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      TEG-1 CD2BP2 regulates stem cell proliferation and sex determination in the C. elegans germ line and physically interacts with the UAF-1 U2AF65 splicing factor.

      Developmental Dynamics
      Adaptor Proteins, Signal Transducing, genetics, metabolism, Alleles, Alternative Splicing, Amino Acid Sequence, Animals, Caenorhabditis elegans, embryology, Caenorhabditis elegans Proteins, Carrier Proteins, Cell Differentiation, Cell Nucleus, Cell Proliferation, Female, Germ Cells, growth & development, Humans, Male, Meiosis, Molecular Sequence Data, Mutation, Nuclear Proteins, Ribonucleoproteins, Sex Determination Processes, Stem Cells, cytology, physiology

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          Abstract

          For a stem cell population to exist over an extended period, a balance must be maintained between self-renewing (proliferating) and differentiating daughter cells. Within the Caenorhabditis elegans germ line, this balance is controlled by a genetic regulatory pathway, which includes the canonical Notch signaling pathway. Genetic screens identified the gene teg-1 as being involved in regulating the proliferation versus differentiation decision in the C. elegans germ line. Cloning of TEG-1 revealed that it is a homolog of mammalian CD2BP2, which has been implicated in a number of cellular processes, including in U4/U6.U5 tri-snRNP formation in the pre-mRNA splicing reaction. The position of teg-1 in the genetic pathway regulating the proliferation versus differentiation decision, its single mutant phenotype, and its enrichment in nuclei, all suggest TEG-1 also functions as a splicing factor. TEG-1, as well as its human homolog, CD2BP2, directly bind to UAF-1 U2AF65, a component of the U2 auxiliary factor. TEG-1 functions as a splicing factor and acts to regulate the proliferation versus meiosis decision. The interaction of TEG-1 CD2BP2 with UAF-1 U2AF65, combined with its previously described function in U4/U6.U5 tri-snRNP, suggests that TEG-1 CD2BP2 functions in two distinct locations in the splicing cascade. Copyright © 2012 Wiley Periodicals, Inc.

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