scholarly journals Live-imaging analysis of germ cell proliferation in the C. elegans adult supports a stochastic model for stem cell proliferation

2017 ◽  
Vol 423 (2) ◽  
pp. 93-100 ◽  
Author(s):  
Simona Rosu ◽  
Orna Cohen-Fix
Keyword(s):  
Cell Proliferation ◽  
Stem Cell ◽  
Stochastic Model ◽  
Germ Cell ◽  
Live Imaging ◽  
Imaging Analysis ◽  
Stem Cell Proliferation ◽  
C Elegans ◽  
Germ Cell Proliferation

scholarly journals mir-35 is involved in intestine cell G1/S transition and germ cell proliferation in C. elegans

Cell Research ◽  
2011 ◽  
Vol 21 (11) ◽  
pp. 1605-1618 ◽  
Author(s):  
Min Liu ◽  
Pengpeng Liu ◽  
Li Zhang ◽  
Qingchun Cai ◽  
Ge Gao ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Germ Cell ◽  
C Elegans ◽  
Intestine Cell ◽  
Germ Cell Proliferation

scholarly journals Mutations that Affect Channel Opening of Innexin Hemichannels in the C. elegans Gonad

2020 ◽  
Author(s):  
Todd Starich ◽  
David Greenstein
Keyword(s):  
Cell Proliferation ◽  
Gap Junctions ◽  
Germ Cell ◽  
Structural Model ◽  
Loss Of Function ◽  
C Elegans ◽  
Somatic Gonad ◽  
Channel Opening ◽  
Germline Proliferation ◽  
Germ Cell Proliferation

In C. elegans, gap junctions couple cells of the somatic gonad with the germline to support germ cell proliferation and gametogenesis. We previously characterized a strong loss-of-function mutation (T239I) affecting the second extracellular loop (EL2) of the somatic INX-8 hemichannel subunit. These mutant hemichannels form non-functional gap junctions with germline-expressed innexins. Here we describe the characterization of mutations that restore germ cell proliferation in the T239I EL2 mutant background. We recovered seven intragenic mutations located in diverse domains of INX-8 but not the EL domains. These second-site mutations compensate for the original channel defect to varying degrees, from nearly complete wild-type rescue, to partial rescue of germline proliferation. One suppressor mutation (E350K) supports the innexin cryo-EM structural model that the channel pore opening is surrounded by a cytoplasmic dome. Two suppressor mutations (S9L and I36N) may form leaky hemichannels that support germline proliferation but cause the demise of somatic sheath cells. Phenotypic analyses of three other suppressors reveal an equivalency in the rescue of germline proliferation and comparable delays in gametogenesis but a graded rescue of fertility. These latter mutations may be useful to probe interactions with the biochemical pathways that produce the molecules transiting through soma-germline gap junctions.

Two mutations in pab-1 encoding poly(A)-binding protein show similar defects in germline stem cell proliferation but different longevity in C. elegans

2010 ◽  
Vol 30 (2) ◽  
pp. 167-172 ◽  
Author(s):  
Sunny Ko ◽  
Jae-Hyung Park ◽  
Ah-Reum Lee ◽  
Eugene Kim ◽  
Jiyoung-Kim ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Stem Cell ◽  
Binding Protein ◽  
Germline Stem Cell ◽  
Stem Cell Proliferation ◽  
C Elegans

scholarly journals Constitutive WNT/CTNNB1 activation triggers spermatogonial stem cell proliferation and germ cell depletion

2017 ◽  
Vol 426 (1) ◽  
pp. 17-27 ◽  
Author(s):  
Anne-Amandine Chassot ◽  
Morgane Le Rolle ◽  
Maxime Jourden ◽  
Maketo M. Taketo ◽  
Norbert B. Ghyselinck ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Stem Cell ◽  
Germ Cell ◽  
Spermatogonial Stem Cell ◽  
Cell Depletion ◽  
Stem Cell Proliferation

scholarly journals The exocyst complex regulates C. elegans germline stem cell proliferation by controlling membrane Notch levels

Development ◽  
2021 ◽  
Vol 148 (15) ◽  
Author(s):  
Kumari Pushpa ◽  
Sunayana Dagar ◽  
Harsh Kumar ◽  
Diksha Pathak ◽  
Sivaram V. S. Mylavarapu
Keyword(s):  
Cell Proliferation ◽  
Stem Cell ◽  
Plasma Membrane ◽  
Notch Signaling ◽  
Mammalian Cells ◽  
Germline Stem Cell ◽  
Stem Cell Proliferation ◽  
C Elegans ◽  
Exocyst Complex ◽  
Membrane Density

ABSTRACT The conserved exocyst complex regulates plasma membrane-directed vesicle fusion in eukaryotes. However, its role in stem cell proliferation has not been reported. Germline stem cell (GSC) proliferation in the nematode Caenorhabditis elegans is regulated by conserved Notch signaling. Here, we reveal that the exocyst complex regulates C. elegans GSC proliferation by modulating Notch signaling cell autonomously. Notch membrane density is asymmetrically maintained on GSCs. Knockdown of exocyst complex subunits or of the exocyst-interacting GTPases Rab5 and Rab11 leads to Notch redistribution from the GSC-niche interface to the cytoplasm, suggesting defects in plasma membrane Notch deposition. The anterior polarity (aPar) protein Par6 is required for GSC proliferation, and for maintaining niche-facing membrane levels of Notch and the exocyst complex. The exocyst complex biochemically interacts with the aPar regulator Par5 (14-3-3ζ) and Notch in C. elegans and human cells. Exocyst components are required for Notch plasma membrane localization and signaling in mammalian cells. Our study uncovers a possibly conserved requirement of the exocyst complex in regulating GSC proliferation and in maintaining optimal membrane Notch levels.

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