2017
DOI: 10.1534/genetics.116.196428
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Evidence for Amino Acid Snorkeling from a High-Resolution,In VivoAnalysis of Fis1 Tail-Anchor Insertion at the Mitochondrial Outer Membrane

Abstract: Proteins localized to mitochondria by a carboxyl-terminal tail anchor (TA) play roles in apoptosis, mitochondrial dynamics, and mitochondrial protein import. To reveal characteristics of TAs that may be important for mitochondrial targeting, we focused our attention upon the TA of the Saccharomyces cerevisiae Fis1 protein. Specifically, we generated a library of Fis1p TA variants fused to the Gal4 transcription factor, then, using next-generation sequencing, revealed which Fis1p TA mutations inhibited membrane… Show more

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Cited by 27 publications
(40 citation statements)
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“…Failure of this fusion protein to insert at its target membrane can allow the Gal4-linked fusion protein to access the nucleus and activate Gal4-responsive promoters that drive proliferation under selective conditions. As previously demonstrated [21], while a membrane-sequestered Gal4-sfGFP-Fis1 fusion protein did not lead to a proliferation defect on non-selective medium (SC-Trp), cells carrying this construct could not survive on medium requiring activation of a Gal4p-driven HIS3 gene (SMM-His+20mM 3-AT) (Fig. 2).…”
Section: Resultssupporting
confidence: 75%
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“…Failure of this fusion protein to insert at its target membrane can allow the Gal4-linked fusion protein to access the nucleus and activate Gal4-responsive promoters that drive proliferation under selective conditions. As previously demonstrated [21], while a membrane-sequestered Gal4-sfGFP-Fis1 fusion protein did not lead to a proliferation defect on non-selective medium (SC-Trp), cells carrying this construct could not survive on medium requiring activation of a Gal4p-driven HIS3 gene (SMM-His+20mM 3-AT) (Fig. 2).…”
Section: Resultssupporting
confidence: 75%
“…Because Fis1p is required for mitochondrial fission in S. cerevisiae , mutants lacking this protein manifest a highly interconnected network of mitochondria due to unbalanced mitochondrial fusion [23-25]. As expected, expression of wild-type Fis1p restored normal mitochondrial distribution in this genetic background, while Fis1p prevented from mitochondrial insertion by a A144D substitution within the Fis1p TA [21] could not restore normal mitochondrial morphology (Figs. 3A and 3B).…”
Section: Resultsmentioning
confidence: 84%
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