Role of <i>SSD1</i> in Phenotypic Variation of <i>Saccharomyces cerevisiae</i> Strains Lacking <i>DEG1</i>-Dependent Pseudouridylation
Yeast phenotypes associated with the lack of wobble uridine (U<sub>34</sub>) modifications in tRNA were shown to be modulated by an allelic variation of <i>SSD1</i>, a gene encoding an mRNA-binding protein. We demonstrate that phenotypes caused by the loss of Deg1-dependent t...
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2021-08-01
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author | Bahar Khonsari Roland Klassen Raffael Schaffrath |
author_facet | Bahar Khonsari Roland Klassen Raffael Schaffrath |
author_sort | Bahar Khonsari |
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description | Yeast phenotypes associated with the lack of wobble uridine (U<sub>34</sub>) modifications in tRNA were shown to be modulated by an allelic variation of <i>SSD1</i>, a gene encoding an mRNA-binding protein. We demonstrate that phenotypes caused by the loss of Deg1-dependent tRNA pseudouridylation are similarly affected by <i>SSD1</i> allelic status. Temperature sensitivity and protein aggregation are elevated in <i>deg1</i> mutants and further increased in the presence of the <i>ssd1-d</i> allele, which encodes a truncated form of Ssd1. In addition, chronological lifespan is reduced in a <i>deg1 ssd1-d</i> mutant, and the negative genetic interactions of the U<sub>34</sub> modifier genes <i>ELP3</i> and <i>URM1</i> with <i>DEG1</i> are aggravated by <i>ssd1-d</i>. A loss of function mutation in <i>SSD1</i>, <i>ELP3</i>, and <i>DEG1</i> induces pleiotropic and overlapping phenotypes, including sensitivity against target of rapamycin (TOR) inhibitor drug and cell wall stress by calcofluor white. Additivity in <i>ssd1 deg1</i> double mutant phenotypes suggests independent roles of Ssd1 and tRNA modifications in TOR signaling and cell wall integrity. However, other tRNA modification defects cause growth and drug sensitivity phenotypes, which are not further intensified in tandem with <i>ssd1-d</i>. Thus, we observed a modification-specific rather than general effect of <i>SSD1</i> status on phenotypic variation in tRNA modification mutants. Our results highlight how the cellular consequences of tRNA modification loss can be influenced by protein targeting specific mRNAs. |
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spelling | doaj.art-1e9aa0f20bf548ff82ece77107dba5972023-11-22T08:00:01ZengMDPI AGInternational Journal of Molecular Sciences1661-65961422-00672021-08-012216875310.3390/ijms22168753Role of <i>SSD1</i> in Phenotypic Variation of <i>Saccharomyces cerevisiae</i> Strains Lacking <i>DEG1</i>-Dependent PseudouridylationBahar Khonsari0Roland Klassen1Raffael Schaffrath2Institut für Biologie, Fachgebiet Mikrobiologie, Universität Kassel, Heinrich-Plett-Str. 40, D-34132 Kassel, GermanyInstitut für Biologie, Fachgebiet Mikrobiologie, Universität Kassel, Heinrich-Plett-Str. 40, D-34132 Kassel, GermanyInstitut für Biologie, Fachgebiet Mikrobiologie, Universität Kassel, Heinrich-Plett-Str. 40, D-34132 Kassel, GermanyYeast phenotypes associated with the lack of wobble uridine (U<sub>34</sub>) modifications in tRNA were shown to be modulated by an allelic variation of <i>SSD1</i>, a gene encoding an mRNA-binding protein. We demonstrate that phenotypes caused by the loss of Deg1-dependent tRNA pseudouridylation are similarly affected by <i>SSD1</i> allelic status. Temperature sensitivity and protein aggregation are elevated in <i>deg1</i> mutants and further increased in the presence of the <i>ssd1-d</i> allele, which encodes a truncated form of Ssd1. In addition, chronological lifespan is reduced in a <i>deg1 ssd1-d</i> mutant, and the negative genetic interactions of the U<sub>34</sub> modifier genes <i>ELP3</i> and <i>URM1</i> with <i>DEG1</i> are aggravated by <i>ssd1-d</i>. A loss of function mutation in <i>SSD1</i>, <i>ELP3</i>, and <i>DEG1</i> induces pleiotropic and overlapping phenotypes, including sensitivity against target of rapamycin (TOR) inhibitor drug and cell wall stress by calcofluor white. Additivity in <i>ssd1 deg1</i> double mutant phenotypes suggests independent roles of Ssd1 and tRNA modifications in TOR signaling and cell wall integrity. However, other tRNA modification defects cause growth and drug sensitivity phenotypes, which are not further intensified in tandem with <i>ssd1-d</i>. Thus, we observed a modification-specific rather than general effect of <i>SSD1</i> status on phenotypic variation in tRNA modification mutants. Our results highlight how the cellular consequences of tRNA modification loss can be influenced by protein targeting specific mRNAs.https://www.mdpi.com/1422-0067/22/16/8753yeast<i>SSD1</i>pseudouridinetRNA modification |
spellingShingle | Bahar Khonsari Roland Klassen Raffael Schaffrath Role of <i>SSD1</i> in Phenotypic Variation of <i>Saccharomyces cerevisiae</i> Strains Lacking <i>DEG1</i>-Dependent Pseudouridylation International Journal of Molecular Sciences yeast <i>SSD1</i> pseudouridine tRNA modification |
title | Role of <i>SSD1</i> in Phenotypic Variation of <i>Saccharomyces cerevisiae</i> Strains Lacking <i>DEG1</i>-Dependent Pseudouridylation |
title_full | Role of <i>SSD1</i> in Phenotypic Variation of <i>Saccharomyces cerevisiae</i> Strains Lacking <i>DEG1</i>-Dependent Pseudouridylation |
title_fullStr | Role of <i>SSD1</i> in Phenotypic Variation of <i>Saccharomyces cerevisiae</i> Strains Lacking <i>DEG1</i>-Dependent Pseudouridylation |
title_full_unstemmed | Role of <i>SSD1</i> in Phenotypic Variation of <i>Saccharomyces cerevisiae</i> Strains Lacking <i>DEG1</i>-Dependent Pseudouridylation |
title_short | Role of <i>SSD1</i> in Phenotypic Variation of <i>Saccharomyces cerevisiae</i> Strains Lacking <i>DEG1</i>-Dependent Pseudouridylation |
title_sort | role of i ssd1 i in phenotypic variation of i saccharomyces cerevisiae i strains lacking i deg1 i dependent pseudouridylation |
topic | yeast <i>SSD1</i> pseudouridine tRNA modification |
url | https://www.mdpi.com/1422-0067/22/16/8753 |
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