 ◽  
Author(s):  
Dan Wang ◽  
Lei Hou ◽  
Shuhei Nakamura ◽  
Ming Su ◽  
Fang Li ◽  
...  
2018 ◽  
Author(s):  
Sarah L. Crittenden ◽  
ChangHwan Lee ◽  
Ipsita Mohanty ◽  
Sindhu Battula ◽  
Judith Kimble

ABSTRACTStem cell maintenance by niche signaling is a common theme across phylogeny. In the Caenorhabditis elegans gonad, the broad outlines of germline stem cell (GSC) regulation are the same for both sexes: GLP-1/Notch signaling from the mesenchymal Distal Tip Cell (DTC) niche maintains GSCs in the distal gonad of both sexes (Austin and Kimble 1987), and does so via two key stem cell regulators, SYGL-1 and LST-1 (Kershneret al. 2014). Most analyses of niche signaling and GSC regulation have focused on XX hermaphrodites, an essentially female sex making sperm in larvae and oocytes in adults. Here we focus on XO males, which are sexually dimorphic in all tissues, including the distal gonad. The architecture of the male niche and the cellular behavior of GSCs are sex-specific. Despite these differences, males maintain a GSC pool similar to the hermaphrodite with respect to size and cell number and the male GSC response to niche signaling is also remarkably similar.


Genetics ◽  
2018 ◽  
Vol 209 (4) ◽  
pp. 1155-1166 ◽  
Author(s):  
Lesley N. Weaver ◽  
Daniela Drummond-Barbosa

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Sneha L. Koneru ◽  
Fu Xiang Quah ◽  
Ritobrata Ghose ◽  
Mark Hintze ◽  
Nicola Gritti ◽  
...  

AbstractDevelopmental 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.


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