2
views
0
recommends
+1 Recommend
0 collections
    0
    shares
      • Record: found
      • Abstract: found
      • Article: not found

      Caenorhabditis elegans homologue of Prox1/Prospero is expressed in the glia and is required for sensory behavior and cold tolerance.

      Read this article at

      ScienceOpenPublisherPubMed
      Bookmark
          There is no author summary for this article yet. Authors can add summaries to their articles on ScienceOpen to make them more accessible to a non-specialist audience.

          Abstract

          The Caenorhabditis elegans (C. elegans) amphid sensory organ contains only 4 glia-like cells and 24 sensory neurons, providing a simple model for analyzing glia or neuron-glia interactions. To better characterize glial development and function, we carried out RNA interference screening for transcription factors that regulate the expression of an amphid sheath glial cell marker and identified pros-1, which encodes a homeodomain transcription factor homologous to Drosophila prospero/mammalian Prox1, as a positive regulator. The functional PROS-1::EGFP fusion protein was localized in the nuclei of the glia and the excretory cell but not in the amphid sensory neurons. pros-1 deletion mutants exhibited larval lethality, and rescue experiments showed that pros-1 and human Prox1 transgenes were able to rescue the larval lethal phenotype, suggesting that pros-1 is a functional homologue of mammalian Prox1, at least partially. We further found that the structure and functions of sensory neurons, such as the morphology of sensory endings, sensory behavior and sensory-mediated cold tolerance, appeared to be affected by the pros-1 RNAi. Together, our results show that the C. elegans PROS-1 is a transcriptional regulator in the glia but is involved not only in sensory behavior but also in sensory-mediated physiological tolerance.

          Related collections

          Author and article information

          Journal
          Genes Cells
          Genes to cells : devoted to molecular & cellular mechanisms
          Wiley
          1365-2443
          1356-9597
          Sep 2016
          : 21
          : 9
          Affiliations
          [1 ] Department of Physiology, Tokyo Women's Medical University School of Medicine, Tokyo, 162-8666, Japan.
          [2 ] The OCU Advanced Research Institute for Natural Science and Technology, Osaka City University, Osaka, 558-8585, Japan.
          [3 ] Graduate School of Human Life Science, Osaka City University, Osaka, 558-8585, Japan.
          [4 ] Laboratory of Molecular and Cellular Regulation, Faculty of Science and Engineering, and Institute for Integrative Neurobiology, Konan University, Kobe, 658-8501, Japan.
          [5 ] Department of Physiology, Tokyo Women's Medical University School of Medicine, Tokyo, 162-8666, Japan. mitani.shohei@twmu.ac.jp.
          Article
          10.1111/gtc.12394
          27402188
          e5cf1384-c455-44d3-940e-c9a8fc675d0f
          History

          Comments

          Comment on this article