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.

scholarly journals The microRNA pathway controls germ cell proliferation and differentiation in C. elegans

Cell Research ◽  
2012 ◽  
Vol 22 (6) ◽  
pp. 1034-1045 ◽  
Author(s):  
Syed Irfan Ahmad Bukhari ◽  
Alejandro Vasquez-Rifo ◽  
Dominic Gagné ◽  
Eric R Paquet ◽  
Monique Zetka ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Germ Cell ◽  
C Elegans ◽  
Cell Proliferation And Differentiation ◽  
Proliferation And Differentiation ◽  
Microrna Pathway ◽  
Germ Cell Proliferation

scholarly journals Dafachronic acid inhibits C. elegans germ cell proliferation in a DAF-12-dependent manner

2017 ◽  
Vol 432 (2) ◽  
pp. 215-221 ◽  
Author(s):  
Madhumati Mukherjee ◽  
Snehal N. Chaudhari ◽  
Riju S. Balachandran ◽  
Alexandra S. Vagasi ◽  
Edward T. Kipreos
Keyword(s):  
Cell Proliferation ◽  
Germ Cell ◽  
Dependent Manner ◽  
C Elegans ◽  
Dafachronic Acid ◽  
Germ Cell Proliferation

scholarly journals Müllerian Inhibiting Substance Is Required for Germ Cell Proliferation during Early Gonadal Differentiation in Medaka (Oryzias latipes)

Endocrinology ◽  
2007 ◽  
Vol 149 (4) ◽  
pp. 1813-1819 ◽  
Author(s):  
Eri Shiraishi ◽  
Norifumi Yoshinaga ◽  
Takeshi Miura ◽  
Hayato Yokoi ◽  
Yuko Wakamatsu ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Germ Cell ◽  
Germ Cells ◽  
Sex Differentiation ◽  
Somatic Cells ◽  
Oryzias Latipes ◽  
Cell Number ◽  
Gonadal Differentiation ◽  
Loss Of Function ◽  
Germ Cell Proliferation

Müllerian inhibiting substance (MIS) is a glycoprotein belonging to the TGF-β superfamily. In mammals, MIS is responsible for the regression of Müllerian ducts in the male fetus. However, the role of MIS in gonadal sex differentiation of teleost fish, which have no Müllerian ducts, has yet to be clarified. In the present study, we examined the expression pattern of mis and mis type 2 receptor (misr2) mRNAs and the function of MIS signaling in early gonadal differentiation in medaka (teleost, Oryzias latipes). In situ hybridization showed that both mis and misr2 mRNAs were expressed in the somatic cells surrounding the germ cells of both sexes during early sex differentiation. Loss-of-function of either MIS or MIS type II receptor (MISRII) in medaka resulted in suppression of germ cell proliferation during sex differentiation. These results were supported by cell proliferation assay using 5-bromo-2′-deoxyuridine labeling analysis. Treatment of tissue fragments containing germ cells with recombinant eel MIS significantly induced germ cell proliferation in both sexes compared with the untreated control. On the other hand, culture of tissue fragments from the MIS- or MISRII-defective embryos inhibited proliferation of germ cells in both sexes. Moreover, treatment with recombinant eel MIS in the MIS-defective embryos dose-dependently increased germ cell number in both sexes, whereas in the MISRII-defective embryos, it did not permit proliferation of germ cells. These results suggest that in medaka, MIS indirectly stimulates germ cell proliferation through MISRII, expressed in the somatic cells immediately after they reach the gonadal primordium.

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