Coordinated regulation of <scp>TORC2</scp> signaling by <scp>MCC</scp>/eisosome‐associated proteins, Pil1 and tetraspan membrane proteins during the stress response

  • Ken‐taro Sakata
    Department of Applied Biological Science, Faculty of Agriculture Kagawa University Miki‐cho Japan
  • Keisuke Hashii
    Department of Applied Biological Science, Faculty of Agriculture Kagawa University Miki‐cho Japan
  • Koushiro Yoshizawa
    Department of Applied Biological Science, Faculty of Agriculture Kagawa University Miki‐cho Japan
  • Yuhei O. Tahara
    Department of Biology, Graduate School of Science Osaka Metropolitan University Osaka Japan
  • Kaori Yae
    Department of Applied Biological Science, Faculty of Agriculture Kagawa University Miki‐cho Japan
  • Ryohei Tsuda
    Department of Applied Biological Science, Faculty of Agriculture Kagawa University Miki‐cho Japan
  • Naotaka Tanaka
    Department of Applied Biological Science, Faculty of Agriculture Kagawa University Miki‐cho Japan
  • Tatsuya Maeda
    Department of Biology Hamamatsu University School of Medicine, Handayama Hamamatsu Japan
  • Makoto Miyata
    Department of Biology, Graduate School of Science Osaka Metropolitan University Osaka Japan
  • Mitsuaki Tabuchi
    Department of Applied Biological Science, Faculty of Agriculture Kagawa University Miki‐cho Japan

抄録

<jats:title>Abstract</jats:title><jats:p>MCCs are linear invaginations of the yeast plasma membrane that form stable membrane microdomains. Although over 20 proteins are localized in the MCCs, it is not well understood how these proteins coordinately maintain normal MCC function. Pil1 is a core eisosome protein and is responsible for MCC‐invaginated structures. In addition, six‐tetraspan membrane proteins (6‐Tsp) are localized in the MCCs and classified into two families, the Sur7 family and Nce102 family. To understand the coordinated function of these MCC proteins, single and multiple deletion mutants of Pil1 and 6‐Tsp were generated and their MCC structure and growth under various stresses were investigated. Genetic interaction analysis revealed that the Sur7 family and Nce102 function in stress tolerance and normal eisosome assembly, respectively, by cooperating with Pil1. To further understand the role of MCCs/eisosomes in stress tolerance, we screened for suppressor mutants using the SDS‐sensitive phenotype of <jats:italic>pil1</jats:italic>Δ <jats:italic>6‐tsp</jats:italic>Δ cells. This revealed that SDS sensitivity is caused by hyperactivation of Tor kinase complex 2 (TORC2)‐Ypk1 signaling. Interestingly, inhibition of sphingolipid metabolism, a well‐known downstream pathway of TORC2‐Ypk1 signaling, did not rescue the SDS‐sensitivity of <jats:italic>pil1</jats:italic>Δ <jats:italic>6‐tsp</jats:italic>Δ cells. These results suggest that Pil1 and 6‐Tsp cooperatively regulate TORC2 signaling during the stress response.</jats:p>

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