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In Saccharomyces cerevisiae, the molecular chaperone proteins Ssb1 and Ssb2 upregulate ABC transporter genes, and their upregulation may play a role in the release of quorum-sensing molecules that induce cell growth arrest during the diauxic shift

  • Received: 09 May 2025 Revised: 18 July 2025 Accepted: 25 July 2025 Published: 02 September 2025
  • In Saccharomyces cerevisiae, the molecular chaperone proteins Ssb1 and Ssb2 (Ssb1/2) and the cochaperone ribosome-associated complex (Zuo1 and Ssz1) localize around the ribosome tunnel exit, assisting in the maturation of nascent polypeptides. Exogenous expression of the Zuo1 C-terminus or the Ssz1 N-terminus—but not Ssb1/2—independently activates the transcription factor Pdr1 (but not Pdr3), enhances the transcription of the ATP-binding cassette (ABC) transporter genes PDR5, SNQ2, and YOR1, and increases pleiotropic drug resistance. Furthermore, upregulation of ABC transporter genes by ZUO1 and SSZ1 leads to the release of quorum-sensing molecules, which cause cell growth arrest during diauxic shifts. In this study, we examined whether SSB1/2 are required for the expression of ABC transporter genes and the release of quorum-sensing molecules that lead to cell growth arrest during diauxic shifts. Our results show that Ssb1/2 increased the mRNA levels of PDR5, SNQ2, and YOR1 during the late logarithmic growth phase and increased resistance to cycloheximide and fluconazole, possibly via the same pathway as Zuo1 or Ssz1. Furthermore, Ssb1/2 induced PDR5 expression and resistance to cycloheximide and fluconazole, possibly via the same pathway as Pdr3 (but not Pdr1). In addition, it was suggested that Ssb1/2 are involved in the release of quorum-sensing molecules into the culture medium, which could signal cell growth arrest during diauxic shifts. This work provides useful knowledge regarding genetic interactions between the ribosome-associated molecular chaperone and cell growth arrest during diauxic shifts.

    Citation: Yoichi Yamada, Mahiro Ota, Atsuki Shiroma, Takaki Matsuzawa. In Saccharomyces cerevisiae, the molecular chaperone proteins Ssb1 and Ssb2 upregulate ABC transporter genes, and their upregulation may play a role in the release of quorum-sensing molecules that induce cell growth arrest during the diauxic shift[J]. AIMS Microbiology, 2025, 11(3): 737-753. doi: 10.3934/microbiol.2025031

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  • In Saccharomyces cerevisiae, the molecular chaperone proteins Ssb1 and Ssb2 (Ssb1/2) and the cochaperone ribosome-associated complex (Zuo1 and Ssz1) localize around the ribosome tunnel exit, assisting in the maturation of nascent polypeptides. Exogenous expression of the Zuo1 C-terminus or the Ssz1 N-terminus—but not Ssb1/2—independently activates the transcription factor Pdr1 (but not Pdr3), enhances the transcription of the ATP-binding cassette (ABC) transporter genes PDR5, SNQ2, and YOR1, and increases pleiotropic drug resistance. Furthermore, upregulation of ABC transporter genes by ZUO1 and SSZ1 leads to the release of quorum-sensing molecules, which cause cell growth arrest during diauxic shifts. In this study, we examined whether SSB1/2 are required for the expression of ABC transporter genes and the release of quorum-sensing molecules that lead to cell growth arrest during diauxic shifts. Our results show that Ssb1/2 increased the mRNA levels of PDR5, SNQ2, and YOR1 during the late logarithmic growth phase and increased resistance to cycloheximide and fluconazole, possibly via the same pathway as Zuo1 or Ssz1. Furthermore, Ssb1/2 induced PDR5 expression and resistance to cycloheximide and fluconazole, possibly via the same pathway as Pdr3 (but not Pdr1). In addition, it was suggested that Ssb1/2 are involved in the release of quorum-sensing molecules into the culture medium, which could signal cell growth arrest during diauxic shifts. This work provides useful knowledge regarding genetic interactions between the ribosome-associated molecular chaperone and cell growth arrest during diauxic shifts.



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    Acknowledgments


    We thank Taichi Nomura and Myu Oie at the School of Biological Science and Technology, Kanazawa University, for technical support. This work was supported by JSPS KAKENHI Grant Number 24K08828.
    Conflict of interest



    The authors declare no conflict of interest.

    Author contributions



    Y.Y. conceived, designed, and supervised the study. Y.Y. wrote the manuscript. Y.Y. and M.O. were responsible for acquiring yeast gene deletion mutants and performing spot dilution assays. Y.Y. conducted the real-time RT–PCR experiments. A.S. and T.M. generated the growth curves of the yeast strains. All authors reviewed and approved the final version of the manuscript.

    Additional information



    Supplementary Information accompanies this paper.
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