Genes and Cells that Determine the Lifespan of C. elegans - Part 2: The Regulation of Aging by Signals from the Reproductive System, and, also, a Link Between Aging and Tumor Growth (37:16)

SciVee ◽  
2009 ◽  
Keyword(s):  
Tumor Growth ◽  
Reproductive System ◽  
C Elegans

scholarly journals Regulation of Actin Dynamics in the C. elegans Somatic Gonad

2019 ◽  
Vol 7 (1) ◽  
pp. 6 ◽  
Author(s):  
Charlotte Kelley ◽  
Erin Cram
Keyword(s):  
Reproductive System ◽  
Cell Types ◽  
Actin Dynamics ◽  
Entry And Exit ◽  
Cell Type ◽  
C Elegans ◽  
Type Study ◽  
Somatic Gonad ◽  
Uterus Contraction

The reproductive system of the hermaphroditic nematode C. elegans consists of a series of contractile cell types—including the gonadal sheath cells, the spermathecal cells and the spermatheca–uterine valve—that contract in a coordinated manner to regulate oocyte entry and exit of the fertilized embryo into the uterus. Contraction is driven by acto-myosin contraction and relies on the development and maintenance of specialized acto-myosin networks in each cell type. Study of this system has revealed insights into the regulation of acto-myosin network assembly and contractility in vivo.

Novel organo-osmium(ii) proteosynthesis inhibitors active against human ovarian cancer cells reduce gonad tumor growth in Caenorhabditis elegans

2021 ◽  
Vol 8 (1) ◽  
pp. 141-155
Author(s):  
Enrique Ortega ◽  
Francisco J. Ballester ◽  
Alba Hernández-García ◽  
Samanta Hernández-García ◽  
M. Alejandra Guerrero-Rubio ◽  
...  
Keyword(s):  
Ovarian Cancer ◽  
Antitumor Activity ◽  
Tumor Growth ◽  
Cancer Cells ◽  
Ovarian Cancer Cells ◽  
Human Ovarian Cancer ◽  
Arene Complexes ◽  
C Elegans

Novel Os(ii) arene complexes with a deprotonated ppy or ppy-CHO C^N ligand have been synthesized to selectively act on cancer cells as proteosynthesis inhibitors in vitro and exert antitumor activity in vivo in C. elegans models.

scholarly journals Tropomyosin and Troponin Are Required for Ovarian Contraction in the Caenorhabditis elegans Reproductive System

2004 ◽  
Vol 15 (6) ◽  
pp. 2782-2793 ◽  
Author(s):  
Kanako Ono ◽  
Shoichiro Ono
Keyword(s):  
Rna Interference ◽  
Caenorhabditis Elegans ◽  
Germ Cells ◽  
Reproductive System ◽  
Regulatory Mechanism ◽  
Striated Muscle ◽  
Troponin C ◽  
Nematode Caenorhabditis Elegans ◽  
C Elegans ◽  
Somatic Gonad

Ovulation in the nematode Caenorhabditis elegans is coordinated by interactions between the somatic gonad and germ cells. Myoepithelial sheath cells of the proximal ovary are smooth muscle-like cells, but the regulatory mechanism of their contraction is unknown. We show that contraction of the ovarian muscle requires tropomyosin and troponin, which are generally major actin-linked regulators of contraction of striated muscle. RNA interference of tropomyosin or troponin C caused sterility by inhibiting ovarian contraction that is required for expelling mature oocytes into the spermatheca where fertilization takes place, thus causing accumulation of endomitotic oocytes in the ovary. Tropomyosin and troponin C were associated with actin filaments in the myoepithelial sheath, and the association of troponin C with actin was dependent on tropomyosin. A mutation in the actin depolymerizing factor/cofilin gene suppressed the ovulation defects by RNA interference of tropomyosin or troponin C. These results strongly suggest that tropomyosin and troponin are the actin-linked regulators for contraction of ovarian muscle in the C. elegans reproductive system.

scholarly journals Production of a Monoclonal Antibody Directed against the Recombinant SEL1L Protein

2002 ◽  
Vol 17 (2) ◽  
pp. 104-111 ◽  
Author(s):  
R. Orlandi ◽  
M. Cattaneo ◽  
F. Troglio ◽  
M. Campiglio ◽  
I. Biunno ◽  
...  
Keyword(s):  
Monoclonal Antibody ◽  
Tumor Growth ◽  
Tumor Progression ◽  
Tumor Cells ◽  
Western Blotting ◽  
Human Gene ◽  
Recombinant Fragment ◽  
C Elegans ◽  
Normal Tissues ◽  
N Terminus

SEL1L, highly similar to the C. elegans sel-1 gene, is a recently cloned human gene whose function is under investigation. SEL1L is differentially expressed in tumors and normal tissues and seems to play a role in tumor growth and aggressiveness. We used the recombinant N-terminus of the SEL1L protein to immunize a Balb/c mouse and produce a monoclonal antibody. A hybridoma secreting an antibody specifically reacting on the SEL1L recombinant fragment was selected. This monoclonal antibody, named MSel1, recognizes the SEL1L protein by Western blotting, immunofluorescence and immunohistochemistry on normal and tumor cells. MSel1 is able to recognize SEL1L even on archival tumor specimens and is therefore particularly appropriate to study SEL1L involvement in tumor progression.

scholarly journals Gα/GSA-1 works upstream of PKA/KIN-1 to regulate calcium signaling and contractility in the Caenorhabditis elegans spermatheca

2020 ◽  
Author(s):  
Perla G. Castaneda ◽  
Alyssa D. Cecchetelli ◽  
Hannah N. Pettit ◽  
Erin J. Cram
Keyword(s):  
Caenorhabditis Elegans ◽  
Protein Kinase ◽  
Calcium Signaling ◽  
Protein Kinase A ◽  
G Protein ◽  
Reproductive System ◽  
The Body ◽  
Cell Contractility ◽  
C Elegans ◽  
Kinase A

AbstractCorrect regulation of cell contractility is critical for the function of many biological systems. The reproductive system of the hermaphroditic nematode C. elegans contains a contractile tube of myoepithelial cells known as the spermatheca, which stores sperm and is the site of oocyte fertilization. Regulated contraction of the spermatheca pushes the embryo into the uterus. Cell contractility in the spermatheca is dependent on actin and myosin and is regulated, in part, by Ca2+ signaling through the phospholipase PLC-1, which mediates Ca2+ release from the endoplasmic reticulum. Here, we describe a novel role for GSA-1/Gαs, and protein kinase A, composed of the catalytic subunit KIN-1/PKA-C and the regulatory subunit KIN-2/PKA-R, in the regulation of Ca2+ release and contractility in the C. elegans spermatheca. Without GSA-1/Gαs or KIN-1/PKA-C, Ca2+ is not released, and oocytes become trapped in the spermatheca. Conversely, when PKA is activated through either a gain of function allele in GSA-1 (GSA-1(GF)) or by depletion of KIN-2/PKA-R, Ca2+ is increased, and waves of Ca2+ travel across the spermatheca even in the absence of oocyte entry. In the spermathecal-uterine valve, loss of GSA-1/Gαs or KIN-1/PKA-C results in sustained, high levels of Ca2+ and a loss of coordination between the spermathecal bag and sp-ut valve. Additionally, we show that depleting phosphodiesterase PDE-6 levels alters contractility and Ca2+ dynamics in the spermatheca, and that the GPB-1 and GPB-2 Gβ subunits play a central role in regulating spermathecal contractility and Ca2+ signaling. This work identifies a signaling network in which Ca2+ and cAMP pathways work together to coordinate spermathecal contractility.Author SummaryOrganisms are full of biological tubes that transport substances such as food, liquids, and air through the body. Moving these substances in a coordinated manner, with the correct directionality, timing, and rate is critical for organism health. In this study we used Caenorhabditis elegans, a small transparent worm, to study how cells in biological tubes coordinate how and when they squeeze and relax. The C. elegans spermatheca is part of the reproductive system, which uses calcium signaling to drive the coordinated contractions that push fertilized eggs out into the uterus. Using genetic analysis and a calcium-sensitive fluorescent protein, we show that the G-protein GSA-1 functions with protein kinase A to regulate calcium release, and contraction of the spermatheca. These findings establish a link between G-protein and cAMP signaling that may apply to similar signaling pathways in other systems.

scholarly journals Positive autoregulation of lag-1 in response to LIN-12 activation in cell fate decisions during C. elegans reproductive system development

Development ◽  
2020 ◽  
Vol 147 (18) ◽  
pp. dev193482
Author(s):  
Katherine Leisan Luo ◽  
Ryan S. Underwood ◽  
Iva Greenwald
Keyword(s):  
Cell Fate ◽  
Reproductive System ◽  
Target Gene ◽  
System Development ◽  
Animal Development ◽  
Cell Fate Decisions ◽  
C Elegans ◽  
Spatiotemporal Regulation ◽  
Target Gene Transcription ◽  
Notch Activation

ABSTRACTDuring animal development, ligand binding releases the intracellular domain of LIN-12/Notch by proteolytic cleavage to translocate to the nucleus, where it associates with the DNA-binding protein LAG-1/CSL to activate target gene transcription. We investigated the spatiotemporal regulation of LAG-1/CSL expression in Caenorhabditis elegans and observed that an increase in endogenous LAG-1 levels correlates with LIN-12/Notch activation in different cell contexts during reproductive system development. We show that this increase is via transcriptional upregulation by creating a synthetic endogenous operon, and identified an enhancer region that contains multiple LAG-1 binding sites (LBSs) embedded in a more extensively conserved high occupancy target (HOT) region. We show that these LBSs are necessary for upregulation in response to LIN-12/Notch activity, indicating that lag-1 engages in direct positive autoregulation. Deletion of the HOT region from endogenous lag-1 reduced LAG-1 levels and abrogated positive autoregulation, but did not cause hallmark cell fate transformations associated with loss of lin-12/Notch or lag-1 activity. Instead, later somatic reproductive system defects suggest that proper transcriptional regulation of lag-1 confers robustness to somatic reproductive system development.

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