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However, the mechanism underlying disease pathogenesis is still unclear. The Senataxin N\u2010terminal protein\u2010interaction and C\u2010terminal<jats:styled-content style=\"fixed-case\">RNA<\/jats:styled-content>\/<jats:styled-content style=\"fixed-case\">DNA<\/jats:styled-content>helicase domains are conserved in the<jats:italic>Saccharomyces cerevisiae<\/jats:italic>homolog, Sen1p. Using genome\u2010wide expression analysis, we first show alterations in key cellular pathways such as: redox, unfolded protein response, and<jats:styled-content style=\"fixed-case\">TOR<\/jats:styled-content>in the yeast<jats:italic>sen1 \u0394N<\/jats:italic>mutant (N\u2010terminal truncation). This mutant exhibited growth defects on nonfermentable carbon sources, was sensitive to oxidative stress, and showed severe loss of mitochondrial<jats:styled-content style=\"fixed-case\">DNA<\/jats:styled-content>. The growth defect could be partially rescued upon supplementation with reducing agents and antioxidants. Furthermore, the mutant showed higher levels of reactive oxygen species, lower<jats:styled-content style=\"fixed-case\">UPR<\/jats:styled-content>activity, and alterations in mitochondrial membrane potential, increase in vacuole acidity, free calcium ions in the cytosol, and resistance to rapamycin treatment. Notably, the<jats:italic>sen1 \u2206N<\/jats:italic>mutant showed increased cell death and shortened chronological life span. Given the strong similarity of the yeast and human Sen1 proteins, our study thus provides a mechanism for the progressive neurological disorders associated with mutations in human senataxin.<\/jats:p>","DOI":"10.1111\/febs.13917","type":"journal-article","created":{"date-parts":[[2016,10,13]],"date-time":"2016-10-13T06:48:50Z","timestamp":1476341330000},"page":"4056-4083","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":34,"title":["Sen1, the homolog of human Senataxin, is critical for cell survival through regulation of redox homeostasis, mitochondrial function, and the<scp>TOR<\/scp>pathway in<i>Saccharomyces cerevisiae<\/i>"],"prefix":"10.1111","volume":"283","author":[{"given":"Santhosh Kumar","family":"Sariki","sequence":"first","affiliation":[{"name":"Laboratory of Chromatin Biology Department of Biological Sciences Indian Institute of Science Education and Research Bhopal 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