Germ-line induction of the
            <i>Caenorhabditis elegans</i>
            vulva

Thompson, Beth E.; Lamont, Liana B.; Kimble, Judith

doi:10.1073/pnas.0510264103

Cited by 15 publications

(21 citation statements)

References 44 publications

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“…Mutations in the FOG and FBF translational inhibitor RNA-binding proteins cause a germline-dependent Muv phenotype, and the FBF proteins can bind to the 3′ UTR of lin-3 in vitro , suggesting that germline lin-3 mRNA is translationally repressed during the larval stage when vulval induction occurs [43]. In many class B synMuv mutants, somatic cells express normally germline-specific genes [19], [44], [45].…”

Section: Discussionmentioning

confidence: 99%

The Caenorhabditis elegans Synthetic Multivulva Genes Prevent Ras Pathway Activation by Tightly Repressing Global Ectopic Expression of lin-3 EGF

et al. 2011

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The Caenorhabditis elegans class A and B synthetic multivulva (synMuv) genes redundantly antagonize an EGF/Ras pathway to prevent ectopic vulval induction. We identify a class A synMuv mutation in the promoter of the lin-3 EGF gene, establishing that lin-3 is the key biological target of the class A synMuv genes in vulval development and that the repressive activities of the class A and B synMuv pathways are integrated at the level of lin-3 expression. Using FISH with single mRNA molecule resolution, we find that lin-3 EGF expression is tightly restricted to only a few tissues in wild-type animals, including the germline. In synMuv double mutants, lin-3 EGF is ectopically expressed at low levels throughout the animal. Our findings reveal that the widespread ectopic expression of a growth factor mRNA at concentrations much lower than that in the normal domain of expression can abnormally activate the Ras pathway and alter cell fates. These results suggest hypotheses for the mechanistic basis of the functional redundancy between the tumor-suppressor-like class A and B synMuv genes: the class A synMuv genes either directly or indirectly specifically repress ectopic lin-3 expression; while the class B synMuv genes might function similarly, but alternatively might act to repress lin-3 as a consequence of their role in preventing cells from adopting a germline-like fate. Analogous genes in mammals might function as tumor suppressors by preventing broad ectopic expression of EGF-like ligands.

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Section: Discussionmentioning

confidence: 99%

The Caenorhabditis elegans Synthetic Multivulva Genes Prevent Ras Pathway Activation by Tightly Repressing Global Ectopic Expression of lin-3 EGF

et al. 2011

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“…In addition to its direct control of the meiotic program, FBF also represses mpk-1 mRNA, lin-3 mRNA, and fog-1 mRNA, which encode the C. elegans homologs of ERK/MAP kinase, TGF-a/EGF, and CPEB, respectively ( Fig. 2B) (Thompson et al , 2006Lee et al 2007a;Kershner and Kimble 2010). MPK-1 and LIN-3 regulate multiple cell fates in somatic tissues (Sundaram 2006); MPK-1 also affects germ cell fate specification (Lee et al 2007b); FOG-1 is one of the terminal regulators of sperm fate specification (Barton and Kimble 1990).…”

Section: Regulators That Promote Germline Self-renewal Directly Reprementioning

confidence: 99%

Molecular Regulation of the Mitosis/Meiosis Decision in Multicellular Organisms

Kimble

2011

Cold Spring Harbor Perspectives in Biology

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“…FBF prevents differentiation by repressing lin-3 mRNA [70], which encodes the C. elegans homolog of EGF [71]. While LIN-3 has no apparent role in the germline, it is a potent regulator of somatic development [40]; indeed when LIN-3 is aberrantly made in fbf-1 fbf-2 germlines, vulval development is defective [70].…”

Section: Germ Cell Intrinsic Controls Of Self-renewalmentioning

confidence: 99%

“…While LIN-3 has no apparent role in the germline, it is a potent regulator of somatic development [40]; indeed when LIN-3 is aberrantly made in fbf-1 fbf-2 germlines, vulval development is defective [70]. The lin-3 case suggests that FBF may repress potent developmental regulators more broadly, not just those that control germline development.…”

Section: Germ Cell Intrinsic Controls Of Self-renewalmentioning

confidence: 99%

Scratching the niche that controls Caenorhabditis elegans germline stem cells

Byrd

Kimble

2009

Seminars in Cell & Developmental Biology

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The C. elegans gonad provides a well-defined model for a stem cell niche and its control of selfrenewal and differentiation. The distal tip cell (DTC) forms a mesenchymal niche that controls germline stem cells (GSCs), both to generate the germline tissue during development and to maintain it during adulthood. The DTC uses GLP-1/Notch signaling to regulate GSCs; germ cells respond to Notch signaling with a network of RNA regulators to control the decision between self-renewal and entry into the meiotic cell cycle.

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Germ-line induction of the Caenorhabditis elegans vulva

Abstract: Development of the

Cited by 15 publications

References 44 publications

The Caenorhabditis elegans Synthetic Multivulva Genes Prevent Ras Pathway Activation by Tightly Repressing Global Ectopic Expression of lin-3 EGF

The Caenorhabditis elegans Synthetic Multivulva Genes Prevent Ras Pathway Activation by Tightly Repressing Global Ectopic Expression of lin-3 EGF

Molecular Regulation of the Mitosis/Meiosis Decision in Multicellular Organisms

Scratching the niche that controls Caenorhabditis elegans germline stem cells

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