Deletion of PIN4 Suppresses the Protein Transport Defects Caused by sec12-4 Mutation in Saccharomyces cerevisiae

Newly synthesized secretory proteins are released into the lumen of the endoplasmic reticulum (ER). The secretory proteins are surrounded by coat protein complex II (COPII) vesicles, and transported from the ER and reach their destinations through the Golgi apparatus. Sec12p is a guanine nucleotide...

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Published inMicrobial Physiology Vol. 30; no. 1-6; pp. 25 - 35
Main Authors Murakami-Sekimata, Akiko, Sekimata, Masayuki, Sato, Natsumi, Hayasaka, Yuto, Nakano, Akihiko
Format Journal Article
LanguageEnglish
Published Basel, Switzerland S. Karger AG 01.12.2020
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ISSN2673-1665
2673-1673
DOI10.1159/000509633

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Abstract Newly synthesized secretory proteins are released into the lumen of the endoplasmic reticulum (ER). The secretory proteins are surrounded by coat protein complex II (COPII) vesicles, and transported from the ER and reach their destinations through the Golgi apparatus. Sec12p is a guanine nucleotide exchange factor for Sar1p, which initiates COPII vesicle budding from the ER. The activation of Sar1p by Sec12p and the subsequent COPII coat assembly have been well characterized, but the events that take place upstream of Sec12p remain unclear. In this study, we isolated the novel extragenic suppressor of sec12-4, PIN4/MDT1, a cell cycle checkpoint target. A yeast two-hybrid screening was used to identify Pin4/Mdt1p as a binding partner of the casein kinase I isoform Hrr25p, which we have previously identified as a modulator of Sec12p function. Deletion of PIN4 suppressed both defects of temperature-sensitive growth and the partial protein transport observed in sec12-4 mutants. The results of this study suggest that Pin4p provides novel aspects of Sec12p modulations.
AbstractList Newly synthesized secretory proteins are released into the lumen of the endoplasmic reticulum (ER). The secretory proteins are surrounded by coat protein complex II (COPII) vesicles, and transported from the ER and reach their destinations through the Golgi apparatus. Sec12p is a guanine nucleotide exchange factor for Sar1p, which initiates COPII vesicle budding from the ER. The activation of Sar1p by Sec12p and the subsequent COPII coat assembly have been well characterized, but the events that take place upstream of Sec12p remain unclear. In this study, we isolated the novel extragenic suppressor of sec12-4, PIN4/MDT1, a cell cycle checkpoint target. A yeast two-hybrid screening was used to identify Pin4/Mdt1p as a binding partner of the casein kinase I isoform Hrr25p, which we have previously identified as a modulator of Sec12p function. Deletion of PIN4 suppressed both defects of temperature-sensitive growth and the partial protein transport observed in sec12-4 mutants. The results of this study suggest that Pin4p provides novel aspects of Sec12p modulations.
Newly synthesized secretory proteins are released into the lumen of the endoplasmic reticulum (ER). The secretory proteins are surrounded by coat protein complex II (COPII) vesicles, and transported from the ER and reach their destinations through the Golgi apparatus. Sec12p is a guanine nucleotide exchange factor for Sar1p, which initiates COPII vesicle budding from the ER. The activation of Sar1p by Sec12p and the subsequent COPII coat assembly have been well characterized, but the events that take place upstream of Sec12p remain unclear. In this study, we isolated the novel extragenic suppressor of sec12-4, PIN4/MDT1, a cell cycle checkpoint target. A yeast two-hybrid screening was used to identify Pin4/Mdt1p as a binding partner of the casein kinase I isoform Hrr25p, which we have previously identified as a modulator of Sec12p function. Deletion of PIN4 suppressed both defects of temperature-sensitive growth and the partial protein transport observed in sec12-4 mutants. The results of this study suggest that Pin4p provides novel aspects of Sec12p modulations. Keywords: Yeast, Membrane traffic, Protein transport, Cell cycle checkpoint
Audience Academic
Author Sekimata, Masayuki
Sato, Natsumi
Murakami-Sekimata, Akiko
Hayasaka, Yuto
Nakano, Akihiko
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  email: *Akiko Murakami-Sekimata, Division of Theoretical Nursing and Genetics, Graduate School of Medical Science, Yamagata University Faculty of Medicine, Iida-Nishi 2-2-2, Yamagata 990-9585 (Japan), s.akiko@med.id.yamagata-u.ac.jp
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  surname: Sekimata
  fullname: Sekimata, Masayuki
  email: *Akiko Murakami-Sekimata, Division of Theoretical Nursing and Genetics, Graduate School of Medical Science, Yamagata University Faculty of Medicine, Iida-Nishi 2-2-2, Yamagata 990-9585 (Japan), s.akiko@med.id.yamagata-u.ac.jp
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Issue 1-6
Keywords Cell cycle checkpoint
Membrane traffic
Yeast
Protein transport
Language English
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Snippet Newly synthesized secretory proteins are released into the lumen of the endoplasmic reticulum (ER). The secretory proteins are surrounded by coat protein...
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SubjectTerms B cells
Genetic aspects
Proteins
Research Article
Title Deletion of PIN4 Suppresses the Protein Transport Defects Caused by sec12-4 Mutation in Saccharomyces cerevisiae
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https://www.ncbi.nlm.nih.gov/pubmed/32958726
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