1,060 research outputs found

    The C. Elegans ROR receptor tyrosine kinase, CAM-1, non-autonomously inhibits the Wnt pathway

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    Inhibitors of Wnt signaling promote normal development and prevent cancer by restraining when and where the Wnt pathway is activated. ROR proteins, a class of Wnt-binding receptor tyrosine kinases, inhibit Wnt signaling by an unknown mechanism. To clarify how RORs inhibit the Wnt pathway, we examined the relationship between Wnts and the sole C. elegans ROR homolog, cam-1, during C. elegans vulval development, a Wnt-regulated process. We found that loss and overexpression of cam-1 causes reciprocal defects in Wnt-mediated cell-fate specification. Our molecular and genetic analyses revealed that the CAM-1 extracellular domain (ECD) is sufficient to non-autonomously antagonize multiple Wnts, suggesting that the CAM-1/ROR ECD sequesters Wnts. A sequestration model is supported by our findings that the CAM-1 ECD binds to several Wnts in vitro. These results demonstrate how ROR proteins help to refine the spatial pattern of Wnt activity in a complex multicellular environment

    C. elegans BED domain transcription factor BED-3 controls lineage-specific cell proliferation during organogenesis

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    The control of cell division is critical to organogenesis, but how this control is achieved is not fully understood. We found that mutations in bed-3, encoding a BED Zn-finger domain transcription factor, confer a phenotype where a specific set of cell divisions during vulval organogenesis is lost. Unlike general cell cycle regulators in Caenorhabditis elegans, the function of bed-3 is restricted to specific lineages. Transcriptional reporters suggest that bed-3 is expressed in a limited number of cell types including vulval cells whose divisions are affected in bed-3 mutants. A bed-3 mutation also affects the expression pattern of the cdh-3 cadherin gene in the vulva. The phenotype of bed-3 mutants is similar to the phenotype caused by mutations in cog-1 (Nkx6), a component of a gene regulatory network controlling cell type specific gene expression in the vulval lineage. These results suggest that bed-3 is a key component linking the gene regulatory network controlling cell-type specification to control of cell division during vulval organogenesis

    A Sound Interpretation of Leśniewski's Epsilon in Modal Logic KTB

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    In this paper, we shall show that the following translation IMI^M from the propositional fragment L1\bf L_1 of Leśniewski's ontology to modal logic KTB\bf KTB is sound: for any formula ϕ\phi and ψ\psi of L1\bf L_1, it is defined as(M1) IM(ϕψ)=IM(ϕ)IM(ψ)I^M(\phi \vee \psi) = I^M(\phi) \vee I^M(\psi),(M2) IM(¬ϕ)=¬IM(ϕ)I^M(\neg \phi) = \neg I^M(\phi),(M3) IM(ϵab)=papa..papb..pbpaI^M(\epsilon ab) = \Diamond p_a \supset p_a . \wedge . \Box p_a \supset \Box p_b .\wedge . \Diamond p_b \supset p_a,where pap_a and pbp_b are propositional variables corresponding to the name variables aa and bb, respectively. In the last, we shall give some comments including some open problems and my conjectures
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